Synaptic Transmission
Excitatory Postsynaptic Potentials
Synapses
Hippocampus
Presynaptic Terminals
Patch-Clamp Techniques
Neurons
Glutamic Acid
Receptors, AMPA
Neuronal Plasticity
Neural Inhibition
Long-Term Potentiation
Disease Transmission, Infectious
Excitatory Amino Acid Antagonists
Inhibitory Postsynaptic Potentials
Receptors, N-Methyl-D-Aspartate
Rats, Sprague-Dawley
Infectious Disease Transmission, Vertical
Action Potentials
Evoked Potentials
Electrophysiology
6-Cyano-7-nitroquinoxaline-2,3-dione
Neurotransmitter Agents
Synaptic Vesicles
Microscopy, Electron, Transmission
Receptors, Glutamate
GABA Antagonists
Pyramidal Cells
Receptors, Metabotropic Glutamate
2-Amino-5-phosphonovalerate
Miniature Postsynaptic Potentials
Calcium
Rats, Wistar
Membrane Potentials
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
Receptors, GABA-A
Bicuculline
Interneurons
Long-Term Synaptic Depression
Receptors, Presynaptic
CA1 Region, Hippocampal
Receptors, Kainic Acid
Tetrodotoxin
Organ Culture Techniques
Picrotoxin
Calcium Channels, N-Type
Excitatory Amino Acid Agents
Spinal Cord
Receptors, GABA-B
N-Methylaspartate
Cells, Cultured
Mossy Fibers, Hippocampal
Posterior Horn Cells
Brain Stem
Calcium Channels, P-Type
Glycine
Calcium Channels
Aminobutyrates
Synaptic Membranes
Models, Neurological
GABA-A Receptor Antagonists
Insect Vectors
Dendrites
Mice, Knockout
Post-Synaptic Density
Kainic Acid
Cycloleucine
Spider Venoms
Strychnine
Cerebral Cortex
Synapsins
Glycine Agents
Solitary Nucleus
Amygdala
Receptors, GABA
Calcium Channel Blockers
Dose-Response Relationship, Drug
Baclofen
Microscopy, Electron, Scanning Transmission
Cannabinoid Receptor Modulators
Cerebellum
Receptors, Nicotinic
Receptors, Glycine
Dendritic Spines
omega-Conotoxin GVIA
Sodium Channel Blockers
Ganglia, Autonomic
Nerve Net
Dentate Gyrus
Dopamine
Endocannabinoids
Receptor, Cannabinoid, CB1
Substantia Gelatinosa
Synaptophysin
Receptors, Neurotransmitter
Phosphinic Acids
Perforant Pathway
HIV Infections
Larva
Chelating Agents
Acetylcholine
Mutation
GABA Agonists
Nerve Endings
Receptor, Adenosine A1
Microscopy, Electron
Ganglia, Invertebrate
Afferent Pathways
Calcium Signaling
Molecular Sequence Data
CA3 Region, Hippocampal
Vesicular Inhibitory Amino Acid Transport Proteins
omega-Agatoxin IVA
Green Fluorescent Proteins
Brain
Exocytosis
Disease Outbreaks
Serotonin
Protein Subunits
Mice, Transgenic
Naphthalenes
Astacoidea
Pregnancy Complications, Infectious
Nerve Fibers
Synaptotagmins
Brain-Derived Neurotrophic Factor
Vesicular Glutamate Transport Protein 1
Adenosine
Analysis of Variance
Periaqueductal Gray
Glutamates
Neocortex
Electrical Synapses
Leeches
Synaptosomes
Cochlear Nucleus
Retina
Cell Adhesion Molecules, Neuronal
Purinergic P1 Receptor Antagonists
Drug Interactions
Methoxyhydroxyphenylglycol
Lampreys
Auditory Pathways
Thalamus
Curare
Models, Biological
Signal Transduction
SNARE Proteins
Benzothiadiazines
Membrane Proteins
Animals, Genetically Modified
Guinea Pigs
Hirudo medicinalis
Corpus Striatum
Xanthenes
Disease Vectors
Ganglia
Zoonoses
Drosophila
Ion Channel Gating
Calcium Channels, R-Type
Immunohistochemistry
Ganglia, Sympathetic
Receptors, Cannabinoid
Septal Nuclei
Nicotinic Antagonists
Cats
Neostriatum
Vesicular Transport Proteins
Disease Reservoirs
Developmental synaptic changes increase the range of integrative capabilities of an identified excitatory neocortical connection. (1/11810)
Excitatory synaptic transmission between pyramidal cells and fast-spiking (FS) interneurons of layer V of the motor cortex was investigated in acute slices by using paired recordings at 30 degrees C combined with morphological analysis. The presynaptic and postsynaptic properties at these identified central synapses were compared between 3- and 5-week-old rats. At these two postnatal developmental stages, unitary EPSCs were mediated by the activation of AMPA receptors with fast kinetics at a holding potential of -72 mV. The amplitude distribution analysis of the EPSCs indicates that, at both stages, pyramidal-FS connections consisted of multiple functional release sites. The apparent quantal size obtained by decreasing the external calcium ([Ca2+]e) varied from 11 to 29 pA near resting membrane potential. In young rats, pairs of presynaptic action potentials elicited unitary synaptic responses that displayed paired-pulse depression at all tested frequencies. In older animals, inputs from different pyramidal cells onto the same FS interneuron had different paired-pulse response characteristics and, at most of these connections, a switch from depression to facilitation occurred when decreasing the rate of presynaptic stimulation. The balance between facilitation and depression endows pyramidal-FS connections from 5-week-old animals with wide integrative capabilities and confers unique functional properties to each synapse. (+info)Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine. (2/11810)
In a slice preparation of rat visual cortex, we discovered that paired-pulse stimulation (PPS) elicits a form of homosynaptic long-term depression (LTD) in the superficial layers when carbachol (CCh) or norepinephrine (NE) is applied concurrently. PPS by itself, or CCh and NE in the absence of synaptic stimulation, produced no lasting change. The LTD induced by PPS in the presence of NE or CCh is of comparable magnitude with that obtained with prolonged low-frequency stimulation (LFS) but requires far fewer stimulation pulses (40 vs 900). The cholinergic facilitation of LTD was blocked by atropine and pirenzepine, suggesting involvement of M1 receptors. The noradrenergic facilitation of LTD was blocked by urapidil and was mimicked by methoxamine, suggesting involvement of alpha1 receptors. beta receptor agonists and antagonists were without effect. Induction of LTD by PPS was inhibited by NMDA receptor blockers (completely in the case of NE; partially in the case of CCh), suggesting that one action of the modulators is to control the gain of NMDA receptor-dependent homosynaptic LTD in visual cortex. We propose that this is a mechanism by which cholinergic and noradrenergic inputs to the neocortex modulate naturally occurring receptive field plasticity. (+info)Activity-dependent metaplasticity of inhibitory and excitatory synaptic transmission in the lamprey spinal cord locomotor network. (3/11810)
Paired intracellular recordings have been used to examine the activity-dependent plasticity and neuromodulator-induced metaplasticity of synaptic inputs from identified inhibitory and excitatory interneurons in the lamprey spinal cord. Trains of spikes at 5-20 Hz were used to mimic the frequency of spiking that occurs in network interneurons during NMDA or brainstem-evoked locomotor activity. Inputs from inhibitory and excitatory interneurons exhibited similar activity-dependent changes, with synaptic depression developing during the spike train. The level of depression reached was greater with lower stimulation frequencies. Significant activity-dependent depression of inputs from excitatory interneurons and inhibitory crossed caudal interneurons, which are central elements in the patterning of network activity, usually developed between the fifth and tenth spikes in the train. Because these interneurons typically fire bursts of up to five spikes during locomotor activity, this activity-dependent plasticity will presumably not contribute to the patterning of network activity. However, in the presence of the neuromodulators substance P and 5-HT, significant activity-dependent metaplasticity of these inputs developed over the first five spikes in the train. Substance P induced significant activity-dependent depression of inhibitory but potentiation of excitatory interneuron inputs, whereas 5-HT induced significant activity-dependent potentiation of both inhibitory and excitatory interneuron inputs. Because these metaplastic effects are consistent with the substance P and 5-HT-induced modulation of the network output, activity-dependent metaplasticity could be a potential mechanism underlying the coordination and modulation of rhythmic network activity. (+info)even-skipped determines the dorsal growth of motor axons in Drosophila. (4/11810)
Axon pathfinding and target choice are governed by cell type-specific responses to external cues. Here, we show that in the Drosophila embryo, motorneurons with targets in the dorsal muscle field express the homeobox gene even-skipped and that this expression is necessary and sufficient to direct motor axons into the dorsal muscle field. Previously, it was shown that motorneurons projecting to ventral targets express the LIM homeobox gene islet, which is sufficient to direct axons to the ventral muscle field. Thus, even-skipped complements the function of islet, and together these two genes constitute a bimodal switch regulating axonal growth and directing motor axons to ventral or to dorsal regions of the muscle field. (+info)Comparative effects of methylmercury on parallel-fiber and climbing-fiber responses of rat cerebellar slices. (5/11810)
The environmental neurotoxicant methylmercury (MeHg) causes profound disruption of cerebellar function. Previous studies have shown that acute exposure to MeHg impairs synaptic transmission in both the peripheral and central nervous systems. However, the effects of MeHg on cerebellar synaptic function have never been examined. In the present study, effects of acute exposure to MeHg on synaptic transmission between parallel fibers or climbing fibers and Purkinje cells were compared in 300- to 350-microm cerebellar slices by using extracellular and intracellular microelectrode-recording techniques. Field potentials of parallel-fiber volleys (PFVs) and the associated postsynaptic responses (PSRs) were recorded in the molecular layer by stimulating the parallel fibers in transverse cerebellar slices. The climbing-fiber responses were also recorded in the molecular layer by stimulating white matter in sagittal cerebellar slices. At 20, 100, and 500 microM, MeHg reduced the amplitude of both PFVs and the associated PSRs to complete block, however, it blocked PSRs more rapidly than PFVs. MeHg also decreased the amplitudes of climbing-fiber responses to complete block. For all responses, an initial increase in amplitude preceded MeHg-induced suppression. Intracellular recordings of excitatory postsynaptic potentials of Purkinje cells were compared before and after MeHg. At 100 microM and 20 microM, MeHg blocked the Na+-dependent, fast somatic spikes and Ca++-dependent, slow dendritic spike bursts. MeHg also hyperpolarized and then depolarized Purkinje cell membranes, suppressed current conduction from parallel fibers or climbing fibers to dendrites of Purkinje cells, and blocked synaptically activated local responses. MeHg switched the pattern of repetitive firing of Purkinje cells generated spontaneously or by depolarizing current injection at Purkinje cell soma from predominantly Na+-dependent, fast somatic spikes to predominantly Ca++-dependent, low amplitude, slow dendritic spike bursts. Thus, acute exposure to MeHg causes a complex pattern of effects on cerebellar synaptic transmission, with apparent actions on both neuronal excitability and chemical synaptic transmission. (+info)Impairment of neocortical long-term potentiation in mice deficient of endothelial nitric oxide synthase. (6/11810)
The role of the possible retrograde messenger nitric oxide (NO) in the induction of long-term potentiation (LTP) was studied in supragranular layers of somatosensory cortical slices obtained from adult mice. High-frequency stimulation produced a slowly rising, long-lasting (50 min) and significant (P < 0.001) increase in the extracellular synaptic response by 23%. The induction of LTP was independent from activation of N-methyl-D-aspartate (NMDA) receptors, but prevented by bath application of NG-nitro-L-arginine methyl ester (L-NAME), indicating that one or several of the different NO synthases (NOS) produced NO within the postsynaptic neuron. No LTP could be induced in knockout mice lacking the endothelial NOS (eNOS) isoform. These data suggest that eNOS is involved in an NMDA receptor-independent form of LTP in the rodent cerebral cortex. (+info)Actions of a pair of identified cerebral-buccal interneurons (CBI-8/9) in Aplysia that contain the peptide myomodulin. (7/11810)
A combination of biocytin back-fills of the cerebral-buccal connectives and immunocytochemistry of the cerebral ganglion demonstrated that of the 13 bilateral pairs of cerebral-buccal interneurons in the cerebral ganglion, a subpopulation of 3 are immunopositive for the peptide myomodulin. The present paper describes the properties of two of these cells, which we have termed CBI-8 and CBI-9. CBI-8 and CBI-9 were found to be dye coupled and electrically coupled. The cells have virtually identical properties, and consequently we consider them to be "twin" pairs and refer to them as CBI-8/9. CBI-8/9 were identified by electrophysiological criteria and then labeled with dye. Labeled cells were found to be immunopositive for myomodulin, and, using high pressure liquid chromatography, the cells were shown to contain authentic myomodulin. CBI-8/9 were found to receive synaptic input after mechanical stimulation of the tentacles. They also received excitatory input from C-PR, a neuron involved in neck lengthening, and received a slow inhibitory input from CC5, a cell involved in neck shortening, suggesting that CBI-8/9 may be active during forward movements of the head or buccal mass. Firing of CBI-8 or CBI-9 resulted in the activation of a relatively small number of buccal neurons as evidenced by extracellular recordings from buccal nerves. Firing also produced local movements of the buccal mass, in particular a strong contraction of the I7 muscle, which mediates radula opening. CBI-8/9 were found to produce a slow depolarization and rhythmic activity of B48, the motor neuron for the I7 muscle. The data provide continuing evidence that the small population of cerebral buccal interneurons is composed of neurons that are highly diverse in their functional roles. CBI-8/9 may function as a type of premotor neuron, or perhaps as a peptidergic modulatory neuron, the functions of which are dependent on the coactivity of other neurons. (+info)Voltage-dependent properties of dendrites that eliminate location-dependent variability of synaptic input. (8/11810)
We examined the hypothesis that voltage-dependent properties of dendrites allow for the accurate transfer of synaptic information to the soma independent of synapse location. This hypothesis is motivated by experimental evidence that dendrites contain a complex array of voltage-gated channels. How these channels affect synaptic integration is unknown. One hypothesized role for dendritic voltage-gated channels is to counteract passive cable properties, rendering all synapses electrotonically equidistant from the soma. With dendrites modeled as passive cables, the effect a synapse exerts at the soma depends on dendritic location (referred to as location-dependent variability of the synaptic input). In this theoretical study we used a simplified three-compartment model of a neuron to determine the dendritic voltage-dependent properties required for accurate transfer of synaptic information to the soma independent of synapse location. A dendrite that eliminates location-dependent variability requires three components: 1) a steady-state, voltage-dependent inward current that together with the passive leak current provides a net outward current and a zero slope conductance at depolarized potentials, 2) a fast, transient, inward current that compensates for dendritic membrane capacitance, and 3) both alpha amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid- and N-methyl-D-aspartate-like synaptic conductances that together permit synapses to behave as ideal current sources. These components are consistent with the known properties of dendrites. In addition, these results indicate that a dendrite designed to eliminate location-dependent variability also actively back-propagates somatic action potentials. (+info)HIV (human immunodeficiency virus) infection is a condition in which the body is infected with HIV, a type of retrovirus that attacks the body's immune system. HIV infection can lead to AIDS (acquired immunodeficiency syndrome), a condition in which the immune system is severely damaged and the body is unable to fight off infections and diseases.
There are several ways that HIV can be transmitted, including:
1. Sexual contact with an infected person
2. Sharing of needles or other drug paraphernalia with an infected person
3. Mother-to-child transmission during pregnancy, childbirth, or breastfeeding
4. Blood transfusions ( although this is rare in developed countries due to screening processes)
5. Organ transplantation (again, rare)
The symptoms of HIV infection can be mild at first and may not appear until several years after infection. These symptoms can include:
1. Fever
2. Fatigue
3. Swollen glands in the neck, armpits, and groin
4. Rash
5. Muscle aches and joint pain
6. Night sweats
7. Diarrhea
8. Weight loss
If left untreated, HIV infection can progress to AIDS, which is a life-threatening condition that can cause a wide range of symptoms, including:
1. Opportunistic infections (such as pneumocystis pneumonia)
2. Cancer (such as Kaposi's sarcoma)
3. Wasting syndrome
4. Neurological problems (such as dementia and seizures)
HIV infection is diagnosed through a combination of blood tests and physical examination. Treatment typically involves antiretroviral therapy (ART), which is a combination of medications that work together to suppress the virus and slow the progression of the disease.
Prevention methods for HIV infection include:
1. Safe sex practices, such as using condoms and dental dams
2. Avoiding sharing needles or other drug-injecting equipment
3. Avoiding mother-to-child transmission during pregnancy, childbirth, or breastfeeding
4. Post-exposure prophylaxis (PEP), which is a short-term treatment that can prevent infection after potential exposure to the virus
5. Pre-exposure prophylaxis (PrEP), which is a daily medication that can prevent infection in people who are at high risk of being exposed to the virus.
It's important to note that HIV infection is manageable with proper treatment and care, and that people living with HIV can lead long and healthy lives. However, it's important to be aware of the risks and take steps to prevent transmission.
1. Group B streptococcus (GBS): This type of bacterial infection is the leading cause of infections in newborns. GBS can cause a range of complications, including pneumonia, meningitis, and sepsis.
2. Urinary tract infections (UTIs): These are common during pregnancy and can be caused by bacteria such as Escherichia coli (E. coli) or Staphylococcus saprophyticus. UTIs can lead to complications such as preterm labor and low birth weight.
3. HIV: Pregnant women who are infected with HIV can pass the virus to their baby during pregnancy, childbirth, or breastfeeding.
4. Toxoplasmosis: This is an infection caused by a parasite that can be transmitted to the fetus through the placenta. Toxoplasmosis can cause a range of complications, including birth defects and stillbirth.
5. Listeriosis: This is a rare infection caused by eating contaminated food, such as soft cheeses or hot dogs. Listeriosis can cause complications such as miscarriage, stillbirth, and premature labor.
6. Influenza: Pregnant women who contract the flu can be at higher risk for complications such as pneumonia and hospitalization.
7. Herpes simplex virus (HSV): This virus can cause complications such as preterm labor, low birth weight, and neonatal herpes.
8. Human parvovirus (HPV): This virus can cause complications such as preterm labor, low birth weight, and stillbirth.
9. Syphilis: This is a sexually transmitted infection that can be passed to the fetus during pregnancy, leading to complications such as stillbirth, premature birth, and congenital syphilis.
10. Chickenpox: Pregnant women who contract chickenpox can be at higher risk for complications such as preterm labor and low birth weight.
It's important to note that the risks associated with these infections are relatively low, and many pregnant women who contract them will have healthy pregnancies and healthy babies. However, it's still important to be aware of the risks and take steps to protect yourself and your baby.
Here are some ways to reduce your risk of infection during pregnancy:
1. Practice good hygiene: Wash your hands frequently, especially before preparing or eating food.
2. Avoid certain foods: Avoid consuming raw or undercooked meat, eggs, and dairy products, as well as unpasteurized juices and soft cheeses.
3. Get vaccinated: Get vaccinated against infections such as the flu and HPV.
4. Practice safe sex: Use condoms or other forms of barrier protection to prevent the spread of STIs.
5. Avoid close contact with people who are sick: If someone in your household is sick, try to avoid close contact with them if possible.
6. Keep your environment clean: Regularly clean and disinfect surfaces and objects that may be contaminated with germs.
7. Manage stress: High levels of stress can weaken your immune system and make you more susceptible to infection.
8. Get enough rest: Adequate sleep is essential for maintaining a healthy immune system.
9. Stay hydrated: Drink plenty of water throughout the day to help flush out harmful bacteria and viruses.
10. Consider taking prenatal vitamins: Prenatal vitamins can help support your immune system and overall health during pregnancy.
Remember, it's always better to be safe than sorry, so if you suspect that you may have been exposed to an infection or are experiencing symptoms of an infection during pregnancy, contact your healthcare provider right away. They can help determine the appropriate course of action and ensure that you and your baby stay healthy.
Zoonoses (zoonosis) refers to infectious diseases that can be transmitted between animals and humans. These diseases are caused by a variety of pathogens, including bacteria, viruses, parasites, and fungi, and can be spread through contact with infected animals or contaminated animal products.
Examples of Zoonoses
Some common examples of zoonoses include:
1. Rabies: a viral infection that can be transmitted to humans through the bite of an infected animal, typically dogs, bats, or raccoons.
2. Lyme disease: a bacterial infection caused by Borrelia burgdorferi, which is spread to humans through the bite of an infected blacklegged tick (Ixodes scapularis).
3. Toxoplasmosis: a parasitic infection caused by Toxoplasma gondii, which can be transmitted to humans through contact with contaminated cat feces or undercooked meat.
4. Leptospirosis: a bacterial infection caused by Leptospira interrogans, which is spread to humans through contact with contaminated water or soil.
5. Avian influenza (bird flu): a viral infection that can be transmitted to humans through contact with infected birds or contaminated surfaces.
Transmission of Zoonoses
Zoonoses can be transmitted to humans in a variety of ways, including:
1. Direct contact with infected animals or contaminated animal products.
2. Contact with contaminated soil, water, or other environmental sources.
3. Through vectors such as ticks, mosquitoes, and fleas.
4. By consuming contaminated food or water.
5. Through close contact with an infected person or animal.
Prevention of Zoonoses
Preventing the transmission of zoonoses requires a combination of personal protective measures, good hygiene practices, and careful handling of animals and animal products. Some strategies for preventing zoonoses include:
1. Washing hands frequently, especially after contact with animals or their waste.
2. Avoiding direct contact with wild animals and avoiding touching or feeding stray animals.
3. Cooking meat and eggs thoroughly to kill harmful bacteria.
4. Keeping pets up to date on vaccinations and preventative care.
5. Avoiding consumption of raw or undercooked meat, particularly poultry and pork.
6. Using insect repellents and wearing protective clothing when outdoors in areas where vectors are prevalent.
7. Implementing proper sanitation and hygiene practices in animal housing and husbandry.
8. Implementing strict biosecurity measures on farms and in animal facilities to prevent the spread of disease.
9. Providing education and training to individuals working with animals or in areas where zoonoses are prevalent.
10. Monitoring for and reporting cases of zoonotic disease to help track and control outbreaks.
Conclusion
Zoonoses are diseases that can be transmitted between animals and humans, posing a significant risk to human health and animal welfare. Understanding the causes, transmission, and prevention of zoonoses is essential for protecting both humans and animals from these diseases. By implementing appropriate measures such as avoiding contact with wild animals, cooking meat thoroughly, keeping pets up to date on vaccinations, and implementing proper sanitation and biosecurity practices, we can reduce the risk of zoonotic disease transmission and protect public health and animal welfare.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are several different types of malaria, including:
1. Plasmodium falciparum: This is the most severe form of malaria, and it can be fatal if left untreated. It is found in many parts of the world, including Africa, Asia, and Latin America.
2. Plasmodium vivax: This type of malaria is less severe than P. falciparum, but it can still cause serious complications if left untreated. It is found in many parts of the world, including Africa, Asia, and Latin America.
3. Plasmodium ovale: This type of malaria is similar to P. vivax, but it can cause more severe symptoms in some people. It is found primarily in West Africa.
4. Plasmodium malariae: This type of malaria is less common than the other three types, and it tends to cause milder symptoms. It is found primarily in parts of Africa and Asia.
The symptoms of malaria can vary depending on the type of parasite that is causing the infection, but they typically include:
1. Fever
2. Chills
3. Headache
4. Muscle and joint pain
5. Fatigue
6. Nausea and vomiting
7. Diarrhea
8. Anemia (low red blood cell count)
If malaria is not treated promptly, it can lead to more severe complications, such as:
1. Seizures
2. Coma
3. Respiratory failure
4. Kidney failure
5. Liver failure
6. Anemia (low red blood cell count)
Malaria is typically diagnosed through a combination of physical examination, medical history, and laboratory tests, such as blood smears or polymerase chain reaction (PCR) tests. Treatment for malaria typically involves the use of antimalarial drugs, such as chloroquine or artemisinin-based combination therapies. In severe cases, hospitalization may be necessary to manage complications and provide supportive care.
Prevention is an important aspect of managing malaria, and this can include:
1. Using insecticide-treated bed nets
2. Wearing protective clothing and applying insect repellent when outdoors
3. Eliminating standing water around homes and communities to reduce the number of mosquito breeding sites
4. Using indoor residual spraying (IRS) or insecticide-treated wall lining to kill mosquitoes
5. Implementing malaria control measures in areas where malaria is common, such as distribution of long-lasting insecticidal nets (LLINs) and indoor residual spraying (IRS)
6. Improving access to healthcare services, particularly in rural and remote areas
7. Providing education and awareness about malaria prevention and control
8. Encouraging the use of preventive medications, such as intermittent preventive treatment (IPT) for pregnant women and children under the age of five.
Early diagnosis and prompt treatment are critical in preventing the progression of malaria and reducing the risk of complications and death. In areas where malaria is common, it is essential to have access to reliable diagnostic tools and effective antimalarial drugs.
There are many different types of epilepsy, each with its own unique set of symptoms and characteristics. Some common forms of epilepsy include:
1. Generalized Epilepsy: This type of epilepsy affects both sides of the brain and can cause a range of seizure types, including absence seizures, tonic-clonic seizures, and atypical absence seizures.
2. Focal Epilepsy: This type of epilepsy affects only one part of the brain and can cause seizures that are localized to that area. There are several subtypes of focal epilepsy, including partial seizures with complex symptoms and simple partial seizures.
3. Tonic-Clonic Epilepsy: This type of epilepsy is also known as grand mal seizures and can cause a loss of consciousness, convulsions, and muscle stiffness.
4. Lennox-Gastaut Syndrome: This is a rare and severe form of epilepsy that typically develops in early childhood and can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
5. Dravet Syndrome: This is a rare genetic form of epilepsy that typically develops in infancy and can cause severe, frequent seizures.
6. Rubinstein-Taybi Syndrome: This is a rare genetic disorder that can cause intellectual disability, developmental delays, and various types of seizures.
7. Other forms of epilepsy include Absence Epilepsy, Myoclonic Epilepsy, and Atonic Epilepsy.
The symptoms of epilepsy can vary widely depending on the type of seizure disorder and the individual affected. Some common symptoms of epilepsy include:
1. Seizures: This is the most obvious symptom of epilepsy and can range from mild to severe.
2. Loss of consciousness: Some people with epilepsy may experience a loss of consciousness during a seizure, while others may remain aware of their surroundings.
3. Confusion and disorientation: After a seizure, some people with epilepsy may feel confused and disoriented.
4. Memory loss: Seizures can cause short-term or long-term memory loss.
5. Fatigue: Epilepsy can cause extreme fatigue, both during and after a seizure.
6. Emotional changes: Some people with epilepsy may experience emotional changes, such as anxiety, depression, or mood swings.
7. Cognitive changes: Epilepsy can affect cognitive function, including attention, memory, and learning.
8. Sleep disturbances: Some people with epilepsy may experience sleep disturbances, such as insomnia or sleepiness.
9. Physical symptoms: Depending on the type of seizure, people with epilepsy may experience physical symptoms such as muscle weakness, numbness or tingling, and sensory changes.
10. Social isolation: Epilepsy can cause social isolation due to fear of having a seizure in public or stigma associated with the condition.
It's important to note that not everyone with epilepsy will experience all of these symptoms, and some people may have different symptoms depending on the type of seizure they experience. Additionally, some people with epilepsy may experience additional symptoms not listed here.
Insects such as mosquitoes, wasps, bees, and hornets are common culprits of bites and stings that cause minor to severe reactions in humans. These reactions may cause pain, redness, swelling, itching, and burning sensations at the site of the bite or sting.
Most insect bites and stings can be treated with over-the-counter medications such as antihistamines, hydrocortisone creams, or calamine lotion. Severe allergic reactions may require medical attention and epinephrine injections to prevent anaphylaxis.
Types of NMJ Diseases:
1. Myasthenia Gravis (MG): An autoimmune disorder that causes muscle weakness and fatigue due to the immune system attacking the NMJs.
2. Lambert-Eaton Myasthenic Syndrome (LEMS): A rare autoimmune disorder that affects the NMJ and can cause muscle weakness, fatigue, and other symptoms.
3. Congenital Myasthenic Syndromes (CMS): A group of rare genetic disorders that affect the development and function of the NMJ, leading to muscle weakness and other symptoms.
4. Neuronal Ceroid Lipofuscinosis (NCL): A group of rare genetic disorders that affect the nervous system and can cause muscle weakness, seizures, and vision loss.
5. Inflammatory Myopathies: A group of muscle disorders caused by inflammation, such as polymyositis or dermatomyositis, which can affect the NMJ and cause muscle weakness.
Symptoms of NMJ Diseases:
1. Muscle weakness or paralysis
2. Fatigue and exhaustion
3. Difficulty swallowing or breathing (in severe cases)
4. Droopy eyelids or double vision
5. Slurred speech or difficulty speaking
6. Weakness in the arms and legs
7. Muscle wasting and loss of muscle mass
8. Seizures or fits
9. Vision loss or blurred vision
10. Cramps or spasms
Diagnosis of NMJ Diseases:
1. Medical history and physical examination
2. Electromyography (EMG) to test muscle activity and strength
3. Nerve conduction studies (NCS) to test nerve function
4. Imaging tests such as MRI or CT scans to rule out other conditions
5. Blood tests to check for autoantibodies or other signs of inflammation
6. Genetic testing to diagnose inherited forms of NMJ diseases
Treatment of NMJ Diseases:
1. Medications such as steroids, immunosuppressants, and anticonvulsants to reduce inflammation and muscle weakness
2. Physical therapy to improve muscle strength and function
3. Occupational therapy to improve daily living skills
4. Speech therapy to improve communication and swallowing difficulties
5. Surgery to relieve compression or repair damaged nerves or muscles
6. Plasmapheresis (plasma exchange) to remove harmful antibodies from the blood
7. Intravenous immunoglobulin (IVIG) therapy to reduce inflammation and modulate the immune system
8. Immunoadsorption therapy to remove antibodies from the blood and restore immune balance
9. Stem cell transplantation to replace damaged cells with healthy ones
10. Gene therapy to repair genetic defects causing NMJ diseases.
It's important to note that the treatment of NMJ diseases is highly individualized and may vary depending on the specific diagnosis, severity of symptoms, and overall health of the patient. A multidisciplinary approach involving neurologists, physical therapists, occupational therapists, speech therapists, and other specialists may be necessary to provide comprehensive care.
There are many different types of seizures, each with its own unique set of symptoms. Some common types of seizures include:
1. Generalized seizures: These seizures affect both sides of the brain and can cause a range of symptoms, including convulsions, loss of consciousness, and muscle stiffness.
2. Focal seizures: These seizures affect only one part of the brain and can cause more specific symptoms, such as weakness or numbness in a limb, or changes in sensation or vision.
3. Tonic-clonic seizures: These seizures are also known as grand mal seizures and can cause convulsions, loss of consciousness, and muscle stiffness.
4. Absence seizures: These seizures are also known as petit mal seizures and can cause a brief loss of consciousness or staring spell.
5. Myoclonic seizures: These seizures can cause sudden, brief muscle jerks or twitches.
6. Atonic seizures: These seizures can cause a sudden loss of muscle tone, which can lead to falls or drops.
7. Lennox-Gastaut syndrome: This is a rare and severe form of epilepsy that can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
Seizures can be diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or imaging studies. Treatment for seizures usually involves anticonvulsant medications, but in some cases, surgery or other interventions may be necessary.
Overall, seizures are a complex and multifaceted symptom that can have a significant impact on an individual's quality of life. It is important to seek medical attention if you or someone you know is experiencing seizures, as early diagnosis and treatment can help to improve outcomes and reduce the risk of complications.
Falciparum malaria can cause a range of symptoms, including fever, chills, headache, muscle and joint pain, fatigue, nausea, and vomiting. In severe cases, the disease can lead to anemia, organ failure, and death.
Diagnosis of falciparum malaria typically involves a physical examination, medical history, and laboratory tests to detect the presence of parasites in the blood or other bodily fluids. Treatment usually involves the use of antimalarial drugs, such as artemisinin-based combination therapies (ACTs) or quinine, which can effectively cure the disease if administered promptly.
Prevention of falciparum malaria is critical to reducing the risk of infection, and this includes the use of insecticide-treated bed nets, indoor residual spraying (IRS), and preventive medications for travelers to high-risk areas. Eliminating standing water around homes and communities can also help reduce the number of mosquitoes and the spread of the disease.
In summary, falciparum malaria is a severe and life-threatening form of malaria caused by the Plasmodium falciparum parasite, which is responsible for the majority of malaria-related deaths worldwide. Prompt diagnosis and treatment are essential to prevent complications and death from this disease. Prevention measures include the use of bed nets, indoor spraying, and preventive medications, as well as reducing standing water around homes and communities.
There are several different types of pain, including:
1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.
The medical field uses a range of methods to assess and manage pain, including:
1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.
It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.
Brain hypoxia is a serious medical condition that requires prompt treatment to prevent long-term damage and improve outcomes for patients. Treatment options may include oxygen therapy, medications to improve blood flow to the brain, and surgery to remove any blockages or obstructions in blood vessels.
Examples of viral STDs include:
1. HIV (Human Immunodeficiency Virus): HIV attacks the body's immune system, making it harder to fight off infections and diseases. It can be spread through sex, sharing needles, or mother-to-child transmission during pregnancy, childbirth, or breastfeeding.
2. Herpes Simplex Virus (HSV): HSV causes genital herpes, which can cause painful blisters and sores on the genitals. It can be spread through skin-to-skin contact with an infected person.
3. Human Papillomavirus (HPV): HPV can cause genital warts, as well as cancer of the cervix, vulva, vagina, penis, or anus. It is usually spread through skin-to-skin contact with an infected person.
4. Hepatitis B Virus (HBV): HBV can cause liver disease and liver cancer. It is usually spread through sex, sharing needles, or mother-to-child transmission during childbirth.
5. Hepatitis C Virus (HCV): HCV can cause liver disease and liver cancer. It is usually spread through sex, sharing needles, or mother-to-child transmission during childbirth.
Preventing the spread of viral STDs includes:
1. Practicing safe sex, such as using condoms and dental dams.
2. Getting vaccinated against HPV and Hepatitis B.
3. Avoiding sharing needles or other drug paraphernalia.
4. Being in a mutually monogamous relationship with someone who has been tested and is negative for STDs.
5. Regularly getting tested for STDs, especially if you have a new sexual partner or engage in risky behavior.
6. Using condoms and other barrier methods consistently and correctly during all sexual activities.
7. Avoiding sexual contact with someone who has symptoms of an STD.
8. Being aware of your own sexual health status and the status of your partners, and being open and honest about your sexual history and any STDs you may have.
9. Seeking medical attention immediately if you suspect you or a partner has an STD.
10. Following safe sex practices and taking precautions to prevent the spread of STDs can help reduce the risk of developing these infections.
It's important to note that not all STDs have symptoms, so it's possible to have an STD and not know it. Regular testing is important for early detection and treatment, which can help prevent long-term health problems and the spread of infection.
In medicine, cross-infection refers to the transmission of an infectious agent from one individual or source to another, often through direct contact or indirect exposure. This type of transmission can occur in various settings, such as hospitals, clinics, and long-term care facilities, where patients with compromised immune systems are more susceptible to infection.
Cross-infection can occur through a variety of means, including:
1. Person-to-person contact: Direct contact with an infected individual, such as touching, hugging, or shaking hands.
2. Contaminated surfaces and objects: Touching contaminated surfaces or objects that have been touched by an infected individual, such as doorknobs, furniture, or medical equipment.
3. Airborne transmission: Inhaling droplets or aerosolized particles that contain the infectious agent, such as during coughing or sneezing.
4. Contaminated food and water: Consuming food or drinks that have been handled by an infected individual or contaminated with the infectious agent.
5. Insect vectors: Mosquitoes, ticks, or other insects can transmit infections through their bites.
Cross-infection is a significant concern in healthcare settings, as it can lead to outbreaks of nosocomial infections (infections acquired in hospitals) and can spread rapidly among patients, healthcare workers, and visitors. To prevent cross-infection, healthcare providers use strict infection control measures, such as wearing personal protective equipment (PPE), thoroughly cleaning and disinfecting surfaces, and implementing isolation precautions for infected individuals.
In summary, cross-infection refers to the transmission of an infectious agent from one individual or source to another, often through direct contact or indirect exposure in healthcare settings. Preventing cross-infection is essential to maintaining a safe and healthy environment for patients, healthcare workers, and visitors.
1. Complete paralysis: When there is no movement or sensation in a particular area of the body.
2. Incomplete paralysis: When there is some movement or sensation in a particular area of the body.
3. Localized paralysis: When paralysis affects only a specific part of the body, such as a limb or a facial muscle.
4. Generalized paralysis: When paralysis affects multiple parts of the body.
5. Flaccid paralysis: When there is a loss of muscle tone and the affected limbs feel floppy.
6. Spastic paralysis: When there is an increase in muscle tone and the affected limbs feel stiff and rigid.
7. Paralysis due to nerve damage: This can be caused by injuries, diseases such as multiple sclerosis, or birth defects such as spina bifida.
8. Paralysis due to muscle damage: This can be caused by injuries, such as muscular dystrophy, or diseases such as muscular sarcopenia.
9. Paralysis due to brain damage: This can be caused by head injuries, stroke, or other conditions that affect the brain such as cerebral palsy.
10. Paralysis due to spinal cord injury: This can be caused by trauma, such as a car accident, or diseases such as polio.
Paralysis can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, work, and participate in social and recreational activities. Treatment options for paralysis depend on the underlying cause and may include physical therapy, medications, surgery, or assistive technologies such as wheelchairs or prosthetic devices.
The diagnosis of absence epilepsy is typically made based on a combination of clinical findings, including:
-A history of recurrent brief loss of awareness or staring spells
-Normal neurological examination between episodes
-Abnormal EEG activity during seizures (spikes or sharp waves)
Treatment for absence epilepsy usually involves medication, such as ethosuximide, valproic acid, or lamotrigine. In some cases, surgery may be considered if medications are ineffective or have significant side effects.
It is important to note that absence epilepsy can be a challenging condition to diagnose and treat, as the spells can be difficult to distinguish from other conditions such as daydreaming or attention deficit hyperactivity disorder (ADHD).
Symptoms of influenza include:
* Fever (usually high)
* Cough
* Sore throat
* Runny or stuffy nose
* Headache
* Muscle or body aches
* Fatigue (tiredness)
* Diarrhea and nausea (more common in children than adults)
Influenza can lead to serious complications, such as pneumonia, bronchitis, and sinus and ear infections. These complications are more likely to occur in people who have a weakened immune system, such as the elderly, young children, and people with certain chronic health conditions (like heart disease, diabetes, and lung disease).
Influenza is diagnosed based on a physical examination and medical history. A healthcare provider may also use a rapid influenza test (RIT) or a polymerase chain reaction (PCR) test to confirm the diagnosis.
Treatment for influenza typically involves rest, hydration, and over-the-counter medications such as acetaminophen (Tylenol) or ibuprofen (Advil, Motrin) to relieve fever and body aches. Antiviral medications, such as oseltamivir (Tamiflu) or zanamivir (Relenza), may also be prescribed to help shorten the duration and severity of the illness. However, these medications are most effective when started within 48 hours of the onset of symptoms.
Prevention is key in avoiding influenza. Vaccination is the most effective way to prevent influenza, as well as practicing good hygiene such as washing your hands frequently, avoiding close contact with people who are sick, and staying home when you are sick.
In birds, the virus can cause respiratory, gastrointestinal, and nervous system disorders. It is transmitted through contact with infected birds or contaminated feces or water. Wild birds and domestic poultry are susceptible to influenza infection. The H5N1 subtype of the virus has caused widespread outbreaks in poultry and wild birds, leading to significant economic losses and public health concerns.
Prevention methods include vaccination, biosecurity measures, and surveillance programs. Vaccines are available for chickens, turkeys, ducks, and other domesticated birds, but the effectiveness of these vaccines can be limited in protecting against certain subtypes of the virus. Biosecurity measures such as sanitation, isolation, and disinfection can help prevent the spread of the disease in poultry flocks. Surveillance programs monitor the presence of the virus in wild and domestic bird populations to detect outbreaks early and prevent the spread of the disease.
The impact of avian influenza on human health is generally minimal, but it can be severe in certain cases. Direct transmission of the virus from birds to humans is rare, but it can occur through close contact with infected birds or contaminated surfaces. Indirect transmission may occur through the handling of contaminated poultry products. People with weakened immune systems, such as young children, the elderly, and those with chronic diseases, are at a higher risk of developing severe symptoms from avian influenza.
Overall, avian influenza is an important disease in birds that can have significant economic and public health implications. Prevention and control measures are essential to minimize the impact of the disease on both bird populations and human health.
Orders of magnitude (voltage)
Ionotropic GABA receptor
Reverse transport
Birdsey Renshaw
Herbert Zimmermann (neuroscientist)
Kainate receptor
Axo-axonic synapse
Willardiine
Alpha cell
Striatum
Cholinesterase inhibitor
Autapse
Nervous system
Neuroeffector junction
AMPA receptor
Krešimir Krnjević
Elizabeth Jonas (neurologist)
Primate basal ganglia
Tripartite synapse
Glia
Emodepside
Cortical cooling
Mauthner cell
VPS35
Andrew Huxley
UCL Neuroscience
SNAPAP
SNAP25
Glutamate (neurotransmitter)
NMDA receptor
Transgenerational stress inheritance
Viral synapse
Voltage-gated ion channel
Pre-Bötzinger complex
Yves De Koninck
CGP-7930
N-Arachidonoyl dopamine
Aloxistatin
Metabotropic glutamate receptor
Mir-188 microRNA precursor family
Synaptic fatigue
Coffin-Lowry syndrome
Motion perception
History of drum and bass
Brain
Sodium- and chloride-dependent glycine transporter 2
Nuclear receptor
Calcium concentration microdomains
SB-334867
Max Planck Institute for Experimental Medicine
Connectome
Alcohol myopia
Brain-computer interface
Evan Harris Walker
Risk factors of schizophrenia
Cadherin-catenin complex in learning and memory
Synaptic noise
Norepinephrine transporter
Phenethylamine
Signaling at the slit: podocytes chat by synaptic transmission
Films Media Group - What is Synaptic Transmission?
Synaptic transmission news and latest updates
NIH VideoCast - Synaptic Transmission at the Ribbon Synapses of the Eye and Ear
Erowid.org: Erowid Reference 8014 : The mysterious trace amines: protean neuromodulators of synaptic transmission in mammalian...
Acid-sensing ion channels contribute to synaptic transmission and inhibit cocaine-evoked plasticity - PubMed
Morphine-sensitive synaptic transmission emerges in embryonic rat microphysiological model of lower afferent nociceptive...
Effect Of Heat Pretreatment On Spontaneous Glutamatergic And Glycinergic Synaptic Transmission During Subsequent Thermal Stress...
Opposing retrograde and astrocyte-dependent endocannabinoid signaling mechanisms regulate lateral habenula synaptic...
Function of glial cells in the inhibitory synaptic transmission of the respiratory network
5-HT7 receptors mediate slow synaptic transmission in myenteric AH neurons of the guinea-pig ileum
Research - Chris McBain Lab | NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human Development
Sialic Acid Enhanced the Antistress Capability under Challenging Situations by Increasing Synaptic Transmission. | J Nutr;2023...
Subjects: Synaptic Transmission - Digital Collections - National Library of Medicine Search Results
Synaptic-like axo-axonal transmission from striatal cholinergic interneurons onto dopaminergic fibers
Encompass - University Presentation Showcase Event: The effects of resting membrane potential and synaptic transmissions by...
Inhibition of calpains improves memory and synaptic transmission in a mouse model of Alzheimer disease
Slow AMPAR Synaptic Transmission Is Determined by Stargazin and Glutamate Transporters<...
Frontiers | Stereotactically Injected Kv1.2 and CASPR2 Antisera Cause Differential Effects on CA1 Synaptic and Cellular...
Synapsin Regulates Activity-Dependent Outgrowth of Synaptic Boutons at the Drosophila Neuromuscular Junction | Journal of...
Nutrients | Free Full-Text | Towards an Integrative Understanding of tRNA Aminoacylation-Diet-Host-Gut Microbiome Interactions...
Social transmission of maternal behavior via oxytocin and synaptic plasticity - ELSC | Edmond & Lily Safra Center for Brain...
Divergent projections of the prelimbic cortex mediate autism- and anxiety-like behaviors | Molecular Psychiatry
Find Your Program Officer-Decision Tree | National Institute of Neurological Disorders and Stroke
2019 Cannabinoid Function in the CNS Conference GRC
Neuronal cell biology and synaptic transmission: driskill graduate enter in existence sciences: feinberg med school:...
Impaired ca2+ sensitivity of a novel gcap1 variant causes cone dystrophy and leads to abnormal synaptic transmission between...
Synaptic transmission and plasticity at inputs to murine cerebellar purkinje cells are largely dispensable for standard...
Biochemistry and Biophysics Center | NHLBI, NIH
Neurons15
- They have successfully recorded synaptic transmission between neurons in a live animal for the first time. (medicalxpress.com)
- As part of our investigation into the effects of hyperthermia on neuronal function, we used standard whole-cell patch clamp techniques to determine whether thermal pretreatment alters the frequency of spontaneous glutamatergic and glycinergic synaptic transmission between neurons of the mouse pre-B�tzinger complex during subsequent hyperthermia. (sicb.org)
- Besides, electrophysiological results revealed SA enhanced synaptic transmission rather than neuronal excitability of mPFC excitatory neurons . (bvsalud.org)
- The SA supplementation enhanced the response capability to stress under challenging situations, and the enhanced synaptic transmission of mPFC excitatory neurons may be the neurological basis of active response under challenging situations. (bvsalud.org)
- With this chapter, we begin to consider the signaling between neurons through the process of synaptic transmission. (mhmedical.com)
- Whereas the Purkinje cell of the cerebellum receives up to 100,000 synaptic inputs, the neighboring granule neurons, the most numerous class of neurons in the brain, receive only around four excitatory inputs. (mhmedical.com)
- Although many of the synaptic connections in the central and peripheral nervous systems are highly specialized, all neurons make use of one of the two basic forms of synaptic transmission: electrical or chemical. (mhmedical.com)
- Recently, we reported that the mesolimbic dopaminergic system was tonically suppressed during chronic pain by enhanced inhibitory synaptic inputs to neurons projecting from the dorsolateral bed nucleus of the stria terminalis (dlBNST) to the ventral tegmental area (VTA), suggesting that tonic suppression of the mesolimbic dopaminergic system by this neuroplastic change may be involved in chronic pain-induced depression-like behaviors. (biomedcentral.com)
- In this study, we hypothesized that inhibitory synaptic inputs to VTA-projecting dlBNST neurons are also enhanced in animal models of depression, thereby suppressing the mesolimbic dopaminergic system. (biomedcentral.com)
- The findings revealed enhanced inhibitory synaptic inputs to VTA-projecting dlBNST neurons in this rat model of depression, suggesting that this neuroplastic change is a neuronal mechanism common to depression and chronic pain that causes dysfunction of the mesolimbic dopaminergic system, thereby inducing depression-like behaviors. (biomedcentral.com)
- Thus, enhanced inhibitory synaptic inputs to VTA-projecting dlBNST neurons should activate VTA GABAergic neurons via a disinhibition mechanism, thereby causing suppression of VTA dopaminergic neurons that may induce depression and anhedonia observed in animal models of chronic pain. (biomedcentral.com)
- Although very close, the neurons do not actually touch each other, but are separated by the synaptic cleft that allows chemical messages to pass across from one neuron to the receptors of another neuron on the other side. (anat.org.au)
- Patterned depolarization of Drosophila motor neurons can rapidly induce the outgrowth of new synaptic boutons at the larval neuromuscular junction (NMJ), providing a model system to investigate mechanisms underlying acute structural plasticity. (jneurosci.org)
- Her graduate work involved studies of synaptic inputs and electrical properties of cochlear type II spiral ganglion afferent neurons in the laboratories of Dr. Paul Fuchs and Dr. Elisabeth Glowatzki. (nih.gov)
- While the phototransduction-associated role of GCAP1 in the photoreceptor outer segment is widely established, its implication in synaptic transmission to downstream neurons remains to be clarified. (unicatt.it)
Plasticity7
- They are presently investigating mechanisms for short-term synaptic plasticity at reciprocal synapses in retinal slices, and multivesicular release at the hair cell synapse using capacitance measurements together with paired recordings of hair cells and their afferent fibers. (nih.gov)
- These differences range from the molecular identity of receptors and channels to mechanisms of short- and long-term synaptic plasticity and signal transduction mechanisms associated with glutamate receptors. (nih.gov)
- We have shown novel forms of synaptic transmission as well as distinct mechanisms of both short- and long term plasticity of synaptic transmission. (nih.gov)
- This synaptic plasticity is crucial for memory and for other higher brain functions. (mhmedical.com)
- basic research on synaptic transmission and plasticity. (nih.gov)
- To characterize the presynaptic mechanisms mediating new synaptic growth induced by patterned activity, we investigated the formation of new boutons in NMJs lacking synapsin [Syn(−)], a synaptic protein important for vesicle clustering, neurodevelopment, and plasticity. (jneurosci.org)
- Synaptic transmission and plasticity at inputs to murine cerebellar purkinje cells are largely dispensable for standard nonmotor tasks. (nin.nl)
Cleft6
- Our genetic results indicate that at glycinergic synapses, the glial transporter GlyT1 catalyses the removal of glycine from the synaptic cleft, whereas GlyT2 is required for the re-uptake of glycine into nerve terminals, thereby allowing for neurotransmitter reloading of synaptic vesicles. (nih.gov)
- In response to the presynaptic neuron being excited by electrical signals, known as action potentials , the vesicles release the neurotransmitters into the synaptic cleft, where they bond with the receptors in a fluid medium. (anat.org.au)
- Desensitization has been studied traditionally with prolonged agonist exposure, whereas the duration of free neurotransmitter in the synaptic cleft is relatively brief. (elsevierpure.com)
- However, the space between the two nerve cells at at synapse, called the synaptic cleft, is no more than 40 nanometers wide. (elifesciences.org)
- Though the probe must be small enough to pass through the synaptic cleft to do this. (elifesciences.org)
- have now developed a quantum dot that is only 10 nanometers wide and therefore small enough to enter the synaptic cleft with an AMPA receptor attached. (elifesciences.org)
Inhibitory2
- Current reports of synaptic actions of eCBs in the LHb are conflicting and lack systematic investigation of eCB regulation of excitatory and inhibitory transmission. (northwestern.edu)
- Work in the McBain Laboratory is targeted towards understanding the development of excitatory and inhibitory synaptic transmission between specific identified neural populations within the hippocampal and cortical formations. (nih.gov)
Mechanisms2
- it remains unknown how new synaptic boutons differentiate and mature and what presynaptic mechanisms mediate their growth. (jneurosci.org)
- In conclusion, the pathological phenotype may rise from a combination of second messengers' accumulation and dysfunctional synaptic communication with bipolar cells, whose molecular mechanisms remain to be clarified. (unicatt.it)
Glutamate3
- However, a 15 min thermal pretreatment at 39.5˚ - 41˚C one hour prior to such hyperthermia significantly reduced the increase in frequency of spontaneous transmission via glutamate to 456.5 � 43.4% above 30˚C baseline (p (sicb.org)
- Here, we report that eCBs differentially regulate glutamatergic and GABAergic transmission in the LHb, exhibiting canonical and circuit-specific inhibition of both systems and an opposing potentiation of synaptic glutamate release mediated via activation of CB 1 receptors on astrocytes. (northwestern.edu)
- Studies of acetylcholine-, glutamate- and GABA-gated channels using rapid agonist application now provide a means to assess the effects of desensitization in shaping synaptic responses and in influencing neuronal excitability. (elsevierpure.com)
Long Term Potenti1
- Using extra- and intracellular techniques, synaptic transmission, long-term potentiation (LTP) and vulnerability to pro-epileptic conditions were analyzed. (frontiersin.org)
Regulation1
- Using electrophysiological, immunohistochemical, anatomical, molecular and genetic approaches we hope to gain significant insight into the developmental- and activity-dependent regulation of cellular and synaptic efficacy under both physiological and pathophysiological conditions. (nih.gov)
Vesicles1
- Unlike mature boutons, new varicosities have synaptic vesicles which are distributed uniformly throughout the bouton and undeveloped postsynaptic specializations. (jneurosci.org)
Neurotransmitter2
- A key event in synaptic transmission is the release of neurotransmitter via vesicle fusion at synaptic terminals. (nih.gov)
- This direct access to the terminal allows the lab to study the kinetics of synaptic vesicle exocytosis and endocytosis, neurotransmitter reuptake, and the modulation of neuronal output patterns by presynaptic receptors and the Na+/K+-ATPase pump. (nih.gov)
Receptors2
- While binding sites or receptors for a few of the trace amines have been advanced, the absence of cloned receptor protein has impeded significant development of their detailed mechanistic roles in the coordination of catecholamine and indolamine synaptic physiology. (erowid.org)
- Transmission from striatal cholinergic interneurons (CINs) controls dopamine release through nicotinic acetylcholine receptors (nAChRs) on dopaminergic axons. (nih.gov)
Inputs1
- The average neuron forms several thousand synaptic connections and receives a similar number of inputs. (mhmedical.com)
Vesicle3
- However, using high time resolution patch-clamp and membrane capacitance measurements, Dr. Von Gersdorff Lab has studied the kinetics of vesicle fusion (exocytosis) and subsequent membrane retrieval (endocytosis) in single, live synaptic terminals from bipolar cells of the goldfish retina and from hair cells of the frog amphibian papilla. (nih.gov)
- Following short depolarizations, a fast form of endocytosis can be observed, indicating that synaptic vesicle membrane is quickly re-internalized after vesicle fusion. (nih.gov)
- We found that budding of new boutons at Syn(−) NMJs was significantly diminished, and that new boutons in Syn(−) preparations were smaller and had reduced synaptic vesicle density. (jneurosci.org)
Neuromuscular2
- The resting membrane potential of larval Drosophila muscle and synaptic transmission at the neuromuscular junction are pH sensitive. (eku.edu)
- Dr. Silinsky, aided by his collaborator and laboratory co-director Dr. Timothy Searl, Research Assistant Professor, studies neuromuscular transmission and it is modulation at both voluntary (skeletal) and involuntary (autonomic) neuromuscular junctions. (futureiplabs.info)
Intracellular1
- The present study investigated the effects of doxapram on membrane potential and synaptic transmission using intracellular recordings of larval Drosophila muscles. (eku.edu)
Kinetics1
- Furthermore, SA supplementation enhanced synaptic transmission mainly by altering the kinetics of synaptic transmission . (bvsalud.org)
Molecular1
- However, despite decades of dedicated research, our understanding of the governing principles of endocannabinoid signaling at the molecular, synaptic and circuit levels has remained rather limited. (grc.org)
GABAergic1
- 13. GABAergic synaptic transmission. (nih.gov)
Fluorescent Dyes1
- However, this has yet to be confirmed directly, in part because conventional fluorescent dyes and quantum dots are too bulky to enter synaptic clefts when bound to a receptor. (elifesciences.org)
Signaling4
- However, the influence of cholinergic transmission on electrical signaling in axons remains unclear. (nih.gov)
- Thus, we reveal that synaptic-like neurotransmission underlies cholinergic signaling onto dopaminergic axons, supporting the idea that striatal dopamine release can occur independently of somatic firing to provide distinct signaling. (nih.gov)
- Endocannabinoid-mediated retrograde signaling is a fundamental counterpart of anterograde synaptic transmission throughout the CNS. (grc.org)
- Why there are different types of endocannabinoids and what is the division of labor between these lipid messengers in synaptic and extrasynaptic signaling? (grc.org)
Efficacy1
- Neuronal networks modify their activity in response to stimulation, and short-term changes in synaptic efficacy can lead to morphological changes in synaptic ultrastructure. (jneurosci.org)
Behavior1
- Because chemical synaptic transmission is so central to understanding brain and behavior, it is examined in detail in the next four chapters. (mhmedical.com)
Neural1
- Synaptic transmission is fundamental to the neural functions we consider in this book, such as perception, voluntary movement, and learning. (mhmedical.com)
Physiology1
- A substantial body of evidence suggests that the trace amines may play very significant roles in the coordination of biogenic amine-based synaptic physiology. (erowid.org)
Membrane1
- GlyT2 is highly enriched at glycinergic nerve terminals, and Ca(2+)-triggered exocytosis and internalization are thought to regulate GlyT2 numbers in the pre-synaptic plasma membrane. (nih.gov)
Protein3
- These beneficial effects of the calpain inhibitors were associated with restoration of normal phosphorylation levels of the transcription factor CREB and involved redistribution of the synaptic protein synapsin I. Thus, calpain inhibition may prove useful in the alleviation of memory loss in AD. (nih.gov)
- Since synapsin is a target of protein kinase A (PKA), we assayed whether activity-dependent synaptic growth is regulated via a cAMP/PKA/synapsin pathway. (jneurosci.org)
- Furthermore, we investigated the role of the presynaptic protein synapsin in activity-dependent synaptic growth. (jneurosci.org)
Terminals2
Nerve1
- Have you got the nerve to explore synaptic transmission? (films.com)
Examine1
- To examine the trafficking of synapsin during synaptic growth, we generated transgenic animals expressing fluorescently tagged synapsin. (jneurosci.org)
Inhibition1
- Here was show that calpain inhibition through E64, a cysteine protease inhibitor, and the highly specific calpain inhibitor BDA-410 restored normal synaptic function both in hippocampal cultures and in hippocampal slices from the APP/PS1 mouse, an animal model of AD. (nih.gov)
Receptor1
- Jones, MV & Westbrook, GL 1996, ' The impact of receptor desensitization on fast synaptic transmission ', Trends in Neurosciences , vol. 19, no. 3, pp. 96-101. (elsevierpure.com)
Terminal1
- However, the abnormal electroretinogram recorded in this patient also suggested that the dysregulation of the GCAP1-cyclase complex further propagates to the synaptic terminal, thereby altering the ON-pathway related to the b-wave generation. (unicatt.it)
Autism1
- 5. Disruptive variants of CSDE1 associate with autism and interfere with neuronal development and synaptic transmission. (nih.gov)
Recordings1
- We examined axo-axonal transmission from CINs onto dopaminergic axons using perforated-patch recordings, which revealed rapid spontaneous EPSPs with properties characteristic of fast synapses. (nih.gov)
Significantly2
- Two hours following thermal pretreatment, hyperthermia-induced increases in spontaneous transmission frequency remained significantly lower than those in tissues undergoing hyperthermia for the first time (p (sicb.org)
- We pretreated preparations with forskolin to raise cAMP levels and found this manipulation significantly enhanced activity-dependent synaptic growth in control but not Syn(−) preparations. (jneurosci.org)
Function1
- Remarkably, axEPSPs triggered spontaneous action potentials, suggesting that these axons perform integration to convert synaptic input into spiking, a function associated with somatodendritic compartments. (nih.gov)
Response1
- These data indicate that exposure of nervous tissue to temperatures experienced during high fever or heat stroke induces an acclimatory response opposing extreme deviation from normal frequencies of spontaneous synaptic transmission. (sicb.org)
Process1
- The generic process that allows sensory stimuli to pass around our body is known as Synaptic Transmission . (anat.org.au)