Prosencephalon
Holoprosencephaly
Mesencephalon
Chick Embryo
Meningitis, Bacterial
Meningitis
Meningitis, Escherichia coli
Meningitis, Viral
Meningitis, Fungal
Meningitis, Pneumococcal
Meningitis, Aseptic
Drug-protein binding and blood-brain barrier permeability. (1/2027)
The permeability surface area (PS) product, an index of permeability of the blood-brain barrier (BBB), was measured by using the in situ perfusion method. In the cerebral circulation, the fraction of drug that permeates into the brain through the BBB is not only the unbound fraction but also the fraction dissociated from the protein in the perfusate. The sum of these two fractions, the apparent exchangeable fraction, was estimated by fitting the parameters of the BBB permeability under the condition of varying BSA concentrations in the perfusate. The unbound fraction of drugs in a buffer containing 0.5 mM BSA was measured by using the ultrafiltration method in vitro, and the apparent exchangeable fraction was measured in vivo by using the intracarotid artery injection method. The apparent exchange fraction was 100% for S-8510, 96.5% for diazepam, 90.9% for caffeine, 38.3% for S-312-d, 33.1% for propranolol, and 6.68% for (+)-S-145 Na, and each of these was higher than the corresponding unbound fraction in vitro in all drugs. The apparent exchangeable fractions, for example, were 8 times higher for diazepam and 38 times for S-312-d than the unbound fractions in vitro. The apparent exchangeable fraction of drugs was also estimated from the parameters obtained with the perfusion method. Because drugs can be infused for an arbitrary length of time in the perfusion method, substances with low permeability can be measured. The apparent exchangeable fractions obtained with this method were almost the same as those obtained with the intracarotid artery injection method. (+info)Alpha-2 adrenergic receptor functional coupling to G proteins in rat brain during postnatal development. (2/2027)
During postnatal development, alpha-2 adrenergic receptors (A2AR) change in both density and distribution. In forebrain, receptor density increases about 4-fold over neonatal levels, reaching adult levels before postnatal day (P) 28, whereas in hindbrain, including cerebellum, there is a decrease in overall receptor density. We examined the coupling of A2AR to G proteins using agonist-stimulated [35S]GTPgammaS binding as a functional assay. In forebrain the A2AR agonist-stimulated [35S]GTPgammaS binding increases rapidly after P7, reaching its highest levels at P21 and then declining slightly to adult levels. This binding increases more slowly than receptor number, suggesting that the appearance of G proteins, rather than the A2AR, determines the developmental appearance of functional A2AR-G protein interactions in forebrain. Basal [35S]GTPgammaS binding and [35S]GTPgammaS binding stimulated by other neurotransmitter receptor systems (GABA-B, mu opiate, and muscarinic) increase with a time course similar to A2AR-stimulated [35S]GTPgammaS binding. In contrast, in hindbrain, A2AR-stimulated [35S]GTPgammaS binding decreases during postnatal development in parallel with the decrease in A2AR levels, whereas [35S]GTPgammaS binding stimulated by other neurotransmitter receptor systems increases in parallel with basal [35S]GTPgammaS binding. Functional receptor-G protein coupling in hindbrain appears to be dependent on the developmental appearance of G proteins for most neurotransmitter systems. However, for A2AR the decrease in receptor density is the overriding factor. These studies 1) demonstrate the functional measurement of A2AR-G protein coupling in native tissue for the first time, 2) demonstrate that A2AR are coupled to G proteins throughout postnatal development, and 3) describe developmental increases and decreases in functional A2AR in brain. (+info)Ethanol exposure differentially alters central monoamine neurotransmission in alcohol-preferring versus -nonpreferring rats. (3/2027)
Individual differences in ethanol preference may be linked to differences in the functional activity of forebrain monoamine systems or their sensitivity to modification by ethanol. To test this hypothesis, basal extracellular concentrations of dopamine (DA) and serotonin (5-HT) in the nucleus accumbens as well as the effects of repeated ethanol pretreatment on the basal release of these transmitters were examined in alcohol-preferring (P), alcohol-nonpreferring (NP), and genetically heterogeneous Wistar rats. All animals received i.p. injections of ethanol (1.0 g/kg) or saline for 5 consecutive days. Fifteen hours after the final pretreatment, basal extracellular concentrations and "in vivo extraction fraction" values for DA and 5-HT were determined by no-net-flux in vivo microdialysis. In ethanol-naive rats, significant line differences were observed with high basal 5-HT release in P rats, low 5-HT release in NP rats, and intermediate 5-HT levels in Wistar rats. No differences among groups were noted in basal DA release. Ethanol pretreatment decreased basal extracellular 5-HT levels in P rats whereas increasing 5-HT efflux was seen in the Wistar and NP lines. In addition, ethanol pretreatment increased extracellular DA concentrations in Wistar and P rats, but not in NP rats. The results confirm a relationship between the functional status of forebrain DA and 5-HT systems and ethanol preference or aversion. Moreover, the data suggest that ethanol exposure can alter basal DA and 5-HT in the nucleus accumbens and that vulnerability to ethanol-induced changes in monoamine neurotransmission may be a factor in genetically determined ethanol preference. (+info)Comparative synteny cloning of zebrafish you-too: mutations in the Hedgehog target gli2 affect ventral forebrain patterning. (4/2027)
Zebrafish you-too (yot) mutations interfere with Hedgehog (Hh) signaling during embryogenesis. Using a comparative synteny approach, we isolated yot as a zinc finger transcription factor homologous to the Hh target gli2. Two alleles of yot contain nonsense mutations resulting in carboxy-terminally truncated proteins. In addition to causing defects in midline development, muscle differentiation, and retinal axon guidance, yot mutations disrupt anterior pituitary and ventral forebrain differentiation. yot mutations also cause ectopic lens formation in the ventral diencephalon. These findings reveal that truncated zebrafish Gli2 proteins interfere with Hh signaling necessary for differentiation and axon guidance in the ventral forebrain. (+info)Ectopic bone morphogenetic proteins 5 and 4 in the chicken forebrain lead to cyclopia and holoprosencephaly. (5/2027)
Proper dorsal-ventral patterning in the developing central nervous system requires signals from both the dorsal and ventral portions of the neural tube. Data from multiple studies have demonstrated that bone morphogenetic proteins (BMPs) and Sonic hedgehog protein are secreted factors that regulate dorsal and ventral specification, respectively, within the caudal neural tube. In the developing rostral central nervous system Sonic hedgehog protein also participates in ventral regionalization; however, the roles of BMPs in the developing brain are less clear. We hypothesized that BMPs also play a role in dorsal specification of the vertebrate forebrain. To test our hypothesis we implanted beads soaked in recombinant BMP5 or BMP4 into the neural tube of the chicken forebrain. Experimental embryos showed a loss of the basal telencephalon that resulted in holoprosencephaly (a single cerebral hemisphere), cyclopia (a single midline eye), and loss of ventral midline structures. In situ hybridization using a panel of probes to genes expressed in the dorsal and ventral forebrain revealed the loss of ventral markers with the maintenance of dorsal markers. Furthermore, we found that the loss of the basal telencephalon was the result of excessive cell death and not a change in cell fates. These data provide evidence that BMP signaling participates in dorsal-ventral patterning of the developing brain in vivo, and disturbances in dorsal-ventral signaling result in specific malformations of the forebrain. (+info)Blockade of N-methyl-D-aspartate receptor activation suppresses learning-induced synaptic elimination. (6/2027)
Auditory filial imprinting in the domestic chicken is accompanied by a dramatic loss of spine synapses in two higher associative forebrain areas, the mediorostral neostriatum/hyperstriatum ventrale (MNH) and the dorsocaudal neostriatum (Ndc). The cellular mechanisms that underlie this learning-induced synaptic reorganization are unclear. We found that local pharmacological blockade of N-methyl-D-aspartate (NMDA) receptors in the MNH, a manipulation that has been shown previously to impair auditory imprinting, suppresses the learning-induced spine reduction in this region. Chicks treated with the NMDA receptor antagonist 2-amino-5-phosphonovaleric acid (APV) during the behavioral training for imprinting (postnatal day 0-2) displayed similar spine frequencies at postnatal day 7 as naive control animals, which, in both groups, were significantly higher than in imprinted animals. Because the average dendritic length did not differ between the experimental groups, the reduced spine frequency can be interpreted as a reduction of the total number of spine synapses per neuron. In the Ndc, which is reciprocally connected with the MNH and not directly influenced by the injected drug, learning-induced spine elimination was partly suppressed. Spine frequencies of the APV-treated, behaviorally trained but nonimprinted animals were higher than in the imprinted animals but lower than in the naive animals. These results provide evidence that NMDA receptor activation is required for the learning-induced selective reduction of spine synapses, which may serve as a mechanism of information storage specific for juvenile emotional learning events. (+info)The Ca2+ channel blockade changes the behavioral and biochemical effects of immobilization stress. (7/2027)
We investigated how the effects of chronic immobilization stress in rats are modified by Ca2+ channel blockade preceding restraint sessions. The application of nifedipine (5 mg/kg) shortly before each of seven daily 2 h restraint sessions prevented the development of sensitized response to amphetamine as well as the stress-induced elevation of the densities of L-type Ca2+ channel in the hippocampus and significantly reduced the elevation of the densities of [3H]nitrendipine binding sites in the cortex and D1 dopamine receptors in the limbic forebrain. Neither stress, nor nifedipine affected the density of alpha 1-adrenoceptors and D1 receptors in the cerebral cortex nor D2 dopamine receptors in the striatum. A single restraint session caused an elevation of blood corticosterone level that remained unaffected by nifedipine pretreatment, but the reduction of this response during the eighth session was significantly less expressed in nifedipine-treated rats. We conclude that L-type calcium channel blockade prevents development of several stress-induced adaptive responses. (+info)Early visual experience shapes the representation of auditory space in the forebrain gaze fields of the barn owl. (8/2027)
Auditory spatial information is processed in parallel forebrain and midbrain pathways. Sensory experience early in life has been shown to exert a powerful influence on the representation of auditory space in the midbrain space-processing pathway. The goal of this study was to determine whether early experience also shapes the representation of auditory space in the forebrain. Owls were raised wearing prismatic spectacles that shifted the visual field in the horizontal plane. This manipulation altered the relationship between interaural time differences (ITDs), the principal cue used for azimuthal localization, and locations of auditory stimuli in the visual field. Extracellular recordings were used to characterize ITD tuning in the auditory archistriatum (AAr), a subdivision of the forebrain gaze fields, in normal and prism-reared owls. Prism rearing altered the representation of ITD in the AAr. In prism-reared owls, unit tuning for ITD was shifted in the adaptive direction, according to the direction of the optical displacement imposed by the spectacles. Changes in ITD tuning involved the acquisition of unit responses to adaptive ITD values and, to a lesser extent, the elimination of responses to nonadaptive (previously normal) ITD values. Shifts in ITD tuning in the AAr were similar to shifts in ITD tuning observed in the optic tectum of the same owls. This experience-based adjustment of binaural tuning in the AAr helps to maintain mutual registry between the forebrain and midbrain representations of auditory space and may help to ensure consistent behavioral responses to auditory stimuli. (+info)The prosencephalon is a term used in the field of neuroembryology, which refers to the developmental stage of the forebrain in the embryonic nervous system. It is one of the three primary vesicles that form during the initial stages of neurulation, along with the mesencephalon (midbrain) and rhombencephalon (hindbrain).
The prosencephalon further differentiates into two secondary vesicles: the telencephalon and diencephalon. The telencephalon gives rise to structures such as the cerebral cortex, basal ganglia, and olfactory bulbs, while the diencephalon develops into structures like the thalamus, hypothalamus, and epithalamus.
It is important to note that 'prosencephalon' itself is not used as a medical term in adult neuroanatomy, but it is crucial for understanding the development of the human brain during embryogenesis.
Holoprosencephaly is a congenital brain malformation that occurs due to the failure of the prosencephalon (the forebrain) to properly divide into the two hemispheres during embryonic development. This condition can vary in severity, from mild anomalies to severe neurological defects and facial abnormalities.
There are four primary types of holoprosencephaly: alobar, semilobar, lobar, and middle interhemispheric variant (MIV). Alobar holoprosencephaly is the most severe form, where the forebrain fails to divide into separate hemispheres, and there is a single ventricle instead of two. Semilobar holoprosencephaly has some separation of the hemispheres but not completely. Lobar holoprosencephaly shows more separation of the hemispheres, with a more typical appearance of the cerebral cortex. MIV is the mildest form and involves an abnormal development of the corpus callosum and third ventricle.
Facial anomalies often accompany holoprosencephaly, such as a single central eye (cyclopia), closely spaced eyes (hypotelorism), a proboscis above the nose, or a flat nasal bridge with a median cleft lip and palate. The severity of these facial abnormalities can correlate with the degree of brain malformation.
Holoprosencephaly is caused by genetic mutations, chromosomal abnormalities, or environmental factors that disrupt normal embryonic development. It affects approximately 1 in 250 conceptuses but has a lower prevalence at birth due to early pregnancy loss. The condition can be diagnosed through prenatal ultrasound, fetal MRI, or postnatal imaging techniques such as CT or MRI scans. Management of holoprosencephaly involves multidisciplinary care, addressing neurological, developmental, and medical needs.
The mesencephalon, also known as the midbrain, is the middle portion of the brainstem that connects the hindbrain (rhombencephalon) and the forebrain (prosencephalon). It plays a crucial role in several important functions including motor control, vision, hearing, and the regulation of consciousness and sleep-wake cycles. The mesencephalon contains several important structures such as the cerebral aqueduct, tectum, tegmentum, cerebral peduncles, and several cranial nerve nuclei (III and IV).
A chick embryo refers to the developing organism that arises from a fertilized chicken egg. It is often used as a model system in biological research, particularly during the stages of development when many of its organs and systems are forming and can be easily observed and manipulated. The study of chick embryos has contributed significantly to our understanding of various aspects of developmental biology, including gastrulation, neurulation, organogenesis, and pattern formation. Researchers may use various techniques to observe and manipulate the chick embryo, such as surgical alterations, cell labeling, and exposure to drugs or other agents.
Bacterial meningitis is a serious infection that causes the membranes (meninges) surrounding the brain and spinal cord to become inflamed. It's caused by various types of bacteria, such as Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae type b.
The infection can develop quickly, over a few hours or days, and is considered a medical emergency. Symptoms may include sudden high fever, severe headache, stiff neck, nausea, vomiting, confusion, and sensitivity to light. In some cases, a rash may also be present.
Bacterial meningitis can lead to serious complications such as brain damage, hearing loss, learning disabilities, and even death if not treated promptly with appropriate antibiotics and supportive care. It is important to seek immediate medical attention if you suspect bacterial meningitis. Vaccines are available to prevent certain types of bacterial meningitis.
Meningitis is a medical condition characterized by the inflammation of the meninges, which are the membranes that cover the brain and spinal cord. This inflammation can be caused by various infectious agents, such as bacteria, viruses, fungi, or parasites, or by non-infectious causes like autoimmune diseases, cancer, or certain medications.
The symptoms of meningitis may include fever, headache, stiff neck, nausea, vomiting, confusion, and sensitivity to light. In severe cases, it can lead to seizures, coma, or even death if not treated promptly and effectively. Bacterial meningitis is usually more severe and requires immediate medical attention, while viral meningitis is often less severe and may resolve on its own without specific treatment.
It's important to note that meningitis can be a serious and life-threatening condition, so if you suspect that you or someone else has symptoms of meningitis, you should seek medical attention immediately.
"Escherichia coli (E. coli) meningitis" is a specific type of bacterial meningitis, which is an inflammation of the membranes covering the brain and spinal cord (meninges). E. coli is a gram-negative, facultatively anaerobic, rod-shaped bacterium that is commonly found in the lower intestine of warm-blooded organisms. While most strains of E. coli are harmless and even beneficial to their hosts, some serotypes can cause severe food poisoning and other illnesses.
E. coli meningitis is relatively rare but can occur in newborns and young infants, particularly those who are premature or have underlying health conditions that weaken their immune systems. The bacteria can enter the bloodstream and travel to the brain, causing meningitis. Symptoms of E. coli meningitis may include fever, vomiting, irritability, lethargy, seizures, and a stiff neck.
E. coli meningitis is a serious medical emergency that requires prompt treatment with antibiotics to prevent complications such as brain damage or hearing loss. Infants who are diagnosed with E. coli meningitis may also require supportive care, such as fluid replacement and respiratory support, to help them recover.
Viral meningitis is a form of meningitis, which is an inflammation of the membranes (meninges) surrounding the brain and spinal cord. It is caused by viral infections, such as enteroviruses, herpesviruses, and HIV. The infection enters the body through the respiratory system or the gastrointestinal tract and then spreads to the central nervous system.
Symptoms of viral meningitis may include fever, headache, stiff neck, photophobia (intolerance to light), and altered mental status. In some cases, patients may also experience vomiting, seizures, or skin rash. However, viral meningitis is generally less severe than bacterial meningitis and has a lower mortality rate.
Most cases of viral meningitis resolve on their own within 7-10 days, and treatment typically involves supportive care such as hydration, pain relief, and fever reduction. Antibiotics are not effective against viruses, so they are not used to treat viral meningitis. In some cases, antiviral medications may be prescribed for certain types of viral meningitis, such as herpes simplex virus (HSV) meningitis.
Preventive measures include practicing good hygiene, such as washing hands frequently and avoiding close contact with people who are sick. There is also a vaccine available to protect against enterovirus D68, which can cause viral meningitis in some cases.
Fungal meningitis is a form of meningitis, which is an inflammation of the membranes (meninges) surrounding the brain and spinal cord. It is specifically caused by the invasion of the meninges by fungi. The most common causative agents are Cryptococcus neoformans and Histoplasma capsulatum.
Fungal meningitis typically occurs in individuals with weakened immune systems, such as those with HIV/AIDS, cancer, or organ transplant recipients. It begins gradually, often with symptoms including headache, fever, stiff neck, and sensitivity to light. Other possible symptoms can include confusion, nausea, vomiting, and altered mental status.
Diagnosis of fungal meningitis typically involves a combination of clinical examination, imaging studies (such as CT or MRI scans), and laboratory tests (such as cerebrospinal fluid analysis). Treatment usually requires long-term antifungal therapy, often administered intravenously in a hospital setting. The prognosis for fungal meningitis depends on several factors, including the underlying immune status of the patient, the specific causative agent, and the timeliness and adequacy of treatment.
Pneumococcal meningitis is a specific type of bacterial meningitis, which is an inflammation of the membranes covering the brain and spinal cord (meninges). It is caused by the bacterium Streptococcus pneumoniae, also known as pneumococcus. This bacterium is commonly found in the upper respiratory tract and middle ear fluid of healthy individuals. However, under certain circumstances, it can invade the bloodstream and reach the meninges, leading to meningitis.
Pneumococcal meningitis is a serious and potentially life-threatening condition that requires immediate medical attention. Symptoms may include sudden onset of fever, severe headache, stiff neck, nausea, vomiting, confusion, and sensitivity to light (photophobia). In some cases, it can also lead to complications such as hearing loss, brain damage, or even death if not treated promptly and effectively.
Treatment typically involves the use of antibiotics that are effective against pneumococcus, such as ceftriaxone or vancomycin. In some cases, corticosteroids may also be used to reduce inflammation and prevent complications. Prevention measures include vaccination with the pneumococcal conjugate vaccine (PCV13) or the pneumococcal polysaccharide vaccine (PPSV23), which can help protect against pneumococcal infections, including meningitis.
Aseptic meningitis is a type of meningitis (inflammation of the membranes covering the brain and spinal cord) that is not caused by bacterial infection. Instead, it can be due to viral infections, fungal infections, or non-infectious causes such as certain medications, chemical irritants, or underlying medical conditions. In aseptic meningitis, the cerebrospinal fluid (CSF) analysis may show increased white blood cells, typically lymphocytes, but no bacterial growth on culture. Common viral causes include enteroviruses, herpes simplex virus, and varicella-zoster virus. Treatment depends on the underlying cause and may include supportive care, antiviral medications, or immunosuppressive therapy in some cases.
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