Galanin
Receptors, Galanin
Receptor, Galanin, Type 2
Receptor, Galanin, Type 1
Receptor, Galanin, Type 3
Receptors, Gastrointestinal Hormone
Galanin-Like Peptide
Receptors, Neuropeptide
Neuropeptides
Adaptation, Psychological
Trauma Centers
Stress Disorders, Post-Traumatic
Questionnaires
Discovery of a receptor related to the galanin receptors. (1/78)
We report the isolation of a cDNA clone named GPR54, which encodes a novel G protein-coupled receptor (GPCR). A PCR search of rat brain cDNA retrieved a clone partially encoding a GPCR. In a library screening this clone was used to isolate a cDNA with an open reading frame (ORF) encoding a receptor of 396 amino acids long which shared significant identities in the transmembrane regions with rat galanin receptors GalR1 (45%), GalR3 (45%) and GalR2 (44%). Northern blot and in situ hybridization analyses revealed that GPR54 is expressed in brain regions (pons, midbrain, thalamus, hypothalamus, hippocampus, amygdala, cortex, frontal cortex, and striatum) as well as peripheral regions (liver and intestine). In COS cell expression of GPR54 no specific binding was observed for 125I-galanin. A recent BLAST search with the rat GPR54 ORF nucleotide sequence recovered the human orthologue of GPR54 in a 3.5 Mb contig localized to chromosome 19p13.3. (+info)Pathogenic Escherichia coli increase Cl- secretion from intestinal epithelia by upregulating galanin-1 receptor expression. (2/78)
Galanin is widely distributed in enteric nerve terminals lining the human gastrointestinal (GI) tract. We have shown previously that galanin-1 receptors (Gal1-R) are expressed by epithelial cells lining the human GI tract, and upon activation cause Cl- secretion. Because expression of this receptor is transcriptionally regulated by nuclear factor-kappa B (NF-kappa B), which is activated by enteric pathogens as a part of the host epithelial response to infection, we investigated whether such bacterial pathogens could directly increase Gal1-R expression in the T84-cell model system. Pathogenic Escherichia coli, but not nonpathogenic E. coli, activate a p50/p65 NF-kappa B complex that binds to oligonucleotides corresponding to a recognition site located within the 5' flanking region of the human GAL1R gene. Pathogenic E. coli, but not normal commensal organisms, increase Gal1-R mRNA synthesis and [(125)I]galanin binding sites. Whereas galanin increases short-circuit current (Isc) approximately 5-fold in uninfected T84 cells, exposure to pathogenic, but not nonpathogenic, E. coli results in galanin increasing Isc approximately 20-fold. To confirm the validity of these in vitro observations, we also studied C57BL/6J mice infected with enterohemorrhagic E. coli (EHEC) by gavage. Infection caused a progressive increase in both NF-kappa B activation and Gal1-R expression, with maximal levels of both observed 3 days after gavage. Ussing chamber studies revealed that colons infected with EHEC, but not those exposed to normal colonic flora, markedly increased Isc in response to galanin. These data indicate that pathogen-induced increases in Gal1-R expression by epithelial cells lining the colon may represent a novel unifying pathway responsible for at least a portion of the excessive fluid secretion observed during infectious diarrhea. (+info)Reverse physiology in drosophila: identification of a novel allatostatin-like neuropeptide and its cognate receptor structurally related to the mammalian somatostatin/galanin/opioid receptor family. (3/78)
By using degenerate oligonucleotide primers deduced from the conserved regions of the mammalian somatostatin receptors, a novel G-protein-coupled receptor from Drosophila melanogaster has been isolated exhibiting structural similarities to mammalian somatostatin/galanin/opioid receptors. To identify the bioactive ligand, a 'reverse physiology' strategy was used whereby orphan Drosophila receptor-expressing frog oocytes were screened against potential ligands. Agonistic activity was electrophysiologically recorded as inward potassium currents mediated through co-expressed G-protein-gated inwardly rectifying potassium channels (GIRK). Using this approach a novel peptide was purified from Drosophila head extracts. Mass spectrometry revealed an octapeptide of 925 Da with a sequence Ser-Arg-Pro-Tyr-Ser-Phe-Gly-Leu-NH(2) reminiscent of insect allatostatin peptides known to control diverse functions such as juvenile hormone synthesis during metamorphosis or visceral muscle contractions. Picomolar concentrations of the synthesized octapeptide activated the cognate receptor response mediated through GIRK1, indicating that we have isolated the 394-amino-acid Drosophila allatostatin receptor which is coupled to the Gi/Go class of G proteins. (+info)Electrophysiological evidence for a hyperpolarizing, galanin (1-15)-selective receptor on hippocampal CA3 pyramidal neurons. (4/78)
The effects of the 29-amino acid neuropeptide galanin [GAL (1-29)], GAL(1-15), GAL(1-16), and the GAL subtype 2 receptor agonist D-tryptophan(2)-GAL(1-29) were studied in the dorsal hippocampus in vitro with intracellular recording techniques. GAL(1-15) induced, in the presence of tetrodotoxin, a dose-dependent hyperpolarization in hippocampal CA3 neurons. Most of the GAL(1-15)-sensitive neurons did not respond to GAL(1-29), GAL(1-16), or D-tryptophan(2)-GAL(1-29). These results indicate the presence of a distinct, yet-to-be cloned GAL(1-15)-selective receptor on CA3 neurons in the dorsal hippocampus. (+info)Isolation and cDNA cloning of a novel galanin-like peptide (GALP) from porcine hypothalamus. (5/78)
Galanin is a widely distributed neuropeptide with a variety of physiological functions. Three galanin receptor subtypes, GALR1, GALR2, and GALR3, have been reported. We isolated a novel galanin-like peptide (GALP) from porcine hypothalamus by observing its activity for increasing [(35)S]GTPgammaS binding to a membrane preparation of GALR2-transfected cells. The peptide had 60 amino acid residues and a non-amidated C terminus. The amino acid sequence of GALP-(9-21) was completely identical to that of galanin-(1-13). A cloned porcine GALP cDNA indicated that GALP was processed from a 120-amino acid GALP precursor protein. The structures of rat and human GALP-(1-60) were deduced from cloned cDNA, which indicated that the amino acid sequences 1-24 and 41-53 were highly conserved between humans, rats, and pigs. Receptor binding studies revealed that porcine GALP-(1-60) had a high affinity for the GALR2 receptor (IC(50) = 0.24 nM) and a lower affinity for the GALR1 receptor (IC(50) = 4.3 nM). In contrast, galanin showed high affinity for the GALR1 (IC(50) = 0.097 nM) and GALR2 receptors (IC(50) = 0.48 nM). GALP is therefore an endogenous ligand that preferentially binds the GALR2 receptor, whereas galanin is relatively non-selective. (+info)Dextran sulfate sodium-induced murine colitis activates NF-kappaB and increases galanin-1 receptor expression. (6/78)
Galanin is widely distributed in enteric nerve terminals and acts to modulate intestinal motility by altering smooth muscle contraction. This ligand causes Cl(-) secretion when colonic epithelial cells express the galanin-1 receptor (Gal1-R) subtype. Because Gal1-R expression by colonic epithelia is upregulated by the transcription factor nuclear factor-kappaB (NF-kappaB), increasingly appreciated as critical in the pathophysiology of inflammatory bowel disease, we wondered whether the diarrhea associated with this condition could be due to NF-kappaB-mediated increases in Gal1-R expression. To test this hypothesis, we provided oral dextran sulfate sodium (DSS) to C57BL/6J mice. Although Gal1-R are not normally expressed by epithelial cells lining the mouse colon, DSS treatment resulted in increased NF-kappaB activation and Gal1-R expression. Whereas galanin had no effect on murine colonic tissues studied ex vivo, it progressively increased short-circuit current and colonic fluid secretion in DSS-treated mice. Concomitant parenteral administration of the NF-kappaB inhibitor dexamethasone attenuated the activation of this transcription factor by DSS, inhibiting the increase in Gal1-R expression. Although Gal1-R-specific antagonists do not exist, intracolonic administration of commercially available galanin antibody diminished the DSS-induced increase in colonic fluid accumulation. Overall, these data demonstrate that a significant component of the excessive fluid secretion observed in DSS-treated mice is due to increased Gal1-R expression. (+info)Antisense properties of peptide nucleic acid. (7/78)
Peptide nucleic acid (PNA) is a nucleic acid mimic in which the deoxyribose phosphate backbone has been replaced by a pseudo-peptide polymer to which the nucleobases are linked. PNA-oligomers can be synthesized in relatively large amounts, are highly stable in biological environments, and bind complementary DNA and RNA targets with remarkably high affinity and specificity. Thus PNA possesses many of the properties desired for a good antisense agent. Until recently, limited uptake of PNA into cells has been the major obstacle for applying PNA as an antisense agent in cell cultures and in vivo. Here, the antisense properties of PNA in vitro and in vivo will be reviewed. In particular, we will focus on recent observations indicating that PNA equipped with or without various uptake moieties may function as an efficient and gene-specific inhibitor of translation in Escherichia coli and in certain mammalian cell types. (+info)Upregulation of galanin binding sites and GalR1 mRNA levels in the mouse locus coeruleus following chronic morphine treatments and precipitated morphine withdrawal. (8/78)
The neuropeptide galanin and its receptors are expressed in the locus coeruleus (LC), a brain area associated with drug dependence and withdrawal. Although galanin peptide mRNA levels do not change during withdrawal, it is not known whether galanin receptor levels are regulated following opiate withdrawal. This study demonstrates that galanin binding in the LC is upregulated by chronic-intermittent morphine administration or by precipitated withdrawal, but not by acute morphine treatment, suggesting that increased activity in the LC may be able to regulate galanin binding sites. Moreover, the increase in galanin binding sites seems to be caused by increased transcription or stabilization of the galanin receptor 1 (GalR1) gene, because there is a dramatic increase in mRNA levels following withdrawal in the LC. It is, therefore, possible that the increase in GalR1 could be an adaptive mechanism that leads to regulation of cAMP levels and possibly firing rate of LC neurons. (+info)Galanin is a neuropeptide, which is a type of small protein molecule that functions as a neurotransmitter or neuromodulator in the nervous system. It is widely distributed throughout the central and peripheral nervous systems of vertebrates and plays important roles in various physiological functions, including modulation of pain perception, regulation of feeding behavior, control of circadian rhythms, and cognitive processes such as learning and memory.
Galanin is synthesized from a larger precursor protein called preprogalanin, which is cleaved into several smaller peptides, including galanin itself, galanin message-associated peptide (GMAP), and alarin. Galanin exerts its effects by binding to specific G protein-coupled receptors, known as the galanin receptor family, which includes three subtypes: GalR1, GalR2, and GalR3. These receptors are widely expressed in various tissues and organs, including the brain, spinal cord, gastrointestinal tract, pancreas, and cardiovascular system.
Galanin has been implicated in several pathological conditions, such as chronic pain, depression, anxiety, epilepsy, and neurodegenerative disorders like Alzheimer's disease and Parkinson's disease. As a result, there is ongoing research into the development of galanin-based therapies for these conditions.
Galanin receptors are a group of G protein-coupled receptors (GPCRs) that bind to and are activated by the neuropeptide galanin. There are three subtypes of galanin receptors, named GalR1, GalR2, and GalR3, each encoded by separate genes. These receptors are widely distributed in the central and peripheral nervous systems, as well as in various endocrine organs.
Galanin receptors play important roles in modulating a variety of physiological functions, including neurotransmission, neuronal excitability, hormone release, and pain perception. Activation of these receptors can lead to either inhibitory or excitatory effects on neurons, depending on the receptor subtype and the specific cellular context.
Galanin has been implicated in several pathological conditions, such as chronic pain, epilepsy, depression, anxiety, and neurodegenerative disorders. Therefore, galanin receptors have become attractive targets for the development of novel therapeutic strategies to treat these conditions.
A galanin type 2 receptor (GAL2R) is a type of G protein-coupled receptor that binds the neuropeptide galanin. Galanin is a naturally occurring neurotransmitter and neuromodulator in the body, involved in various physiological functions such as regulation of feeding behavior, anxiety, pain perception, and memory.
The gene for the human GAL2R is called GALR2 and is located on chromosome 17. The receptor is widely expressed throughout the central nervous system, including in areas involved in reward processing, emotion regulation, and cognitive function.
Activation of the GAL2R by galanin can lead to a variety of intracellular signaling pathways, depending on the specific cell type and context. These signaling pathways can ultimately result in changes in neuronal excitability, neurotransmitter release, and gene expression.
Abnormalities in the galanin system have been implicated in several neurological and psychiatric disorders, including Alzheimer's disease, Parkinson's disease, depression, and chronic pain. As such, GAL2R has become a target of interest for drug development in these areas.
A galanin type 1 receptor (GAL1R) is a type of G protein-coupled receptor (GPCR) that binds the neuropeptide galanin. Galanin is a naturally occurring neurotransmitter in the body that plays a role in various physiological functions, including regulation of feeding behavior, anxiety, pain perception, and memory.
The GAL1R is widely expressed throughout the central nervous system and peripheral tissues. Once galanin binds to the GAL1R, it activates a signaling cascade that can have either excitatory or inhibitory effects on neuronal activity, depending on the specific cell type and location.
The activation of GAL1R has been implicated in various pathophysiological conditions, such as pain, depression, and neurodegenerative disorders. Therefore, GAL1R is considered a potential therapeutic target for the development of new drugs to treat these conditions.
A "Galanin Receptor, Type 3" (GAL3R or GalR3) is a type of G protein-coupled receptor that binds the neuropeptide galanin. Galanin is a naturally occurring neurotransmitter and neuromodulator in the body that plays roles in various physiological functions, including regulation of feeding behavior, anxiety, pain perception, and memory.
GalR3 is expressed in both the central and peripheral nervous systems and has been shown to have high affinity for galanin. Activation of GalR3 can lead to a variety of intracellular signaling pathways that ultimately influence cellular responses. The specific functions of GalR3 are still being studied, but it is believed to play roles in modulating pain perception, reducing inflammation, and regulating the release of other neurotransmitters.
It's important to note that while there is a significant body of research on galanin receptors, including GalR3, much remains to be learned about their precise functions and therapeutic potential.
Gastrointestinal (GI) hormone receptors are specialized protein structures found on the surface of cells in the gastrointestinal tract. These receptors recognize and respond to specific hormones that are released by enteroendocrine cells in the GI tract. Examples of GI hormones include gastrin, secretin, cholecystokinin (CCK), motilin, and ghrelin.
When a GI hormone binds to its specific receptor, it triggers a series of intracellular signaling events that ultimately lead to changes in cell function. These changes can include increased or decreased secretion of digestive enzymes, altered motility (movement) of the GI tract, and regulation of appetite and satiety.
Abnormalities in GI hormone receptors have been implicated in a variety of gastrointestinal disorders, including functional dyspepsia, irritable bowel syndrome, and obesity. Therefore, understanding the role of these receptors in GI physiology and pathophysiology is an important area of research.
Galanin-like peptide (GLP) is a neuropeptide belonging to the galanin family, which also includes galanin and galanin message-associated peptide (GMAP). GLP shares structural similarity with galanin but has distinct biological activities. It is encoded by the GALP gene and is primarily expressed in the hypothalamus, specifically in the arcuate nucleus.
GLP plays a role in various physiological functions, including energy balance, feeding behavior, and reproductive processes. It acts through specific G protein-coupled receptors, such as GalR1, GalR2, and GalR3, which are widely distributed throughout the central nervous system and peripheral tissues.
GLP has been implicated in several pathological conditions, including obesity, diabetes, and neurodegenerative disorders. However, its precise role and therapeutic potential in these diseases remain to be fully elucidated.
Neuropeptide receptors are a type of cell surface receptor that bind to neuropeptides, which are small signaling molecules made up of short chains of amino acids. These receptors play an important role in the nervous system by mediating the effects of neuropeptides on various physiological processes, including neurotransmission, pain perception, and hormone release.
Neuropeptide receptors are typically composed of seven transmembrane domains and are classified into several families based on their structure and function. Some examples of neuropeptide receptor families include the opioid receptors, somatostatin receptors, and vasoactive intestinal peptide (VIP) receptors.
When a neuropeptide binds to its specific receptor, it activates a signaling pathway within the cell that leads to various cellular responses. These responses can include changes in gene expression, ion channel activity, and enzyme function. Overall, the activation of neuropeptide receptors helps to regulate many important functions in the body, including mood, appetite, and pain sensation.
Neuropeptides are small protein-like molecules that are used by neurons to communicate with each other and with other cells in the body. They are produced in the cell body of a neuron, processed from larger precursor proteins, and then transported to the nerve terminal where they are stored in secretory vesicles. When the neuron is stimulated, the vesicles fuse with the cell membrane and release their contents into the extracellular space.
Neuropeptides can act as neurotransmitters or neuromodulators, depending on their target receptors and the duration of their effects. They play important roles in a variety of physiological processes, including pain perception, appetite regulation, stress response, and social behavior. Some neuropeptides also have hormonal functions, such as oxytocin and vasopressin, which are produced in the hypothalamus and released into the bloodstream to regulate reproductive and cardiovascular function, respectively.
There are hundreds of different neuropeptides that have been identified in the nervous system, and many of them have multiple functions and interact with other signaling molecules to modulate neural activity. Dysregulation of neuropeptide systems has been implicated in various neurological and psychiatric disorders, such as chronic pain, addiction, depression, and anxiety.
Psychological adaptation refers to the process by which individuals adjust and cope with stressors, challenges, or changes in their environment or circumstances. It involves modifying thoughts, feelings, behaviors, and copabilities to reduce the negative impact of these stressors and promote well-being. Psychological adaptation can occur at different levels, including intrapersonal (within the individual), interpersonal (between individuals), and cultural (within a group or society).
Examples of psychological adaptation include:
* Cognitive restructuring: changing negative thoughts and beliefs to more positive or adaptive ones
* Emotion regulation: managing and reducing intense or distressing emotions
* Problem-solving: finding solutions to practical challenges or obstacles
* Seeking social support: reaching out to others for help, advice, or comfort
* Developing coping strategies: using effective ways to deal with stressors or difficulties
* Cultivating resilience: bouncing back from adversity and learning from negative experiences.
Psychological adaptation is an important aspect of mental health and well-being, as it helps individuals adapt to new situations, overcome challenges, and maintain a sense of control and optimism in the face of stressors or changes.
A Trauma Center is a hospital that has specialized resources and capabilities to provide comprehensive care for severely injured patients. It is a designated facility that has met strict criteria established by the American College of Surgeons (ACS) and/or state or regional trauma systems. These criteria include having a dedicated trauma team, available 24/7, with specially trained healthcare professionals who can promptly assess, resuscitate, operate, and provide critical care to patients suffering from traumatic injuries.
Trauma centers are categorized into levels (I-V), based on the resources and capabilities they offer. Level I trauma centers have the highest level of resources and are capable of providing comprehensive care for all types of traumatic injuries, including conducting research and offering education in trauma care. In contrast, lower-level trauma centers may not have the same extent of resources but still provide essential trauma care services to their communities.
The primary goal of a trauma center is to ensure that severely injured patients receive prompt, high-quality care to minimize the risk of complications, reduce long-term disability, and improve overall outcomes.
Psychological stress is the response of an individual's mind and body to challenging or demanding situations. It can be defined as a state of emotional and physical tension resulting from adversity, demand, or change. This response can involve a variety of symptoms, including emotional, cognitive, behavioral, and physiological components.
Emotional responses may include feelings of anxiety, fear, anger, sadness, or frustration. Cognitive responses might involve difficulty concentrating, racing thoughts, or negative thinking patterns. Behaviorally, psychological stress can lead to changes in appetite, sleep patterns, social interactions, and substance use. Physiologically, the body's "fight-or-flight" response is activated, leading to increased heart rate, blood pressure, muscle tension, and other symptoms.
Psychological stress can be caused by a wide range of factors, including work or school demands, financial problems, relationship issues, traumatic events, chronic illness, and major life changes. It's important to note that what causes stress in one person may not cause stress in another, as individual perceptions and coping mechanisms play a significant role.
Chronic psychological stress can have negative effects on both mental and physical health, increasing the risk of conditions such as anxiety disorders, depression, heart disease, diabetes, and autoimmune diseases. Therefore, it's essential to identify sources of stress and develop effective coping strategies to manage and reduce its impact.
Multiple trauma, also known as polytrauma, is a medical term used to describe severe injuries to the body that are sustained in more than one place or region. It often involves damage to multiple organ systems and can be caused by various incidents such as traffic accidents, falls from significant heights, high-energy collisions, or violent acts.
The injuries sustained in multiple trauma may include fractures, head injuries, internal bleeding, chest and abdominal injuries, and soft tissue injuries. These injuries can lead to a complex medical situation requiring immediate and ongoing care from a multidisciplinary team of healthcare professionals, including emergency physicians, trauma surgeons, critical care specialists, nurses, rehabilitation therapists, and mental health providers.
Multiple trauma is a serious condition that can result in long-term disability or even death if not treated promptly and effectively.
Post-traumatic stress disorder (PTSD) is a psychiatric condition that can occur in people who have experienced or witnessed a traumatic event such as a natural disaster, serious accident, war combat, rape, or violent personal assault. According to the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5), PTSD is characterized by the following symptoms, which must last for more than one month:
1. Intrusion symptoms: These include distressing memories, nightmares, flashbacks, or intense psychological distress or reactivity to internal or external cues that symbolize or resemble an aspect of the traumatic event.
2. Avoidance symptoms: Persistent avoidance of stimuli associated with the traumatic event, including thoughts, feelings, conversations, activities, places, or people.
3. Negative alterations in cognitions and mood: This includes negative beliefs about oneself, others, or the world; distorted blame of self or others for causing the trauma; persistent negative emotional state; decreased interest in significant activities; and feelings of detachment or estrangement from others.
4. Alterations in arousal and reactivity: This includes irritable behavior and angry outbursts, reckless or self-destructive behavior, hypervigilance, exaggerated startle response, problems with concentration, and sleep disturbance.
5. Duration of symptoms: The symptoms must last for more than one month.
6. Functional significance: The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
It is essential to note that PTSD can occur at any age and can be accompanied by various physical and mental health problems, such as depression, substance abuse, memory problems, and other difficulties in cognition. Appropriate treatment, which may include psychotherapy, medication, or a combination of both, can significantly improve the symptoms and overall quality of life for individuals with PTSD.
A questionnaire in the medical context is a standardized, systematic, and structured tool used to gather information from individuals regarding their symptoms, medical history, lifestyle, or other health-related factors. It typically consists of a series of written questions that can be either self-administered or administered by an interviewer. Questionnaires are widely used in various areas of healthcare, including clinical research, epidemiological studies, patient care, and health services evaluation to collect data that can inform diagnosis, treatment planning, and population health management. They provide a consistent and organized method for obtaining information from large groups or individual patients, helping to ensure accurate and comprehensive data collection while minimizing bias and variability in the information gathered.
An "ecosystem" is not a term that has a specific medical definition, as it is a concept that is more commonly used in the fields of ecology and environmental science. However, I can provide you with the general ecological definition of an ecosystem:
An ecosystem is a community of living organisms interacting with each other and their non-living environment, including both biotic factors (plants, animals, microorganisms) and abiotic factors (climate, soil, water, and air). These interactions create a complex network of relationships that form the foundation of ecological processes, such as energy flow, nutrient cycling, and population dynamics.
While there is no direct medical definition for an ecosystem, understanding the principles of ecosystems can have important implications for human health. For example, healthy ecosystems can provide clean air and water, regulate climate, support food production, and offer opportunities for recreation and relaxation, all of which contribute to overall well-being. Conversely, degraded ecosystems can lead to increased exposure to environmental hazards, reduced access to natural resources, and heightened risks of infectious diseases. Therefore, maintaining the health and integrity of ecosystems is crucial for promoting human health and preventing disease.