« GABA Receptors GABAA Receptor The GABAA receptor is a member of the superfamily of ligand-activated ion channels in the cell membrane. ...» Document abstract
$4.95
5 word format
Language : english
psychology
presentation
date published
26/11/2007
review : not yet assessed
level : Advanced
requested 0 times
SummaryGABAA Receptor The GABAA receptor is a member of the superfamily of ligand-activated ion channels in the cell membrane. GABA type A (GABAA) receptors are most closely related to strychnine-sensitive glycine receptors, more distantly related to acetylcholine nicotonic receptors and serotonin 5-hydroxytryptamine (5-HT) [5-HT] type receptors, and even more distantly related to glutamate ionotropic receptors (AMPA and kainate receptors and NMDA receptors). GABAA receptors are heteropentameric protein complexes, which when activated undergo a series of conformational changes that form an open channel (pore) selectively permeable to anions, specifically chlorine anion (Cl–) and to a lesser degree (HCO–3). Receptor activation normally results in an influx of Cl– which rapidly and transiently hyperpolarizes the membrane, a process generally referred to as the generation of an inhibitory postsynaptic potential. The increase in Cl– flux also decreases the resistance of the membrane, which acts as a shunt to impede the ability of depolarizing excitatory postsynaptic potentials to elicit action potentials (nerve impulses).
Table of Contents
- GABAA receptors are heteromeric in that the receptor can comprise at least four types of subunit proteins, termed a, b, g, and d. It is pentameric in that each receptor has a total of five proteins
- A variety of pharmacological agents can influence the activity of GABAA receptors
- GABAB Receptors The metabotropic GABAB receptors are a member of the superfamily of G-protein-coupled receptors expressed in the cell membrane.
- However, it is likely that a breakdown in the regulation of glutamate is a major factor.
- Epilepsy Epilepsy is a group of neurological disorders characterized by spontaneous recurrent seizures.
- Although many neurobiological factors may contribute to seizure formation, a prominent feature of most seizures is an abnormal and excessive firing of glutamatergic neural pathways.
- Kindling, which is a gradual induction of a hyperexcitable neuronal state, can occur by focal repetitive subconvulsive stimulation of the hippocampus, amygdala, or some other brain areas.
- Neuropathic Pain Activation of afferent C fibers with nociceptive stimuli produces pain sensations that are enhanced during pathological conditions.
- A pregnane-derived synthetic neurosteroid is in clinical trials for treatment of epilepsy.
- Substance Abuse Ethanol enhances GABA receptor function in some in vitro preparations potentially via a protein-binding site.
« For example, benzodiazepines act via GABA receptors, cocaine blocks the reuptake of monoamines, and opioids act via an array of opiate receptor subtypes. ...» Document abstract
$3.95
4 word format
Language : english
biology
research papers
date published
26/11/2007
review : not yet assessed
level : Advanced
requested 0 times
SummaryIn its simplest form, the postsynaptic response to neurotransmitter release can be mediated by a single protein complex. For example, nicotinic acetylcholine receptors are self-contained stimulus-response modules that both detect a stimulus, acetylcholine, and generate a response, passage of ion currents. In a similar vein, other members of this superfamily of ionotropic receptors, including g-aminobutyric acid (GABA) and glutamate receptors, have the ability to function in a manner that is independent of the intracellular signaling pathways discussed. Thus, in contrast to growth factor or G-protein–coupled receptors, which often recruit elaborate cascades to elicit a response, the simplicity of self-sufficient ionotropic receptor complexes represents an optimal design for achieving reliability, precision, and speed. However, this view of ionotropic receptors as insulated from their social environment has had to be abandoned in the face of overwhelming evidence that this class of receptors is dynamically regulated by intraneuronal signaling pathways. Although these receptors do not rely on intraneuronal signaling pathways to operate ion channels, because these channels are an intrinsic feature of the receptor complex the linkage between ligand binding and ion channel gating is nevertheless subject to regulation by the network of intraneuronal signaling pathways just described. For example, phosphorylation of the GABA or glutamate receptors modulates their response to ligand exposure.
Table of Contents
- Long-Term Depression The principle that ion channels are regulated by second messenger pathways is of central importance in considering how neuronal responses are altered by experience.
- Long-Term Potentiation The notion that coactivation of multiple second messenger pathways can have a qualitatively different impact than any one individually is also borne out in another well-known model of synaptic plasticity, long-term potentiation.
- This unusual property of NMDA receptors provides a molecular mechanism for conferring associative properties on long-term potentiation.
- Role of Phosphorylation The associative property of this model of synaptic plasticity has focused attention on deciphering the intraneuronal signaling pathways that mediate the long-term change in synaptic transmission triggered by NMDA receptor stimulation.
- Actions of Psychotropic Drugs In addition to providing insight into the molecular mechanism underlying synaptic plasticity, studies of intraneuronal signaling pathways are also directly relevant to deciphering the mode of action of psychotropic drugs.
- Evidence supporting this theory has been provided by recent studies demonstrating that opiate withdrawal is attenuated in transgenic animals that are deficient in CREB.
« Out of the many types of GABA(A) receptors in the nervous system, it is believed that only a few are affected by benzodiazepines. ...» Document abstract
$3.95
4 word format
Language : english
biology
school essay
date published
17/09/2007
review : not yet assessed
level : General public
requested 0 times
SummaryThe GABA(A) receptor plays a vital role in the mammalian brain and is responsible for a large majority of inhibitory neurotransmissions in the central nervous system (Perrine 144). The GABA(A) receptor is a member of the ionotropic (ligand gated) family of receptors that uses GABA, otherwise known as γ-aminobutyric acid, as its ligand. The binding of GABA to the receptor opens the associated ion channel, which in this case is selectively permeable to chlorine ions as they pass down their electrochemical gradient. The negatively charged chlorine ions passing into the cell further negate the postsynaptic membrane potential, usually hyperpolarizing it. This makes it more difficult to depolarize the cell and decreases the probability of further propagation of action potential.
Table of Contents
- The GABA(A) receptor plays a vital role in the mammalian brain and is responsible for a large majority of inhibitory neurotransmissions in the central nervous system
- The GABA(A) receptor consists of five glycoprotein subunits
- Other binding sites exist along the protein shell of the GABA(A) receptor complex, including binding sites for agonists (activating ligands) such as barbiturates(sedatives), certain steroids and benzodiazepines
- Diazepam, commonly known as Valium, with its trademark electron attracting group at the 7th position
- with an ' subunit but the aforementioned two GABA ligands are still necessary for the ion channel to open
- Out of the many types of GABA(A) receptors in the nervous system, it is believed that only a few are affected by benzodiazepines
- There exist three types of benzodiazepines, short lasting, intermediate lasting and long lasting.
- With all these positive effects of benzodiazepines, there is always the risk of taking too much.
- With all these positive effects of benzodiazepines, there is always the risk of taking too much.
« Subsequent studies found that muscle-type nicotinic receptors are part of a superfamily that includes neuronal nicotinic, GABA type A (GABAA), glycine, and ...» Document abstract
$2.95
3 word format
Language : english
biology
research papers
date published
26/11/2007
review : not yet assessed
level : Advanced
requested 1 times
SummaryClasses of Neurotransmitters Much of the information transfer between neurons in the CNS occurs via chemical synapses. These synapses use a variety of messengers (neurotransmitters) that are released in a Ca2+-dependent fashion from presynaptic terminals and act on specific protein receptors to produce biochemical and excitability changes in the receiving cell. There are two primary groups of neurotransmitters—low–molecular-weight amines and neuroactive peptides. These agents act on two classes of receptors, ligand-gated ion channels, at which the binding of the transmitter directly opens ion channels in the membrane, and G protein coupled receptors. The activated G protein then acts on ion channels or alters biochemical second-messenger systems. Physiologists classify synaptic transmission according to the speed of transmission (fast or slow) and according to the nature of the response (excitatory or inhibitory).
Table of Contents
- Currently, there are nine low–molecular-weight amines that serve as neurotransmitters.
- Conductance Mechanisms Underlying Neurotransmitter Actions
- Structure of Neurotransmitter Receptors Considerable information now exists about the primary structure of neurotransmitter receptors.
- The ligand-gated ion channels gated by extracellular ATP (called P2X receptors) are exceptions to the scheme described above and have structures more typical of the inwardly rectifying K+ channels.
- G-protein coupled receptors have a distinctly different structure from the ligand-gated ion channels.
« GABA6-producing neurons and GABAA receptors are widely distributed in brain. receptor after anxiolytic steroid binding increases the affinity of GABA for this ...» Document abstract
$1.95
2 word format
Language : english
medical studies
research papers
date published
26/11/2007
review : not yet assessed
level : Advanced
requested 0 times
SummaryA variety of maladies, sometimes disabling, beset many ovulatory women in a recurrent manner during the luteal phase of each ovarian cycle. Although the biological basis for this association is not defined, evidence points to a causal relationship between progesterone secretion and withdrawal and the development of these premenstrual syndromes (PMS). As reviewed by MacDonald and associates (1991), symptoms include disorders in mood, behavior, and physical well-being. Commonly, there is a characteristic cluster of the same symptoms in a given woman month after month.
Table of Contents
- RECURRENT PROGESTERONE SECRETION: AN ENDOCRINOPATHY?
- PROGESTERONE AND PMS
- PROGESTERONE METABOLISM.
- SAFE CONTRACEPTION, WITHOUT MENSTRUATION
« molecules that also includes those for g-aminobutyric acid (GABA), glycine, and In contrast to monoaminergic receptors, there is evidence for only a single ...» Document abstract
$2.95
3 word format
Language : english
psychology
presentation
date published
13/11/2007
review : not yet assessed
level : Advanced
requested 2 times
SummaryIn addition to similarities in neuronal organization, monoaminergic systems are similar with regard to their synthesis, storage, and degradation. Monoamines are synthesized within neurons from common amino acid precursors and taken up into synaptic vesicles via a vesicular monoamine transporter. Upon stimulation, vesicles within nerve terminals release neurotransmitter into the synaptic cleft. Once released, the monoamines interact with postsynaptic receptors to alter the excitability of postsynaptic cells. Monoamines may also interact with presynaptic autoreceptors located on the nerve terminal to suppress further release. In addition, released monoamines may be taken back up from the synaptic cleft into the nerve terminal by plasma membrane transporter proteins. Reuptake plays an important role in limiting the magnitude and duration of action of synaptically released monoamines. Once monoamines are taken up, they may be subject to enzymatic degradation or they may be protected from degradation by uptake into vesicles. The processing of acetylcholine differs from this scheme, and is described below.
Table of Contents
- Serotonin The CNS contains less than 2 percent of the serotonin in the body; peripheral serotonin is located in platelets, mast cells, and enterochromaffin cells of the gastrointestinal system.
- The first step in the degradation of serotonin is mediated by monoamine oxidase (MAO) type A
- Two enzymes that play major roles in the degradation of catecholamines are monoamine oxidase and catechol O-methyltransferase
- Histamine As is the case for serotonin, the brain contains only a small portion of the histamine found in the body.
- Plasma Membrane Transporters A great deal of progress has been made in the molecular characterization of the monoamine plasma membrane transporter proteins.
- Vesicular Monoamine Transporter In addition to the reuptake of monoamines into the presynaptic nerve terminal, a second transport process serves to concentrate and store monoamines within synaptic vesicles.
« Acetylcholine, acting at muscarinic receptors, blocks several K+ currents leading CNS regions, the neurotransmitters g-aminobutyric acid (GABA), serotonin, and ...» Document abstract
$5.95
6 word format
Language : english
biology
research papers
date published
26/11/2007
review : not yet assessed
level : Advanced
requested 0 times
SummaryStructure and Function of Voltage-Gated Ion Channels Voltage-gated ion channels allow the flow of ions in response to changes in membrane voltage and are key elements in neuronal excitation and inhibition. Although ion channels can usually pass more than a single type of ion, voltage-gated channels are named according to the predominant ion that flows when the channel is open. Ion channels that are selective for Na+, K+, Ca2+, or Cl– have been described in neuronal membranes. Certain ion channels that are gated directly by chemical neurotransmitters such as glutamate and acetylcholine are selective for Na+, K+, and Ca2+ but exclude Cl– and are called nonselective cationic channels.
Table of Contents
- Sodium (Na+) Channels Na+ channels are primarily responsible for the fast upstroke of action potentials, although in some neurons Na+ channels also contribute to lower-level depolarizations and pacemaker firing.
- Relations between primary protein structure and ion channel function in Na+ channels have been examined using mutations of specific amino acid residues.
- The net effect is similar to the scorpion toxins. Finally, certain local anesthetic drugs, including lidocaine and procaine, block Na+ channels by binding reversibly to sites within the hydrophobic regions of the ion channel.
- Delayed-rectifier channels open slowly and show little inactivation during prolonged depolarizations.
- M channels represent a class of K+ channels that are activated in a time- and voltage-dependent fashion but are blocked by the neurotransmitter, acetylcholine, acting at muscarinic receptors.
- KATP channels exist in the CNS and appear to be involved in regulating the release of certain neurotransmitters and perhaps in determining the response of some neurons to changes in intracellular energy levels.
- Calcium (Ca2+) Channels Because Ca2+ is involved in numerous cellular events including enzyme activation, gene expression, and neurotransmitter release, the regulation of intracellular Ca2+ levels is of major importance to neurons.
- Most structural information about Ca2+ channels comes from skeletal muscle HVA Ca2+ channels.
« Although CNS neuropeptides are found predominantly in neurons, peptide receptors have been Somatostatin has been found in g-aminobutyric acid (GABA) neurons of ...» Document abstract
$6.95
7 word format
Language : english
biology
research papers
date published
26/11/2007
review : not yet assessed
level : Advanced
requested 1 times
SummaryThe past several decades have witnessed a veritable explosion of knowledge about the central nervous system (CNS), and in no area has this been as impressive as in peptide neurobiology. Numerous peptide neurotransmitter candidates have been identified and characterized, their CNS distributions mapped, and their genes cloned. The tenet “one neuron-one transmitter” erroneously attributed to Dale has been convincingly refuted with numerous demonstrations of neurons containing multiple peptides or combinations of peptide and nonpeptide neurotransmitters. Additionally, since the early 1980s there has been an embarrassment of riches in the form of knowledge about neurotransmitter receptor diversity, diversity of receptor-effector coupling, and neurotransmitter transporters. These discoveries have not yet been fully integrated into what is known about normal or aberrant CNS function, although dysfunction at virtually any level could conceivably lead to neuropsychiatric deficits.
Table of Contents
- By definition, a neuropeptide is a chain of two or more amino acids linked by peptide bonds, and differs from other proteins only in the length of the amino acid chain.
- Many of the known behavioral effects of neuropeptides are observed only after their direct injection into the CNS because most peptides do not penetrate the blood-brain barrier in amounts sufficient to produce effects before being inactivated by serum and tissue enzymes that degrade them.
- The tertiary structure for recognition is also used by the immune system for the production of specific antibodies, as well as by biological receptors.
- Neuropeptides are found throughout the CNS, as well as in various peripheral organs, such as the gastrointestinal tract, pancreas, and adrenal glands.
- In the cortex of rats SRIF is found in some of the large stellate-shaped neurons and in abundance among the fusiform-shaped, nonpyramidal neurons of layers II to V, and particularly in layer V of the sensory cortex.
- Through the use of retrograde tracing methods and dual staining techniques, several pathways for certain peptides have now been delineated.
- Some of the noradrenergic locus ceruleus neurons, in turn, project to the hypothalamic paraventricular nucleus where their input increases CRF synthesis and release.
- The neurotensin-neuromedin N gene was originally cloned from canine ileal mucosa, and complementary deoxyribonucleic acid (cDNA) probes constructed against this form were used to clone the rat gene.
« 5-HT]) type 1A [HT1A], 5-HT2, g-aminobutyric acid (GABA), as well and met-enkephalin, 5-HT1A and 5-HT2 muscarinic cholinergic, glutamate and GABAA receptors. ...» Document abstract
$6.95
7 word format
Language : english
psychology
research papers
date published
13/11/2007
review : not yet assessed
level : Advanced
requested 0 times
SummaryThe wonder of development is that a structure as complex as the human brain originates from a flat sheet of embryologic ectoderm. The final, formed brain shows remarkable order in its predictable cortical layering, its diversity of cortical areas, and the numerous networks linking specific cortical areas and subcortical structures. To have cells choosing to become a certain neuronal type, attaining the correct laminar position, finding the correct target, and expressing the correct neurotransmitters at first seems overwhelmingly difficult. However, the final, breathtakingly complex set of connections in the human brain depends on a series of much simpler decisions as neurons become progressively more restricted in the choices they make. These decisions require the subtle interplay of genetic and environmental factors; much has been learned at a molecular level about these processes. At first glance this information seems most relevant to mental retardation or autistic disorder, in which abnormal brain development results in lifelong disability. However, even schizophrenia is believed to originate in subtle aberrant brain development, and understanding it requires an understanding of its etiology.
Table of Contents
- Neurogenesis and Neural Identity The cerebral cortex possesses an orderly six-layered array of neuronal and glial cell types; layer I is the most superficial layer closest to the meninges, layer VI lies deeper, closest to white matter.
- The first postmitotic neurons leave the neuroepithelium and accumulate beneath the pial surface to form the preplate.
- The microenvironment may also provide other information about a neuron's fate, such as what kind of cortex to become.
- Neuronal Migration Once neurons are born in the ventricular zone, they migrate past earlier born neurons to assume their final laminar position.
- The leading edge of the axon, the growth cone, has an array of molecules on its surface.
- Cell Death Once cortical neurons are created and assume their connections, there is a period of naturally occurring cell death (apoptosis) in widespread areas.
- Implications for Psychiatry What happens when the developmental plan goes awry?
- Such subtle developmental anomalies are being discovered in many animal species.
- One dysfunctional neural network in schizophrenia links the association cortices of the frontal, parietal, and temporal lobes and the limbic cortex and subcortical structures.
- Postmortem morphometric studies of brains from patients with schizophrenia are consistent with in vivo imaging studies.
- A neuron-specific stain for nicotinamide-adenine dinucleotide phosphate-diaphorase (NADPH-d) has been used to study brains from patients with schizophrenia.
- Molecules crucial to normal brain development and postnatal plasticity are being investigated in schizophrenia.
- If abnormal brain development causes schizophrenia, why does onset of symptoms occur in late adolescence or early adulthood?
1
knowledge network
Sort by
Subject :
Type :
Extension :
Language :
Size :