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Gamma-aminobutyric neurons

Danik M, Puma C, Quirion R, et al. Widely expressed transcripts for chemokine receptor CXCR1 in identified glutamatergic, gamma-aminobutyric acidergic, and cholinergic neurons and astrocytes of the rat brain a single-cell reverse transcription-multiplex polymerase chain reaction study. J Neurosci Res 2003 74 286-295. [Pg.365]

Yuan CS, Mehendale S, Xiao Y, Aung HH, Xie JT, Ang-Lee MK. The gamma-aminobutyric acidergic effects of valerian and valerenic acid on rat brainstem neuronal activity. Anesth Analg 2004 98 353-358. [Pg.159]

Janowski, M. P. Sesack, S. R. (2004). Prefrontal cortical projections to the rat dorsal raphe nucleus ultrastructural features and association with serotonin and gamma-aminobutyric acid neurons. J. Comp. Neurol. 468, 518-29. [Pg.271]

Jarry H, Leonhardt S, Wuttke W (1991) Gamma-aminobutyric acid neurons in the preoptic/anterior hypothalamic area synchronize the phasic activity of the gonadotropinreleasing hormone pulse generator in ovariectomized rats. Neuroendocrinology 53 261-267... [Pg.143]

Bai, D., Zhu, G., Pennefather, P, Jackson, M. F., MacDonald, J. F., and Orser, B. A. (2001) Distinct functional and pharmacological properties of tonic and quantal inhibitory postsy-naptic currents mediated by gamma-aminobutyric acid(A) receptors in hippocampal neurons. Mol. Pharmacol. 59, 814-824. [Pg.92]

E Ng, G. Y., Bertrand, S., Sullivan, R., et al. (2001) Gamma-aminobutyric acid type B receptors with specific heterodimer composition and postsynaptic actions in hippocampal neurons are targets of anticonvulsant gabapentin action. Mol. Pharmacol. 59,144-152. [Pg.141]

Iversen, L. L. and Kelly, J. S. (1975) Uptake and metabolism of gamma-aminobutyric acid by neurones and glial cells. Biochem. Pharmacol. 24, 933-938. [Pg.189]

Larsson, O. M., Griffiths, R., Allen, I. C., and Schousboe, A. (1986) Mutual inhibition kinetic analysis of gamma-aminobutyric acid, taurine and beta-alanine high-affinity transport into neurons, and astrocytes evidence for similarity between the taurine and beta-ala-nine carriers in both cell types. J. Neurochem. 47,426 132. [Pg.189]

Schousboe, A., Larsson, O. M., Wood, J. D., and Krogsgaard-Larsen, P. (1983) Transport and metabolism of gamma-aminobutyric acid in neurons and glia implications for epilepsy. Epilepsia. 24, 531-538. [Pg.189]

Figure 1.2 Serotonin is one of the brain s neurotransmitters. This image depicts serotonin transmission between neurons and the drug Ecstasy s effects on that transmission. Serotonin is normally removed from the synapse shortly after being released. Ecstasy blocks this mechanism, increasing the amount of serotonin in the synapse. This causes the postsynaptic neuron to be overstimulated by serotonin. Serotonin is one of many neurotransmitters that nerve cells can secrete. Other common neurotransmitters include dopamine, glutamate, gamma aminobutyric acid (GABA), noradrenaline, and endorphins. Figure 1.2 Serotonin is one of the brain s neurotransmitters. This image depicts serotonin transmission between neurons and the drug Ecstasy s effects on that transmission. Serotonin is normally removed from the synapse shortly after being released. Ecstasy blocks this mechanism, increasing the amount of serotonin in the synapse. This causes the postsynaptic neuron to be overstimulated by serotonin. Serotonin is one of many neurotransmitters that nerve cells can secrete. Other common neurotransmitters include dopamine, glutamate, gamma aminobutyric acid (GABA), noradrenaline, and endorphins.
The diagram below shows the pathway of pain transmission from the peripheral nerves to the cerebral cortex. There are three levels of neuronal involvement and the signals may be modulated at two points during their course to the cerebral cortex. Descending inhibitory pathways arise in the midbrain and pass to the dorsal horn as shown. Multiple different neurotransmitters are involved in the pathway and include gamma-aminobutyric acid (GABA), N-methyl-D-aspartate (NMDA), noradrenaline and opioids. [Pg.199]

In simple terms, messages travel along neurons (nerve cells) in the form of an electrical current that moves from one end of the neuron to its opposite end. The electric current is produced by a flow of sodium ions (Na ") and potassium ions (K ) across the nerve membrane, as shown in the diagram on page 11. When the electrical current reaches the end of the neuron, it causes the release of a chemical known as a neurotransmitter. Some examples of neurotransmitters are acetylcholine, serotonin, dopamine, GABA (gamma-aminobutyric acid), and norepinephrine. [Pg.10]

The mechanism of action of acamprosate in the maintenance of alcohol abstinence is not completely understood. Chronic alcohol exposure is hypothesized to alter the normal balance between neuronal excitation and inhibition. Studies suggest acamprosate may interact with glutamate and gamma-aminobutyric acid (GABA) neurotransmitter systems centrally, and have led to the hypothesis that acamprosate restores this balance. [Pg.1326]

Davis M, Myers KM (2002) The role of glutamate and gamma-aminobutyric acid in fear extinction clinical implications for exposure therapy. Biol Psychiatry 52 998-1007 Dawson VL, Kizushi VM, Huang PL, Snyder SH, Dawson TM (1996) Resistance to nemotox-icity in cortical cultures from neuronal nitric oxide synthase-deficient mice. J Nemosci... [Pg.520]

Mechanism of Action An anticonvulsant that blocks repetitive, sustained firing of neurons by enhancing the ability of gamma-aminobutyric acid to induce an influx of chloride ions into the neurons may also block sodium channels. Therapeutic Effect Decreases seizure activity... [Pg.1245]

Pereira EFR, Reinhardt-Maehcke S, Schrattenholz A, et al Identification and functional characterization of a new agonist site on nicotinic acetylchohne receptors of cultured hippocampal neurons. J Pharmacol Exp Ther 265 1474-1491, 1993 Perez de la Mora N, Hemandez-Gomez AM, et al Cholecystokinin-8 increases K -evoked [ H] gamma-aminobutyric acid release in shces from various brain areas. Eur J Pharmacol 250 423-430, 1993... [Pg.717]

It is beta-4 (chlorophenyl)-gamma aminobutyric acid. It is a powerful neuronal depressant. It reduces the release of excitatory transmitter and is antinociceptive in animal studies. It inhibits monosynaptic and polysynaptic reflex transmission at spinal level, probably by stimulating the GABAg... [Pg.113]

Perhaps the most well-known example is the acetylcholine receptor located on the postsynaptic membrane of the neuromuscular junction49 56 (Fig. 4-1). When bound by acetylcholine molecules, the receptor activates and opens a pore through the cell membrane, thereby increasing the permeability of the muscle cell to sodium.38 56 This action results in depolarization and excitation of the cell because of sodium influx. Another important example of a receptor-ion channel system is the gamma-aminobutyric acid (GABA)-benzodiazepine-chloride ion channel complex found on neuronal membranes in the central nervous sys-... [Pg.41]


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See also in sourсe #XX -- [ Pg.176 ]

See also in sourсe #XX -- [ Pg.176 ]




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