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Neurotransmitters inhibitory

Picrotoxin has been instmmental in estabUshing an inhibitory neurotransmitter role for the amino acid, gamma-aminobutyric acid (GABA), quantitatively the most important inhibitory neurotransmitter in the mammalian CNS. Whereas glycine is predominately localized in the spinal cord, GABA... [Pg.461]

The mechanism by which the methylxanthines produce CNS stimulation is not clearly estabUshed. These agents may function, ia part, to limit chloride channel activation ia a manner similar to that of pentylenetetra2ol (7) or hicuculline (8). Another possibiUty is a specific antagonism of the inhibitory neurotransmitter adenosiae [58-61-7] (19) (19). [Pg.464]

GABA is the predominant inhibitory neurotransmitter in the CNS. Baclofen acts centrally as an agonist at the GABAb receptor, which increases inhibition of nerves. 3-Aminopropylphosphinic acid (3-APPi) has been shown experimentally to act as an antitussive at peripheral nerves and preclinical evidence suggests that baclofen indeed has antitussive actions clinically [3]. [Pg.195]

GABAb receptors mediate the slow and prolonged physiological effects of the inhibitory neurotransmitter GABA. Functional GABAb receptors are comprised of two subunits, GABAbR1 and GABAbR2. Both subunits are G-protein-coupled receptors, which couple to the Gi/o family and are densely expressed at spinal nociceptive synapses. [Pg.515]

An inhibitory postsynaptic potential is a local hypetpo-larizing potential at a postsynaptic membrane, which is elicited by the release of an inhibitory neurotransmitter via an inhibitory postsynaptic current. [Pg.664]

GABA is the most prominent inhibitory neurotransmitter in the mammalian nervous system and acts via GABA receptors. Activation of GABAb receptors by GABA released from local spinal interneurons (Fig. 1) negatively modulates nociceptive transmission in the spinal cord. Agonists at GABAb receptors... [Pg.931]

Synaptic vesicles isolated from brain exhibit four distinct vesicular neurotransmitter transport activities one for monoamines, a second for acetylcholine, a third for the inhibitory neurotransmitters GABA and glycine, and a fourth for glutamate [1], Unlike Na+-dependent plasma membrane transporters, the vesicular activities couple to a proton electrochemical gradient (A. lh+) across the vesicle membrane generated by the vacuolar H+-ATPase ( vacuolar type proton translocating ATPase). Although all of the vesicular transport systems rely on ApH+, the relative dependence on the chemical and electrical components varies (Fig. 1). The... [Pg.1279]

GABA receptors. Receptors for y-aminobutyric acid. GABA is an amino acid that acts as an inhibitory neurotransmitter in the CNS. [Pg.250]

Lamina II is also known as the substantia gelatinosa (SG) and can be divided into two layers, the outer layer (IIo) and the inner layer (Ili). This layer is densely packed with small neurons and lacks myelinated axons. Neurons with cell bodies in Hi receive inputs from low-threshold mechanoreceptive primary afferents, while those in IIo respond to inputs from high-threshold and thermoreceptive afferents. The intrinsic cells which comprise the SG are predominantly stalk and islet cells. Stalk cells are found located in lamina IIo, particularly on the border of lamina I, and most of their axons have ramifications in lamina I although some also project to deeper layers. These cells are thought to predominantly relay excitatory transmission. Islet cells, on the other hand, are located in Hi and have been demonstrated to contain the inhibitory neurotransmitters, y-aminobutyric acid (GABA), glycine and enkephalins in their dendrites. Hence these cells have been proposed to be inhibitory interneurons. [Pg.461]

Regardless of the underlying etiology, all seizures involve a sudden electrical disturbance of the cerebral cortex. A population of neurons fires rapidly and repetitively for seconds to minutes. Cortical electrical discharges become excessively rapid, rhythmic, and synchronous. This phenomenon is presumably related to an excess of excitatory neurotransmitter action, a failure of inhibitory neurotransmitter action, or a combination of the two. In the individual patient, however, it is usually impossible to identify which neurochemical factors are responsible. [Pg.444]

The major inhibitory neurotransmitter in the cerebral cortex is y-aminobutyric acid (GABA). It attaches to neuronal membranes and opens chloride channels. When chloride flows into the neuron, it becomes hyperpolarized and less excitable. This mechanism is probably critical for shutting off seizure activity by controlling the excessive neuronal firing. Some antiepileptic drugs, primarily barbiturates and benzodiazepines, work by enhancing the action of GABA. [Pg.444]

Status epilepticus occurs because the brain fails to stop an isolated seizure. The exact reason for this failure is unknown and probably involves many mechanisms. A seizure is likely to occur due to a mismatch of excitatory and inhibitory neurotransmitters in the brain. The primary excitatory neurotransmitter in the brain is glutamate. Glutamate stimulates postsynaptic N-methyl-D-aspartate (NMDA) receptors in the brain, causing an influx of calcium into the cells and depolarization of the neuron. Sustained depolarization may maintain SE and eventually cause neuronal injury and death.7 The primary... [Pg.462]

Harris-Warrick R. (2005). Synaptic chemistry in single neurons GABA is identified as an inhibitory neurotransmitter. J. Neurophysiol. 93, 3029-31. [Pg.50]

An unanswered question about adenosine is how this inhibitory neurotransmitter activates the ventrolateral preoptic area of the hypothalamus (VLPO), which contains a population of sleep-active neurons and is hypothesized to be... [Pg.442]


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