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Jai-hyun Hwang - One of the best experts on this subject based on the ideXlab platform.
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effect of subarachnoid GABApentin on tactile evoked allodynia in a surgically induced neuropathic pain model in the rat
Regional anesthesia, 1997Co-Authors: Jai-hyun Hwang, Tony L YakshAbstract:Background and Objectives Spinal gamma-aminobutyric acid (GABA) Receptors have been shown to modulate post-nerve injury-induced allodynia. This study sought to examine the antiallodynic effects of a GABA analog GABApentin [1-(aminomethyl)cyclohexaneacetic acid], given by subarachnoid injection in a rat neuropathic pain model. Methods The rats were prepared with lumbar subarachnoid catheters, and allodynia was induced in rats by ligation of the L5-6 nerve roots (Chung model). Results Spinal injection of GABApentin resulted in a dose-dependent (10-1,000 μg) antagonism of the allodynia at doses that had no detectable effect on motor function. Subarachnoid injection of either the GABA A antAgonist bicuculline (0.3 μg), or the GABA B antAgonist CGP 35348 (30 μg) 5 minutes before or 60 minutes after injection of GABA Receptor Agonist did not reverse the antiallodynic effects produced by GABApentin. Conclusions GABApentin shows antiallodynic effect, but its mechanism is not known. The failure to reverse this effect by GABA A or B antAgonists at doses that reverse the effects of the respective Agonists suggests that GABApentin is involved in the modulation of spinal systems by mechanisms that do not involve either a GABA A or a GABA B site.
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the effect of spinal GABA Receptor Agonists on tactile allodynia in a surgically induced neuropathic pain model in the rat
Pain, 1997Co-Authors: Jai-hyun Hwang, Tony L YakshAbstract:Abstract This study evaluated the effects of spinal gamma-aminobutyric acid (GABA) Receptor Agonists on the tactile allodynia observed in rats with ligation of the L5/L6 nerve roots (Chung model) and chronic lumbar intrathecal catheters. In these rats, the spinal injection of the GABA b Agonist baclofen (BAC; 0.03–0.3 μg) and GABA a Agonist muscimol (MUS; 0.1–1.0 μg) resulted in a dose-dependent antagonism of the allodynia at doses which had no detectable effect upon motor function. Intrathecal injection of the GABA b antAgonist CGP 35348 (CGP; 30 μg) or the GABA a antAgonist bicuculline (BIC; 0.3 μg) prior to injection of each GABA Receptor Agonist had little effect upon normal or tactile allodynic thresholds, but significantly reversed the anti-allodynic effects produced by the respective Receptor Agonists. The antAgonistic effects were limited to the Agonist of the respective Receptor. These observations indicate that spinal GABA a and GABA b Receptors modulate spinal systems activated by low threshold mechanoReceptors which mediate the allodynia observed following peripheral nerve injury.
Tony L Yaksh - One of the best experts on this subject based on the ideXlab platform.
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effect of subarachnoid GABApentin on tactile evoked allodynia in a surgically induced neuropathic pain model in the rat
Regional anesthesia, 1997Co-Authors: Jai-hyun Hwang, Tony L YakshAbstract:Background and Objectives Spinal gamma-aminobutyric acid (GABA) Receptors have been shown to modulate post-nerve injury-induced allodynia. This study sought to examine the antiallodynic effects of a GABA analog GABApentin [1-(aminomethyl)cyclohexaneacetic acid], given by subarachnoid injection in a rat neuropathic pain model. Methods The rats were prepared with lumbar subarachnoid catheters, and allodynia was induced in rats by ligation of the L5-6 nerve roots (Chung model). Results Spinal injection of GABApentin resulted in a dose-dependent (10-1,000 μg) antagonism of the allodynia at doses that had no detectable effect on motor function. Subarachnoid injection of either the GABA A antAgonist bicuculline (0.3 μg), or the GABA B antAgonist CGP 35348 (30 μg) 5 minutes before or 60 minutes after injection of GABA Receptor Agonist did not reverse the antiallodynic effects produced by GABApentin. Conclusions GABApentin shows antiallodynic effect, but its mechanism is not known. The failure to reverse this effect by GABA A or B antAgonists at doses that reverse the effects of the respective Agonists suggests that GABApentin is involved in the modulation of spinal systems by mechanisms that do not involve either a GABA A or a GABA B site.
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the effect of spinal GABA Receptor Agonists on tactile allodynia in a surgically induced neuropathic pain model in the rat
Pain, 1997Co-Authors: Jai-hyun Hwang, Tony L YakshAbstract:Abstract This study evaluated the effects of spinal gamma-aminobutyric acid (GABA) Receptor Agonists on the tactile allodynia observed in rats with ligation of the L5/L6 nerve roots (Chung model) and chronic lumbar intrathecal catheters. In these rats, the spinal injection of the GABA b Agonist baclofen (BAC; 0.03–0.3 μg) and GABA a Agonist muscimol (MUS; 0.1–1.0 μg) resulted in a dose-dependent antagonism of the allodynia at doses which had no detectable effect upon motor function. Intrathecal injection of the GABA b antAgonist CGP 35348 (CGP; 30 μg) or the GABA a antAgonist bicuculline (BIC; 0.3 μg) prior to injection of each GABA Receptor Agonist had little effect upon normal or tactile allodynic thresholds, but significantly reversed the anti-allodynic effects produced by the respective Receptor Agonists. The antAgonistic effects were limited to the Agonist of the respective Receptor. These observations indicate that spinal GABA a and GABA b Receptors modulate spinal systems activated by low threshold mechanoReceptors which mediate the allodynia observed following peripheral nerve injury.
G. Bartholini - One of the best experts on this subject based on the ideXlab platform.
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GABA Receptor Agonists: pharmacological spectrum and therapeutic actions.
Medicinal Research Reviews, 2006Co-Authors: G. BartholiniAbstract:Abstract From the data discussed in this review it appears that GABA Receptor Agonists exhibit a variety of actions in the central nervous system, some of which are therapeutically useful (Table V). GABA Receptor Agonists, by changing the firing rate of the corresponding neurons accelerate noradrenaline turnover without changes in postsynaptic Receptor density and diminish serotonin liberation with an up-regulation of 5HT2 Receptors. These effects differ from those of tricyclic antidepressants which primarily block monoamine re-uptake and cause down-regulation of beta-adrenergic and 5HT2 Receptors. The GABA Receptor Agonist progabide has been shown to exert an antidepressant action which is indistinguishable from that of imipramine in patients with major affective disorders. The fact that: (a) GABA Receptor Agonists and tricyclic antidepressants affect noradrenergic and serotonergic transmission differently; and (b) tricyclic antidepressants alter GABA-related parameters challenges the classical monoamine hypothesis of depression and suggests that GABA-mediated mechanisms play a role in mood disorders. Decreases in cellular excitability produced by GABAergic stimulation leads to control of seizures in practically all animal models of epilepsy. GABA Receptor Agonists have a wide spectrum as they antagonize not only seizures which are dependent on decreased GABA synaptic activity but also convulsant states which are apparently independent of alterations in GABA-mediated events. These results in animals are confirmed in a wide range of human epileptic syndromes. GABA Receptor Agonists decrease dopamine turnover in the basal ganglia and antagonize neuroleptic-induced increase in dopamine release. On repeated treatment, progabide prevents or reverses the neuroleptic-induced up-regulation of dopamine Receptors in the rat striatum and antagonizes the concomitant supersensitivity to dopaminomimetics. Behaviorally, GABA Receptor Agonists diminish the stereotypies induced by apomorphine or L-DOPA suggesting that GABAergic stimulation results also in an antidopaminergic action which is exerted beyond the dopamine synapse. These effects of GABA Receptor Agonists may represent the basis of the antidyskinetic action of these compounds which, however, remains to be fully confirmed. GABA Receptor Agonists reduce striatal acetylcholine turnover, an effect which occurs at doses much lower than those which affect dopamine neurons. Since hyperactivity of cholinergic neurons plays a determinant role in the pathogenesis of some parkinsonian symptoms, it is conceivable that GABAergic stimulation is effective in ameliorating Parkinson's disease.(ABSTRACT TRUNCATED AT 400 WORDS)
I V Pavlova - One of the best experts on this subject based on the ideXlab platform.
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effects of administration of an Agonist and an antAgonist of GABA a Receptors into the amygdala in rabbits on the respiratory and cardiac components of conditioned reflex fear
Neuroscience and Behavioral Physiology, 2015Co-Authors: I V Pavlova, M P RysakovaAbstract:The role of the GABAergic system of the amygdala in the autonomic and behavioral manifestations of conditioned reflex fear was studied in groups of “active” and “passive” rabbits selected on the basis of testing in an open field and a dark-light chamber. The animals were trained to a conditioned reflex by combining light (4 sec) and electrocutaneous stimulation of the hindlimbs (1 sec, 10 Hz). The extent of conditioned reflex fear was assessed in terms of changes in heart rate and respiratory movements in response to the conditioned and unconditioned stimuli as compared with rates prior to training. After training, a GABA Receptor Agonist (muscimol, 0.1 μg/1 μl) or antAgonist bicuculline metabromide, 0.5 μg/1 μl) was applied locally into the right or left basal nucleus of the amygdala via a cannula. Administration of muscimol into the amygdala induced more extensive autonomic changes in passive rabbits than in active, eliminating the reduction in the rate of respiratory movements in response to the conditioned stimulus typical of freezing, as well as weakening or altering responses to electrocutaneous stimulation, as judged by heart and respiratory rates. Activation of the left amygdala with bicuculline increased the probability of active motor reactions in active rabbits, while activation of the right amygdala, conversely, increased the probability of freezing. These results provide evidence of the nonequivalence of the GABAergic system of the amygdala in animals with active and passive behavioral strategies.
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effects of the GABA Receptor Agonist phenibut on spike activity and interactions between neocortex and hippocampus neurons in emotionally negative situations
Neuroscience and Behavioral Physiology, 2010Co-Authors: E A Zyablitseva, I V PavlovaAbstract:The nature of the spike activity of single neurons and interactions of neighboring cells in the hippocampus (field CA1) and parietal-temporal areas of the neocortex were compared in rabbits in emotionally negative situations in normal conditions and with decreased anxiety levels produced by systemic administration of the GABA Receptor Agonist phenibut. Analysis of the shapes of neuron spike activity autocorrelograms showed that phenibut increased the grouping of discharges in both structures, decreased interspike intervals within trains, increased the numbers of neurons with oscillations in the delta frequency range, and decreased the numbers of neurons with oscillations in the theta-1 range; in the hippocampus there was also an increase in frequencies in the theta-2 range. After phenibut, stimuli induced smaller rearrangements in neuron spike activity than in normal conditions. Analysis of cross-correlation histogram shapes showed that phenibut increased the numbers of common inputs to the neuron pairs being recorded and decreased the numbers of excitatory connections between cells in both structures; the hippocampus also showed an increase in the number of inhibitory connections. These changes provide evidence of a reduced level of activation of the hippocampus and neocortex after phenibut, with increases in neuron synchronization and decreases in the propagation of excitation between cells within structures, which correlated with decreases in the animals’ behavioral reactivity and anxiety.
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effects of the GABA Receptor Agonist phenibut on behavior and respiration in rabbits in emotionally negative situations
Neuroscience and Behavioral Physiology, 2008Co-Authors: E A Zyablitseva, I V PavlovaAbstract:Three groups of rabbits differing in terms of movement activity in an open field (active, passive, and intermediate animals) were used to study the effects of systemic administration of the GABA Receptor Agonist phenibut (40 mg/kg, s.c.) on behavior in the open field, behavioral reactivity, and changes in measures of respiration during exposure to emotionally negative stimuli. Phenibut administration led to decreases in horizontal movement activity and some elements of investigative behavior in rabbits in the open field, along with decreases in the reactivity of the animals to emotionally significant stimuli. There were reductions in the probabilities of both active (orientational-investigative, active defensive) and passive defensive (freezing) reactions. The effects of phenibut depended on the typological characteristics of the rabbits: its actions on behavior were most marked in active rabbits and were less marked in passive animals; phenibut had virtually no effect on the behavior of intermediate rabbits. The duration of inhalation by the rabbits on exposure to emotionally significant stimuli increased after phenibut, which contrasted with a reduction seen in normal animals; this is evidence for changes in the autonomic reactivity of the animals.
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Effect of GABA Receptor Agonist phenibut on behavior and respiration of rabbits in the negative emotional situation
Zhurnal vysshei nervnoi deiatelnosti imeni I P Pavlova, 2007Co-Authors: E A Ziablitseva, I V PavlovaAbstract:The influence of systemic injection of GABA-Receptor Agonist--phenibut (40 mg/kg, s/c) on open field behavior, behavioral reactivity and changes in respiratory parameters after exposure of negative emotional stimuli was studied in three rabbit groups differentiated by locomotor activity in open field (active, passive and medium-active animals). The injection of phenibut results in decrease of rabbits horizontal locomotor activity and some components of research behavior in open field and also decrease of behavioral reactivity on emotional stimuli. At the same time the probability of both an active orienting exploratory or defensive reactions and passive reactions (freezing) were decreased. The influence of phenibut depended on typological features of rabbits: the most potent effect occurred upon behavior of active rabbits, less on passive animals and practically none on medium-active rabbits. The phenibut injection results in increase of duration of inhalation during exposure to emotional stimuli, whereas it decreased in normal.
S.a. Greenfield - One of the best experts on this subject based on the ideXlab platform.
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The effects of gamma-hydroxybutyrate on the membrane properties of guinea-pig pars compacta neurons in the substantia nigra in vitro
Neuroscience, 2003Co-Authors: N.c. Harris, C. Webb, S.a. GreenfieldAbstract:Abstract The effects of gamma-hydroxybutyrate have been studied on the membrane properties of pars compacta neurons within the guinea-pig substantia nigra maintained in vitro . The effects of gammahydroxybutyrate are to (i) lower input resistance, (ii) hyperpolarize the cell membrane in a dose-dependent manner and (iii) facilitate calcium conductances. These effects are resistant to the blockade of sodium channels with tetrodotoxin and blockade of potassium channels with tetraethylammonium or 4-aminopyridine. Furthermore, these effects are only partially blocked by high doses of the GABA Receptor antAgonist bicuculline: indeed the effects of the GABA Receptor Agonist muscimol can be differentiated from those of gamma-hydroxybutyrate in that the latter is sensitive to application of barium ions. The results suggest that gamma-hydroxybutyrate acts to increase utilization of calcium, which in turn leads to an initiation of calcium-dependent events. The functional consequences of these effects of gamma-hydroxybutyrate are discussed with regard to its possible endogenous modulatory actions.
