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At least 343 records · Page 19Linked to original sources
PubMed1985

Enhanced depressor effect of muscimol in the DOCA/NaCl hypertensive rat: evidence for altered GABAergic activity in brain.

To elucidate the role of the central gamma-aminobutyric acid (GABA) system in the maintenance of deoxycorticosterone (DOCA)NaCl hypertension, the responses of mean arterial pressure (MAP), plasma norepinephrine (NE), and epinephrine (EP) to intracerebroventricular (ICV) administration of muscimol, a GABA agonist, and the responses of MAP to bicuculline, a GABA antagonist, and to clonidine, an alpha 2-adrenoceptor agonist known to lower blood pressure by inhibiting sympathetic tone, were examined in conscious, unrestrained 4 week DOCA/NaCl hypertensive rats and age-matched uninephrectomized control rats. Muscimol (50-1000 ng/300 g, ICV) caused dose-dependent decreases in MAP which were greater in DOCA/NaCl rats than in controls. Basal plasma NE and EP were significantly higher in DOCA/NaCl rats than in controls. Muscimol (1000 ng/300 g, ICV) induced decreases in plasma EP which were greater in DOCA/NaCl rats than in controls without changing NE levels in either group. Bicuculline (3 micrograms/300 g, ICV) caused increases in MAP which were the same in both groups. The depressor response to clonidine (5 micrograms/300 g) was greater in DOCA/NaCl rats than in controls. These results suggest that the activity of the central GABAergic system is altered in the rat with established DOCA/NaCl hypertension and that the alteration in central GABAergic function may be related to the increased sympathoadrenal activity and the maintenance of hypertension in this model.

Animals↗
PubMed2000

Forebrain lesions differentially affect drinking elicited by dipsogenic challenges and injections of muscimol into the median raphe nucleus.

Injections of muscimol into the median raphe nucleus (MR) elicit intense drinking in normally hydrated rats. To determine whether this response is dependent on forebrain systems mediating other aspects of water intake, the authors examined the effects of lesions of the subfornical organ (SFO), median preoptic nucleus (MnPO), lateral preoptic area (LPO), or lateral hypothalamus (LH) on the drinking. Lesions of the SFO or LH attenuated muscimol-elicited drinking, whereas lesions of the MnPO or LPO increased water intake after the treatment. All of the lesion groups showed a deficit in drinking to injections of polyethylene glycol and at least one of the doses of hypertonic saline. Only the SFO- and LH-lesioned groups showed a suppression of drinking to systemic injections of angiotensin II, suggesting that the drinking elicited by intra-MR injections of muscimol may involve changes in the central circuits mediating angiotensin-induced drinking.

Animals↗
PubMed2000

Huperzine A reverses scopolamine- and muscimol-induced memory deficits in chick.

AIM: To study the effects of huperzine A on disruption of spatial memory induced by scopolamine (a muscarinic antagonist) and muscimol (a GABAA agonist) in passive avoidance task. METHODS: One-trial passive avoidance task was used to investigate the effects of huperzine A. The avoidance rate was used to evaluate memory retention. RESULTS: Both scopolamine (100 ng) and muscimol (50 ng), injected intracranially 5 min before training, resulted in a decreased avoidance rate. Huperzine A (25 ng), injected intracranially 15 min before training, reversed memory deficits induced by scopolamine and muscimol at 30 min after training, and this reversal persisted at least 1 h. The improving effects of huperzine A exhibited a bell-shaped dose-response curve. CONCLUSION: Huperzine A improved the process of memory formation not only by acting as a highly potent and selective inhibitor of AChE, but also by antagonizing effects mediated through the GABAA receptor.

Alkaloids↗
PubMed1992

[Effects of GABA antagonist-induced seizures on 3H-muscimol and 3H-diazepam binding in the rat striatum].

The binding of 3H-muscimol and 3H-diazepam to rat striatum membranes after picrotoxin- and bicuculline-induced seizures was characterized. No alteration in the maximal binding capacity (Bmax) of 3H-muscimol was observed. However, bicuculline produced a 27% decrease in Kd. Both picrotoxin and bicuculline increased the binding capacity of 3H-diazepam. Bicuculline produced a 86% increase in Kd. These results suggest that the GABA antagonists-induced seizures may modulate 3H-muscimol and 3H-diazepam binding in rat striatum.

Animals↗
PubMed1978

[Ventrobulbular hypotensive action of muscimol].

Muscimol, a rigid analogue of GABA has been injected in the CNS of urethane anesthetized, normotensive cats. Injected either intracisternally (1 or 2 microgram/kg, 0.05 ml) or directly by microinjection in a restricted ventrolateral region of the brain stem (0.5 or 1 microgram/kg, 0.5 microliter), muscimol induced hypotension and bradycardia. These central cardiovascular effects of muscimol were antagonized by bicuculline, a "specific" GABA antagonist agent. These data emphasize the involvement of gabergic mechanisms in the central cardiovascular control, at least in the ventrolateral part of the medulla oblongata.

Animals↗
PubMed1990

Changes in succinate dehydrogenase activity of rats after intraventricular injections of GABA, muscimol and picrotoxin.

Effects of intraventricular injections of GABA, and a GABA agonist, muscimol and an antagonist, picrotoxin on succinate dehydrogenase (SDH) enzyme activity in plasma and a few hypothalamic nuclei of brain of rats have been investigated using biochemical, histochemical and cytophotometric techniques. Results show that SDH decreased by GABA and muscimol treatment, and increased after picrotoxin injection. From the above findings, it is apparent that GABA, muscimol and picrotoxin influence SDH activity of plasma and hypothalamic nuclei.

Animals↗
PubMed1987

[Effects of systemic administration of muscimol (gamma-aminobutyric acid agonist) on the corticotropic adenohypophysis].

A short and moderate increase in plasma ACTH and corticosterone levels was observed after i.v. injection of the GABA-agonist, muscimol as a bolus of 0.5 mg . kg-1. Doses lower than 0.3 mg . kg-1 were ineffective. 6 hrs. after i.v. injection of 1 ml of an undiluted immune serum raised against oCRF41, resting hormone levels were markedly diminished, stress-induced responses were almost completely suppressed, whereas i.v. injection of muscimol still resulted in an unaltered adrenocorticotropic stimulation. Adenohypophysectomized animals displayed a low basal adrenal function, no stress-induced response and interestingly enough no longer responded to i.v. muscimol injection. Consequently, acute GABA-ergic stimulation appears to act directly onto the pituitary corticotroph cells. It cannot be inferred so far whether this action is of physiological importance but it can at least contribute to elucidate some controversial data prevailing in this field.

Adrenocorticotropic Hormone↗
PubMed1986

Localization of 3H-GABA, -muscimol, and -glycine in goldfish retinas stained for glutamate decarboxylase.

Glutamic acid decarboxylase (GAD), the synthesizing enzyme for the neurotransmitter GABA, has been localized in goldfish retina using a new antiserum. We observed at least six types of GAD-immunoreactive amacrine cells, one of which was large and pyriform (Ab type). In addition, immunoreactive synaptic terminals were located throughout the inner plexiform layer (IPL). Amacrine cells that were GAD-immunoreactive also had high-affinity uptake mechanisms for both 3H-GABA and 3H-muscimol that were detectable autoradiographically. Type Ab pyriform amacrine cells were heavily labeled because of 3H-GABA uptake and were GAD-immunoreactive. Other types of GAD-immunoreactive amacrine cells, including a subpopulation of Ab amacrines, were lightly labeled because of 3H-GABA uptake. Because the same neurons that were GAD-immunoreactive also accumulated 3H-GABA and 3H-muscimol, these three are appropriate markers for GABAergic cells in the goldfish retina. However, the uptake of 3H-muscimol by many non-GAD-immunoreactive cells, detectable at longer autoradiographic exposure times, indicates that this label must be used with caution. Thirty percent of goldfish retinal amacrine cells are GABAergic, and their processes are distributed throughout all levels of the IPL. Few GAD-immunoreactive amacrine cells accumulated 3H-glycine, so the goldfish retina contains distinct populations of glycinergic and GABAergic amacrine cells.

Animals↗
PubMed1982

Single channel currents activated by gamma-aminobutyric acid, muscimol, and (-)-pentobarbital in cultured mouse spinal neurons.

The patch electrode technique was used to record single channel current pulses in tissue-cultured mouse spinal cord neurons. In agreement with earlier noise studies, channels activated by gamma-aminobutyric acid (GABA), muscimol, and (-)-pentobarbital were found to have equal unit conductances. The kinetics of channel closing were studied by analyzing the distributions of open state lifetimes. Channels activated by (-)-pentobarbital and muscimol had longer mean open times than channels activated by GABA. As a result, the kinetics of (-)-pentobarbital- and muscimol-activated channels could be studied in greater detail. Most observed open state lifetime distributions were not exponential but contained an excess of short duration events. A sum of two exponential functions gave a much better fit than a single exponential function to most observed open state lifetime distributions. A critical comparison of noise analysis with single channel recording shows that the fast process responsible for the rapid closures would be very difficult to detect in a noise experiment. The channel noise is dominated by the slower process, and as a result, the relaxation time of the slower kinetic component derived from single channel studies is close to the mean open state lifetime derived from noise measurements. The observation of a faster process points toward either an additional population of channels or a scheme for the channel closing transition which is not a simple first order process.

Animals↗
PubMed1981

Central cardiovascular effects of taurine: comparison with homotaurine and muscimol.

The central cardiovascular effects of taurine were compared with those of homotaurine and muscimol. The drugs were injected i.c.v. in cumulative doses into pentobarbital-anesthetized cats. Muscimol (0.1-30 microgram/kg) produced dose-dependent hypotension and bradycardia, with a maximum effect of 70 +/- 5 mm Hg and 75 +/- 5 beats/min, respectively. Homotaurine led to a dose-related fall in blood pressure and heart rate; maximum effects were obtained with 300 microgram/kg and averaged 55 +/- 3 mm Hg and 73 +/- 3 beats/min. For both drugs, the dose-response curves were shifted to the right by pretreatment with 10 microgram/kg of bicuculline i.c.v. This antagonism confirms that the central cardiovascular effects of muscimol and homotaurine are mediated by a stimulation of gamma-aminobutyric acid receptors. Taurine produced dose-related hypotension and bradycardia. The depressive effects of taurine started at a dose of 10 microgram/kg; at a dose of 1000 microgram/kg, the maximum effects observed were a 55 +/- 7 mm Hg hypotension and a 53 +/- 8 beats/min bradycardia. These effects were not affected by bicuculline pretreatment, but strychnine (i.c.v) prevented the effects of taurine. These findings indicate that glycine-type receptors may be involved in the taurine effects rather than gamma-aminobutyric acid type receptors. However, these results do not exclude the involvement of taurine-type receptors for which the specific antagonists is not yet available.

Animals↗
PubMed1995

Intrathecal baclofen and muscimol, but not midazolam, are antinociceptive using the rat-formalin model.

Both gamma-aminobutyric acid (GABA)A and GABAB receptor subtypes have been implicated in spinally mediated antinociception in acute pain models. In the current study, the formalin test was used as a model of protracted nociception to examine the effect of intrathecally (i.t.) administered baclofen (GABAB agonist), muscimol (GABAA agonist) or midazolam (a benzodiazepine) on antinociception. At doses that did not affect motor function, baclofen (0.3 and 1.0 micrograms, i.t.) decreased the flinch response in a dose-dependent manner during Phase 1 and Phase 2. This effect was reversible by the GABAB-specific antagonist, CGP35348 ([P-(3-aminopropyl)-P-diethoxymethyl-phosphinic acid]). Muscimol (0.3 and 1.0 microgram i.t.) evoked a dose-dependent, bicuculline-reversible decrease in flinching during Phase 1 and Phase 2, but midazolam had no effect on either phase. No attenuation of the quiescent period between Phase 1 and Phase 2 was seen upon administration of baclofen, muscimol or midazolam. Additionally, no increase in nocifensive behavior was observed upon administration of either GABAA or GABAB antagonists alone. Therefore, our conclusions are that both GABAA and GABAB agonists are antinociceptive at the spinal cord level and that endogenous spinal GABA levels are insufficient for a GABA potentiator to act alone in an antinociceptive manner.

Animals↗
PubMedDate not supplied

Effect of vinconate against alterations in [3H]naloxone, [3H]MK-801 and [3H]muscimol bindings after transient cerebral ischemia in gerbils.

We examined the alterations of opioid (naloxone), N-methyl-D-aspartate and gamma-aminobutyric acidA receptors in the gerbil brain 7 days after cerebral ischemia using [3H]naloxone, [3H]MK-801 and [3H]muscimol autoradiography, respectively. We also evaluated the effect of vinconate against the alterations in these receptors. Transient cerebral ischemia was induced for 10 minutes, and vinconate (100 and 300 mg/kg) was given intraperitoneally 10 minutes before ischemia. [3H]MK-801 binding showed a more severe reduction than [3H]naloxone binding 7 days after cerebral ischemia, whereas [3H]muscimol binding was unchanged in almost all brain regions. Vinconate showed a significant prevention against the reduction in [3H]naloxone binding in all brain areas. This drug also prevented a significant reduction in [3H]MK-801 binding in most of the brain regions. Furthermore, [3H]muscimol binding in vinconate-treated gerbils exhibited a significant increase compared with that in sham-operated animals. These results show that opioid and N-methyl-D-aspartate receptors are very sensitive to transient cerebral ischemia, whereas gamma-aminobutyric acidA receptors are particularly resistant. They also suggest that vinconate has a potent protective effect against the alterations of opioid and N-methyl-D-aspartate receptors. These findings might be of interest in relation to the mechanism of ischemic neuronal damage.

Animals↗
PubMed1996

Laminar distribution of MK-801, kainate, AMPA, and muscimol binding sites in cat visual cortex: a developmental study.

We used quantitative autoradiography to determine whether the development of glutamate receptors correlates with the sensitive period for monocular deprivation in the visual cortex. To study glutamate receptors, we incubated sections of cat visual cortex with tritiated (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10imin e-maleate (MK-801), tritiated kainate, and tritiated amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA). [3H]MK-801 is a noncompetitive ligand for the N-methyl-D-aspartate (NMDA) receptor. [3H]kainate and [3H]AMPA are competitive ligands for non-NMDA receptors. We used [3H]muscimol, which binds to GABAA receptors, so that we would have one control ligand that binds to a nonglutamate receptor. When all layers were combined, the results confirmed our previous studies with homogenate binding. [3H]MK-801 and [3H]kainate binding were significantly greater at 42 days than at earlier or later times. [3H]AMPA and [3H]muscimol binding did not show such a peak. This suggests that MK-801 and kainate binding sites are more likely to be involved in plasticity than are AMPA and muscimol binding sites. In layers 2/3, MK-801 had the greatest age-dependent changes; in layers 5 and 6, kainate binding changed most with age. This suggests that the mechanisms of plasticity may vary with cortical layer.

Animals↗
PubMed1982

Characterization of solubilized benzodiazepine and muscimol binding sites from rat brain.

Binding sites for muscimol and flunitrazepam were solubilized and their properties studied by ultrafiltration, isoelectro-focusing and cation-exchange chromatography methods. The heterogenity of binding sites for flunitrazepam was demonstrated in the ultrafiltration experiments: the binding sites with a molecular weight of more than 300,000 dalton were sensitive to stimulation by gamma-aminobutyric acid (GABA) and those with a molecular weight of less than 300,000 dalton were not. The binding sites for flunitrazepam appeared to be low acidic molecules with pI 5.6-6.0 and binding sites for muscimol an apparently more heterogenous distribution in the range of pH 4.6 to 5.9 was detected. Cation-exchange chromatography revealed two subpopulations of binding sites for muscimol one of which copurified together with binding sites for flunitrazepam. Each subpopulation exhibited only one class of binding site with Kd = 20 nM for a subpopulation copurifying together with binding sites for flunitrazepam and Kd = 9 nM for the other.

Animals↗
PubMed1978

Quantitative visualization of gamma-aminobutyric acid receptors in hippocampus and area dentata demonstrated by [3H]muscimol autoradiography.

Muscimol, a potent gamma-aminobutyric acid (GABA) agonist, was used in a radioactively labeled form for the quantitative localization of GABA receptors in the rat's hippocampus (CA(1) to CA(4)) and area dentata. [(3)H]Muscimol was injected directly in vivo or used in the incubation medium of tissue slices, and the tissues were then fixed and prepared for autoradiography. [(3)H]Muscimol-bound GABA receptors are weakly though evenly distributed over the fimbria of the fornix. There was a laminar distribution in CA(1) to CA(4) and the area dentata, with an increasing density of the GABA receptors in that order. The lowest density was found in the alveus of CA(1) and CA(2) and the highest in the stratum granulosum of the area dentata. The greatest density was found in the neuropil between granule cells, in which are found dendrites and the basket-like plexuses of the inhibitory GABA-containing local circuit neurons. The molecular layers of the area dentata, CA(1), and CA(2) also have a high density of GABA receptors, indicating a probable distribution over the dendrites of granule and pyramidal cells. The laminar distribution of GABA receptors in the hippocampus and area dentata is similar to the distributions of the GABA-synthesizing enzyme, glutamate decarboxylase, and of GABA previously published. Neurons with label of various density are found in the polymorphic cell layer of the area dentata, in the stratum radiatum of CA(3), and in CA(4). These are possibly the GABA-containing basket local circuit neurons.

Amanita↗
PubMed1999

Tremor arrest with thalamic microinjections of muscimol in patients with essential tremor.

Six patients undergoing stereotactic procedures for essential tremor received microinjections of muscimol (a gamma-aminobutyric acid-A [GABA(A)] agonist) into the ventralis intermedius thalamus in areas where tremor-synchronous cells were identified electrophysiologically with microelectrode recordings and where tremor reduction occurred with electrical microstimulation. Injections of muscimol but not saline consistently reduced tremor in each patient. The effect had a mean latency of 7 minutes and lasted an average of 9 minutes. We propose that GABA-mediated thalamic neuronal inhibition may represent a mechanism underlying the effectiveness of surgery for tremor and that GABA analogues could potentially be used therapeutically.

Aged↗
PubMed1983

Neuronal subpopulations in cat retina which accumulate the GABA agonist, (3H)muscimol: a combined Golgi and autoradiographic study.

Golgi impregnation techniques were combined with electron microscopic autoradiography of (3H-muscimol in order to provide morphological identification of labeled neurons in the cat retina. This gamma-aminobutyric acid (GABA) agonist has been shown to label the same neurons which accumulate (3H)GABA. Selected cells were photographed and drawn by the aid of a camera lucida drawing tube prior to being thin sectioned for autoradiography. The (3H)muscimol-accumulating neurons which were identified include an interplexiform cell, five classes of conventional amacrine cell, and another cell with its soma located in the ganglion cell layer which is either a ganglion cell or a displaced amacrine. The conventional amacrine cells were compared with the recent morphological classification of Kolb et al. (Vision Res. 21: 1081-1114, '81) and identified as A2, A10, A13, A17, and A19 amacrine cells. These cells exhibit a widespread distribution providing input to all five strata of the inner plexiform layer.

Animals↗
PubMedDate not supplied

Affinities and densities of high-affinity [3H]muscimol (GABA-A) binding sites and of central benzodiazepine receptors are unchanged in autopsied brain tissue from cirrhotic patients with hepatic encephalopathy.

The integrity of GABA-A receptors and of central benzodiazepine receptors was evaluated in membrane preparations from prefrontal cortex and caudate nuclei obtained at autopsy from nine cirrhotic patients who died in hepatic coma and an equal number of age-matched control subjects. Histopathological studies revealed Alzheimer Type II astrocytosis in all cases in the cirrhotic group; controls were free from neurological, psychiatric or hepatic diseases. Binding to GABA-A receptors was studied using [3H]muscimol as radioligand. The integrity of central benzodiazepine receptors was evaluated using [3H]flunitrazepam and [3H]Ro15-1788. Data from saturation binding assays was analyzed by Scatchard plot. No modifications of either affinities (Kd) or densities (Bmax) of [3H]muscimol of central benzodiazepine binding sites were observed. These findings do not support recent suggestions that alterations of either high-affinity GABA or benzodiazepine receptors play a significant role in the pathogenesis of hepatic encephalopathy.

Affinity Labels↗