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PubMed1984

Autoradiographic studies of [3H]-glycine, [3H]-GABA, and [3H]-muscimol uptake in the mudpuppy retina.

Autoradiographic studies showed selective accumulation of [3H]-glycine, [3H]-GABA, and the GABA agonist [3H]-muscimol by neurons of the mudpuppy retina. [3H]-Glycine was taken up by bipolar cells, amacrine cells, and displaced amacrine or ganglion cells. Both [3H]-GABA and [3H]-muscimol were also accumulated by bipolar cells, amacrine cells and ganglion layer cells. However, the [3H]-GABA uptake pattern differed from that of [3H]-muscimol in showing labeling of horizontal cells, an increased percentage of cells in the ganglion cell layer, and a band in the most proximal portion of the inner plexiform layer. Variations in grain density suggested the presence of multiple subpopulations of [3H]-glycine- and [3H]-GABA-labeled amacrine cells. The labeled cells may play a role in inhibitory pathways in the inner retina.

Animals↗
PubMed1982

Stimulatory and protective effects of benzodiazepines on GABA receptors labeled with [3H]muscimol.

We investigated the effects of benzodiazepines on [3H]muscimol binding to rat brain membranes and on heat inactivation of GABA receptors. Scatchard analysis of [3H]muscimol binding to frozen and 0.05% Triton X-100 treated membranes revealed two components; a higher affinity (Kd = 2.2 nM, Bmax = 1.2 pmol/mg protein) and a lower affinity component (Kd = 15.9 nM, Bmax = 4.4 pmol/mg protein). Diazepam and flurazepam (3 microM) increases significantly the specific binding of 40 nM but not of 2 nM [3H]muscimol. This stimulation was attributed to an increase in the affinity of the lower affinity component for GABA receptors. The time course of heat inactivation of GABA receptors revealed rapidly and then slowly denaturating Phases. These observations would suggest that there are multiple GABA receptors with different sensitivities to the heat treatment. Diazepam depressed remarkably the slowly denaturating phase(s). After heat treatment for 50 min, the single component of GABA receptors with Kd of 14.3 nM and Bmax of 0.6 pmol/mg protein survived, whereas in the membranes preincubated with 3 microM diazepam, the Kd and Bmax of the still viable GABA receptors were 14.8 nM and 1.14 pmol/mg protein, respectively. In light of these findings, the stimulation of the lower affinity component of GABA receptors may be related to the protective effects of these drugs against heat inactivation.

Animals↗
PubMed1987

[3H]muscimol binding sites increased in autopsied brains of chronic schizophrenics.

[3H]muscimol binding and glutamic acid decarboxylase (GAD) activity in the prefrontal cortex and caudate nucleus of autopsied brains from 19 chronic schizophrenics and 17 control subjects were investigated. In the schizophrenics, saturation analysis with varying concentrations of [3H]muscimol revealed an increase in the number of GABAA receptors, but there was no significant difference in the affinity. In addition, the enhancement of [3H]muscimol binding by diazepam was significantly greater in schizophrenics than in controls. GAD activity did not differ between controls and schizophrenics. The possibility that GABAergic mechanisms might play a role in case of chronic schizophrenia should be given further attention.

Adult↗
PubMed1982

On the involvement of GABA in the analgesia produced by baclofen, muscimol and morphine.

In the mouse hot-plate test (50 degrees C), muscimol produced analgesia which was blocked by bicuculline but not by picrotoxin. Analgesia produced by baclofen was dose-dependent and stereoselective, but was not blocked by bicuculline, picrotoxin or naloxone. Morphine-induced analgesia was not altered by bicuculline. The inhibitors of GABA-transaminase, amino-oxyacetic acid, gamma-acetylenic GABA and gamma-vinyl GABA, produced analgesia which was much more prolonged than that observed with muscimol, baclofen or morphine. The analgesic action of these agents was not significantly altered by bicuculline. At a higher plate temperature (55 degrees C), GABA-transaminase inhibitors produced minimal analgesia but significantly enhanced the analgesic action of baclofen. gamma-Vinyl GABA markedly increased both the peak effect and the duration of analgesia but gamma-acetylenic GABA and amino-oxyacetic acid caused smaller increases. In the mouse hot-plate test, bicuculline-sensitive GABA receptors appear to mediate the analgesic action fo muscimol. Analgesia produced by baclofen, morphine and inhibitors of GABA-transaminase may involve another class of GABA receptors which are insensitive to bicuculline.

4-Aminobutyrate Transaminase↗
PubMed1984

Blockade of bicuculline-induced pressor and tachycardic responses by forebrain administration of muscimol.

To determine whether i.v. administered bicuculline acts in the forebrain to increase arterial blood pressure and heart rate, this agent was administered i.v. to chloralose anesthetized cats that had muscimol injected into and restricted to the forebrain ventricles. Bicuculline (0.5 mg/kg i.v.) given alone increased arterial pressure by 56 +/- 8 mm Hg and heart rate by 45 +/- 11 beats/min. Bicuculline given to animals exposed to muscimol exhibited no increase in either of these parameters. Muscimol localized to the forebrain did not alter the pressor response to a non-GABA antagonist agent, strychnine, indicating a specific interaction of the drugs with GABA receptors in the forebrain.

Animals↗
PubMed1986

Low doses of muscimol produce anticonflict actions in the lateral septum of the rat.

Muscimol microinjected into the lateral septum of the rat produced a dose dependent increase in punished responding over the dose range of 100 pg-5 ng. The higher doses used (10 ng and 1 microgram) produced sedation and ataxia, markedly reducing the number of approaches to the water spout. This steep, biphasic dose response curve for the anticonflict actions of muscimol may explain contradictory findings in the literature concerning GABAergic involvement in the anxiolytic actions of benzodiazepines. The low dose of muscimol needed to produce a significant anticonflict effect in the lateral septum suggests that this nucleus may be a critical site in anxiety-related behaviors.

Animals↗
PubMed1989

Comparative studies of locomotor behavior following microinjections of muscimol into various sites in the paramedian tegmentum.

Microinjections of various doses of muscimol into the median raphe nucleus, the dorsal raphe nucleus or the caudal portion of the ventral tegmental area elicited dose-dependent increases in locomotor activity. In contrast, injections into the rostral portion of the ventral tegmental area or the midline pontine tegmentum caudal to the median raphe were ineffective. Lower doses of muscimol were required to produce hyperactivity after injections into the median raphe than after injections into any of the other sites. These findings suggest that the median raphe nucleus is the most sensitive site in the paramedian tegmentum for the elicitation of hyperactivity by muscimol.

Animals↗
PubMed1990

Effects of post-training bicuculline and muscimol on retention: lack of state dependency.

Immediate post-training intraperitoneal injections of the GABA antagonist bicuculline (0.25 or 0.5 mg/kg) or of the GABA agonist muscimol (1.0 or 2.0 mg/kg) improved and impaired, respectively, retention of CD1 mice tested 24 h after training in a one-trial inhibitory avoidance task. Administration of bicuculline or muscimol prior to the retention test did not modify retention latencies of mice that had received either saline or the same drug immediately after training. These findings indicate that the effects of post-training administration of bicuculline and muscimol on retention are not state dependent and, thus, argue against a general state-dependency interpretation of the effects of post-training treatments affecting retention. The findings are consistent with previous evidence indicating that GABAergic drugs affect retention through influences on memory storage processes.

Animals↗
PubMed1994

Perfusion of the preoptic area with muscimol or prostaglandin E2 stimulates cardiovascular function in anesthetized rats.

The effect of unilateral perfusion of the preoptic area (POA) utilizing in vivo microdialysis with the GABAergic agonist, muscimol, or prostaglandin E2 (PGE2) on cardiovascular function (heart rate, blood pressure and cutaneous blood flow) was determined in halothane-anesthetized rats. Perfusion of muscimol or PGE2 increased the heart rate, 55 +/- 6 beats/min and 69 +/- 12 betas/min, respectively (P < 0.01). Cutaneous paw blood flow tended to decrease. Blood pressure did not change in response to the perfusion of muscimol, but increased 9 mmHg in response to the perfusion of PGE2 (P < 0.01). The increases in heart rate and blood pressure were blocked by systemic administration of propranolol or adrenalectomy (P < 0.01), suggesting that these effects were due to the activation of the sympathetic innervation of the heart or adrenal gland. It is proposed that the POA provides a tonic inhibitory afferent to posterior hypothalamus neurons which regulate cardiovascular function.

Adrenal Medulla↗
PubMed1987

Age-related changes in striatal dopamine activity following nigral muscimol infusions.

Microinfusions of muscimol into the substantia nigra pars reticulata produced marked increases in striatal dopamine (DA) utilization without affecting striatal DA concentration in adult rats. In contrast, muscimol increased striatal DA concentration and decreased DA utilization in 16-day-old rat pups. The striatal norepinephrine concentration was not altered in either group. Since previous studies have shown that similar infusions of muscimol are anticonvulsant in adults and proconvulsant in rat pups, our results suggest that the nigrostriatal pathway may play an important role in mediating the nigral effects on seizures.

Aging↗
PubMed1994

Chronic NMDA receptor blockade or muscimol inhibition of cerebellar cortical neuronal activity alters the development of spinocerebellar afferent topography.

The requirement for cerebellar cortical neuronal activity in the development of spinocerebellar afferent topography was investigated in neonatal rats. In adult rats lower thoracic-upper lumbar spinocerebellar projections are localized to sharply circumscribed patches in the granule cell layer of the cerebellar anterior lobe. In transverse sections these patches appear as sagittally oriented stripes. This pattern develops postnatally as many spinal axons which initially project between the incipient stripes are eliminated thereby sharpening the stripe boundaries. We attempted to alter cerebellar cortical neuronal activity in neonatal animals to study the effects of these changes on the development of spinocerebellar stripes. In some experiments glutaminergic excitatory synaptic transmission was chronically blocked with the N-methyl-D-aspartate (NMDA) receptor antagonist 2-aminophosphovaleric acid (APV). In other experiments postsynaptic activity was directly inhibited by the gamma-aminobutyric acid agonist muscimol. Chronic exposure to APV or to muscimol did not affect the initial development of spinocerebellar projections; many spinal axons were present in the anterior lobe and arranged in incipient stripes. Both the APV and the muscimol appeared to prevent the elimination of interstripe projections; consequently the boundaries of the stripes remained poorly defined. These findings suggest that cerebellar cortical neuronal activity is a necessary requirement for the refinement of spinal afferent topography in the anterior lobe.

2-Amino-5-phosphonovalerate↗
PubMed1992

Muscimol-induced reduction of GABAA receptor alpha 1-subunit mRNA in primary cultured cerebral cortical neurons.

The expression of mRNA for GABAA receptor alpha 1-subunit in mouse cerebral cortical neurons in primary culture was examined using RNA blot analysis and ribonuclease protection assay following the treatment of neurons with muscimol, a selective agonist of GABAA receptor. The level of mRNA for GABAA receptor alpha 1-subunit showed a decrease in comparison with that in non-treated cells, whereas no changes in the level of beta-actin mRNA were noted under the same experimental conditions. This muscimol-induced reduction in GABAA receptor alpha 1-subunit mRNA was counteracted by the simultaneous exposure of neurons to both bicuculline, an antagonist of GABAA receptor, and muscimol. The expression of mRNA for GABAA receptor alpha 1-subunit also showed a decline by the treatment of cells with flunitrazepam alone, an agonist of benzodiazepine receptor, and this change was also abolished by the simultaneous exposure of cells to flunitrazepam and Ro15-1788, an antagonist for central benzodiazepine receptor. These results suggest that the continuous stimulation of cerebral GABAA receptor complex may induce the reduced expression of mRNA for the receptor complex.

Animals↗
PubMed1984

In vitro effects of melatonin on [3H]muscimol binding in rat brain.

The possible interaction of melatonin with the GABAergic system at the receptor level was investigated. The effect of melatonin on the binding of the GABA agonist, [3H]muscimol, in crude synaptic membrane preparations was assayed. In fresh membrane preparations, melatonin increased [3H]muscimol binding in the rat striatum and frontal cortex. Treatment of membrane preparations with Triton X-100 appeared to abolish or depress the enhancing effect of melatonin. The use of Tris HCl as buffer appeared to be more effective than Tris-Citrate buffer suggesting a possible important ionic effect. The present findings suggest that melatonin is capable of enhancing [3H]muscimol binding in vitro, perhaps at the benzodiazepine-GABA-receptor-ionophore complex.

Animals↗
PubMed1979

Turning behaviour induced by injection of muscimol or picrotoxin into the substantia nigra demonstrates dual GABA components.

Injection of the GABA agonist muscimol into rat caudal substantia nigra caused contralateral turning, whereas injection into the rostral substantia nigra caused ipsilateral turning. The GABA antagonist picrotoxin had the opposite effect. These findings support the hypothesis that GABA has dual actions in the substantia nigra. Ipsilateral turning induced by injection of muscimol into rostral nigra was abolished by haloperidol pretreatment, indicating the involvement of dopaminergic mechanisms. Haloperidol pre-treatment did not prevent turning induced by muscimol injected into the caudal nigra, supporting the existence of a non-dopaminergic nigral output system.

Animals↗
PubMed1990

Behavioral interactions between muscimol and compounds selective for the D1 and D2 dopamine receptor subtypes.

The present study investigated the effects of the GABA agonist muscimol on the behaviors produced by acute injections of selective D1 and D2 agonists and antagonists. Muscimol potentiated the intensity of stereotyped behaviors shown by rats treated with the D2 agonist quinpirole; in contrast, it suppressed the repetitive bouts of grooming shown by rats treated with SKF38393. Muscimol potentiated the catalepsy produced by either a D1 (SCH23390) or D2 (metoclopramide) antagonist, suggesting that the cataleptic behaviors produced by these compounds may contain a common GABAergic mechanism.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Muscimol-induced increase in dopamine release and metabolism is not observed in kainic acid-lesioned striatum of conscious rats: an in vivo microdialysis study.

Local application of muscimol through the striatal dialysis membrane caused a significant increase in both dopamine release and dopamine metabolism in the striatum of conscious rats, however, both elevations induced by muscimol were significantly lower in the kainic acid-lesioned striatum when assessed with in vivo brain microdialysis. These findings show that intra-striatal muscimol indirectly stimulates nigrostriatal dopaminergic function by possibly causing an inhibition of striatal gamma-aminobutyric acid neurons.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

The enhancement of muscimol-stimulated 36C1 influx by the antispastic 5-aryl-3-(alkylsulfonyl)-4H-1,2,4-triazole (MDL 27,531) in rat brain membrane vesicles.

The antispastic triazole, 4-methyl-3-methylsulphonyl-5-phenyl-4H-1,2,4-triazole (MDL 27,531) was tested in glycine- and muscimol-stimulated 36Cl- influx into brain membrane preparations. MDL 27,531 (100 nM) had no effect on glycine- (100 nM-400 microM) stimulated 36Cl- influx in brain stem tissue; on the other hand, MDL 27,531 (10 nM-10 microM) enhanced muscimol- (1 microM) stimulated 36Cl- influx in cerebellar but not cortical membranes. In the presence of the benzodiazepine (BZD) antagonist, flumazenil (10 microM), MDL 27,531 inhibited muscimol-stimulated flux. These data suggest a novel interaction of this triazole with subtypes of the gamma-aminobutyric acid (GABA)A receptor complex and the BZD receptor.

Animals↗
PubMed1996

Fos oncoprotein expression in the rat forebrain following muscimol-induced absence seizures.

Fos oncoprotein expression is a marker of neuronal activation following seizures. Here, using this method we examined the anatomical locations of muscimol-induced absence seizures in the rat forebrain. Six hours after a systemic injection of muscimol a massive Fos immunoreactivity appeared in the olfactory system, retrosplenial cortex and paraventricular thalamic nucleus, whereas other cortical areas contained low level of Fos expression. These results provide the first functional morphological evidence suggesting that these forebrain structures with Fos expression may play an important role in the pathophysiology of muscimol-induced absence seizures.

Animals↗