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PubMed1988

Colocalization of [3H]muscimol uptake and choline acetyltransferase immunoreactivity in amacrine cells of the cat retina.

High affinity uptake of [3H]muscimol, a gamma-aminobutyric acid (GABA) analogue, followed by autoradiography, labelled practically all amacrine cells which expressed GABA-like immunoreactivity. Hence it is a good marker for putative GABAergic amacrine cells. All amacrine cells, which were stained with antibodies against choline acetyltransferase, a marker for cholinergic neurones, also accumulated [3H]muscimol. This makes it likely that cholinergic amacrine cells of the cat retina are a subpopulation of putative GABAergic amacrine cells.

Animals↗
PubMed1989

[3H]muscimol labels neurons in both the superficial and deep layers of cat superior colliculus.

We examined the pattern of [3H]muscimol labeling in cat superior colliculus to determine if it matches that of [3H] gamma-aminobutyric acid ([3H]-GABA) labeling or GABA antibody immunoreactivity. Injections in the superficial layers labeled cell bodies in only the superficial layers. Of 204 labeled cells, 68% were located within the upper 200 microns of the superior colliculus, 31% within the deep superficial gray layer, and only 1% below that layer, a pattern similar to that seen with [3H]GABA labeling. By contrast, an injection in the deep layers of the colliculus resulted in cell labeling in both the superficial and deep layers, including 68% in the superficial gray layer, 24% in the optic layer, and 8% in the intermediate and deep gray layers. This pattern approximates that seen with GABA immunocytochemistry. We conclude that the pattern of accumulation of [3H]muscimol depends critically upon the location of the injection and reasonably matches the pattern of GABA immunoreactivity if the injection involves the deep layers of the colliculus.

Animals↗
PubMed1991

Ammonia-induced alterations in glutamate and muscimol binding to cerebellar synaptic membranes.

Binding of glutamate and muscimol (an agonist for GABAA receptors) to their respective receptors has been studied in the cerebellum of normal and hyperammonemic rats. There was a decrease in both high- and low-affinity binding of glutamate in the cerebellum during hyperammonemia. Kinetic studies revealed that the decrease is due to a reduction in the number of binding sites, but not due to changes in the binding affinities. Further studies also revealed that the decrease was only in the N-methyl-D-aspartate (NMDA)-specific binding sites without any alterations in the binding to non-NMDA sites represented by kianic acid (KA)- and quisqualic acid (QQ)-sensitive receptor sites. These effects were also mimicked when the membrane preparations from the cerebellum of normal animals were incubated with ammonium acetate. Enhancement of muscimol binding was observed in animals injected with ammonium acetate. It is concluded that hyperammonemic states, even in the presence of a functional liver, are capable of altering amino acid neurotransmission and this might play an important role in cerebral dysfunction under these conditions.

Ammonia↗
PubMed1991

Microinjections of muscimol and bicuculline into the pontine reticular formation modify the sleep-waking cycle in the rat.

The role of gamma-aminobutyric acid (GABA) in the sleep-waking cycle was evaluated by means of microinjections of muscimol and bicuculline into the rat pontine reticular formation (PRF). Muscimol (20 ng) produced a marked increase in wakefulness (70%), a decrease in slow-wave sleep (SWS) (35%) and a remarkable delay in the onset of both SWS and paradoxical sleep, without modifying the percentage of the latter. Bicuculline (4 ng) shortened SWS latency by about 70%. These results suggest that GABAergic transmission in the PRF is involved in the regulation of sleep-waking cycle in the rat.

Animals↗
PubMed1993

Differential effect of chronic ethanol treatment on barbiturate and steroid modulation of muscimol-binding to rat brain cortex.

We report the differential alterations produced by chronic ethanol treatment on the modulation, by the barbiturate thiopental and the steroid 5 beta-pregnan-3 alpha-ol-20-one, of the binding of [3H]muscimol to membrane preparations from rat brain cortex. We found a clear barbiturate- and steroid-promoted enhancement of muscimol-binding to membranes in both control and ethanol-treated animals. However, the enhancements were higher in control animals, using the barbiturate, and in ethanol-treated rats, using the steroid, Bmax and Kd values were also differentially affected in control and ethanol-treated animals by the presence of the barbiturate or the steroid.

Animals↗
PubMed1984

Single class of muscimol binding sites in the solubilized gamma-aminobutyrate-benzodiazepine receptor complex.

The gamma-aminobutyrate-benzodiazepine receptor complex was solubilized from the rat brain and bovine cortex and partially purified by means of gel chromatography. Analysis of binding parameters of [3H]muscimol indicates that the complex includes only one class of binding sites which presumably represent an apparently low affinity class of two classes of gamma-aminobutyrate A receptors described on the brain membranes. Analysis of the [3H] flunitrazepam specific binding also shows the presence of one class of binding sites sensitive to gamma-aminobutyrate stimulation. The concentration of muscimol binding sites in the gamma-aminobutyrate-benzodiazepine receptor complex was observed to be twice as high as the concentration of benzodiazepine binding sites.

Animals↗
PubMed1993

Alterations in [3H]MK-801, [3H]muscimol, [3H]cyclic AMP, and [3H]rolipram binding in the gerbil hippocampus following repeated ischemic insults.

Using [3H]MK-801, [3H]muscimol, [3H]cyclic AMP, and [3H]rolipram, we performed quantitative in vitro autoradiography to determine sequential alterations in the binding of N-methyl-D-aspartate and GABAA receptors, particulate cyclic AMP-dependent protein kinase, and cyclic AMP-selective phosphodiesterase, respectively, in the gerbil hippocampus following repeated brief ischemic insults. Changes from 1 h to 28 days after three 2-min ischemic insults at 1-h intervals were compared with those after 2 and 6 min of ischemia. We observed no alterations in the binding of all the four ligands throughout the observation period following 2 min of ischemia which produced no histological neuronal damage except for transient reductions in [3H]cyclic AMP binding during the early reperfusion period. [3H]Cyclic AMP binding in the CA1 subfield decreased one day after 6 min of ischemia and four days after three 2-min ischemic insults, and 62-65% of the binding was lost after 28 days. [3H]Rolipram binding in the CA1 subfield decreased one day after 6 min of ischemia and the binding was reduced by 45-50% after four and 28 days. Following three 2-min ischemic insults, [3H]rolipram binding decreased in the CA1 at one day, and decreased by 25-33% after 28 days. Both [3H]MK-801 and [3H]muscimol binding was preserved during the early reperfusion period after 6 min of ischemia and three 2-min ischemic insults. Reductions in [3H]MK-801 binding in CA1 were observed four days after ischemic insults when CA1 neuronal destruction was seen. After one month, approximately 50% of [3H]MK-801 binding was lost in CA1 in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1990

Regional brain [3H]muscimol binding in kindled rat brain: a quantitative autoradiographic examination.

Quantitative [3H]muscimol autoradiography was used to perform a comprehensive examination of the GABAA receptor site in entorhinal cortex kindled and handled control rats. Ninety-eight brain areas were analyzed 24 h or 28 days after the last kindled seizure. A significant post-kindling change was observed in only one area, the fascia dentata of the hippocampus, which showed an increase of 55% at 24 h, but not at 28 days. This acute change appeared in both the dorsal and ventral divisions of the hippocampus and in both the infrapyramidal and suprapyramidal blades of the fascia dentata. These data closely parallel the pattern previously obtained with [3H]flunitrazepam in the same animals. The comprehensive nature of this examination further suggests that the fascia dentata is the only site in the brain which shows altered GABAA binding after kindling. Although our data indicate that elevated [3H]muscimol binding is not a permanent feature of the kindled state, the possibility exists that the fascia dentata change observed at 24 h reflects a permanent alteration in the acute reactivity of hippocampal GABAA receptors to electrical stimulation.

Animals↗
PubMed2003

Intracerebroventricular injection of muscimol, baclofen or nipecotic acid stimulates food intake in layer-type, but not meat-type, chicks.

This study was designed to compare the effects of muscimol (GABA(A) agonist), baclofen (GABA(B) agonist) and nipecotic acid (GABA uptake inhibitor) on food intake in two chicken strains (meat-type and layer-type chicks). The intracerebroventricular (ICV) injection of all GABA agents induced hyperphagia in layer-type chicks. However, in broiler chicks, there were similar tendencies with muscimol and nipecotic acid but not significantly different. Conversely, ICV injection of baclofen depressed feeding of broiler chicks. These results suggest that there are some differences in central GABAergic systems between these strains of chicks, but GABAergic systems have an important role in the regulation of food intake in neonatal chicks.

Animals↗
PubMed2004

Muscimol injection into the lateral hypothalamus inhibits the hypotension and bradycardia caused by somato-visceral nociception.

This study investigated whether the lateral hypothalamus (LH) contributes to the depressor response evoked by somato-visceral nociception. Lidocaine (2%; 0.1, 0.3 or 1.0 microl) or muscimol (0.34 nmol; 0.5 microl) was microinjected into the rostral LH of halothane-anesthetized rats bilaterally and somato-visceral nociception was induced 2 min later by injecting 5% acetic acid (0.5 ml) intraperitoneally. Lidocaine and muscimol inhibited the hypotension and bradycardia caused by somato-visceral nociception significantly without affecting cardiovascular function in normotensive animals.

Animals↗
PubMed2004

Prolonged initiation latency in Morris water maze learning in rats with ibotenic acid lesions to medial striatum: effects of systemic and intranigral muscimol administration.

The contribution of the rat striatonigral GABAergic system to spatial navigation was investigated in this study. We first tested the effects of ibotenic acid lesions of the striatum on place navigation performance in Morris water maze. Medial but not lateral striatal lesions produced a significant increase of escape latency, and this deficit was clarified as mainly caused by a marked increase of initiation latency rather than of thigmotaxis time (experiment 1). Next we tested the effects of systemic (0.5 mg/kg) and intranigral (2.0 ng/side) administrations of muscimol, a GABA receptor agonist, on the place navigation deficits produced by medial striatal lesions. Systemic muscimol administration significantly ameliorated the increase of initiation latency, while intranigral administration was not sufficiently effective (experiment 2). The results suggest that neural circuits containing medial striatal neurons play an essential role in place navigation performance probably through some movement preparation processes that precede movement execution, and the GABAergic system may be involved in this initiation process, although whether it is the striatonigral GABAergic system that is involved remains unclear.

Animals↗
PubMed2004

In vitro and in vivo effects of GABA, muscimol, and bicuculline on lamprey GnRH concentration in the brain of the sea lamprey (Petromyzon marinus).

gamma-Aminobutyric acid (GABA) is a neurotransmitter with a demonstrated neuroregulatory role in reproduction in most representative species of vertebrate classes via the hypothalamus. The role of GABA on the hypothalamus-pituitary axis in lampreys has not been fully elucidated. Recent immunocytochemical and in situ hybridization studies suggest that there may be a neuroregulatory role of GABA on the gonadotropin-releasing hormone (GnRH) system in lampreys. To assess possible GABA-GnRH interactions, the effects of GABA and its analogs on lamprey GnRH in vitro and in vivo were studied in adult female sea lampreys (Petromyzon marinus). In vitro perfusion of GABA and its analogs at increasing concentrations (0.1-100 microM) was performed over a 3-h time course. There was a substantial increase of GnRH-I and GnRH-III following treatment of muscimol at 100 microM. In in vivo studies, GABA or muscimol injected at 200 microg/kg significantly increased lamprey GnRH concentration in the brain 0.5 h after treatment compared to controls in female sea lampreys. No significant change in lamprey GnRH-I or GnRH-III was observed following treatment with bicuculline. These data provide novel physiological data supporting the hypothesis that GABA may influence GnRH in the brain of sea lamprey.

Animals↗
PubMed2005

Behavioral responses to injections of muscimol into the subthalamic nucleus: temporal changes after nigrostriatal lesions.

Changes in cellular activity in the subthalamic nucleus are a cardinal feature of Parkinson's disease and occur in rodents after lesions of the nigrostriatal pathway, a model of Parkinson's disease. GABA-ergic neurons from the globus pallidus provide a major input to the subthalamic nucleus. Previous electrophysiological studies revealed temporal changes in the activity of pallidal neurons after nigrostriatal lesions in rats. However, little is known about the impact of these changes on GABAergic transmission in the subthalamic nucleus. We have examined the behavioral responses to a local administration of the GABA A agonist muscimol into the subthalamic nucleus. Muscimol (0.01 and 0.1 microg) induced orofacial dyskinesia in normal rats; this response was blunted 2 weeks but enhanced 2 months after a unilateral lesion of the nigrostriatal pathway. The early decrease in the behavioral response occurred at a time when increased expression of mRNA for glutamic acid decarboxylase, the enzyme of GABA synthesis, and burst firing have been reported in the globus pallidus, suggesting an adaptive post-synaptic response to increased GABAergic transmission in the subthalamic nucleus. In contrast, we now show that glutamic acid decarboxylase mRNA is unchanged in the globus pallidus at the later time point, when electrophysiological changes also subside in this region. The increased behavioral response at this later time point may reflect a decreased activity in GABAergic inputs to the subthalamic nucleus. The results show time-dependent changes in behavioral responses to GABA A receptor stimulation in the subthalamic nucleus which may reflect adaptive changes in postsynaptic inhibitory responses after dopaminergic lesions.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1986

[3H]muscimol photolabels the gamma-aminobutyric acid receptor binding site on a peptide subunit distinct from that labeled with benzodiazepines.

Affinity column-purified GABA-benzodiazepine receptor protein from bovine brain was photoaffinity labeled with both [3H]flunitrazepam and [3H]muscimol. Gel electrophoresis in sodium dodecyl sulfate revealed that the benzodiazepine binding site labeled with [3H]flunitrazepam was primarily associated with a major peptide subunit revealed by protein staining with Mr = 52 kiloDaltons, with minor labeling of a second peptide of Mr = 57 kiloDaltons, corresponding to a second major stained band. Covalent incorporation of [3H]muscimol was limited to the 57 kiloDalton band, with no labeling of the 52 kiloDalton peptide, showing that the GABA binding site is carried by a subunit distinct from that carrying the benzodiazepine binding site.

Affinity Labels↗
PubMed1996

Effect of microinjection of muscimol into the dorsomedial or paraventricular hypothalamic nucleus on air stress-induced neuroendocrine and cardiovascular changes in rats.

The paraventricular nucleus (PVN) contains neurons that release corticotrophin-releasing factor (CRH) and thus provide the stimulus for the release of adrenocorticotrophic hormone (ACTH), the neuroendocrine hallmark of the response to stress. However, inhibition of neuronal activity in the nearby dorsomedial hypothalamic nucleus (DMH) by microinjection of the GABA(A) receptor agonist muscimol suppresses cardiovascular changes seen in air stress in conscious rats, while similar treatment in the PVN has no effect. Because the DMH projects to the PVN and also contains CRH neurons, we decided to investigate the role of neuronal activity in the DMH in the neuroendocrine response to stress. In control rats or after microinjection of saline vehicle into either the PVN or the DMH, air stress resulted in equivalent increases in plasma levels of ACTH, heart rate, and arterial pressure. Bilateral microinjection of muscimol 80 pmol/100 nl/side into either the PVN or the DMH prior to air stress reduced the associated increases in plasma ACTH (-37% and -71%, respectively), while only injection into the DMH attenuated the accompanying tachycardia (-62%) and pressor (-83%) effects. Thus, neurons in the DMH, but not in the PVN, play a role in both the cardiovascular and neuroendocrine response to air stress.

Adrenocorticotropic Hormone↗
PubMed1997

Intra-septal infusions of glucose potentiate inhibitory avoidance deficits when co-infused with the GABA agonist muscimol.

This experiment examined the effects of co-infusions of glucose with the gamma-aminobutyric acid (GABA) agonist muscimol into the medial septum on memory for inhibitory avoidance learning. Co-infusions of muscimol (3 nmol) and glucose (33 nmol) impaired memory, but neither drug did so when administered alone. Thus, although glucose typically reverses memory deficits, these results indicate that glucose potentiates the memory-impairing effects of a GABA agonist.

Animals↗
PubMed2000

Lesion or muscimol in the rostral ventral medulla reduces ventilatory output and the CO(2) response in decerebrate piglets.

Developmental abnormalities have been described in the arcuate nucleus of sudden infant death syndrome (SIDS) victims. The arcuate nucleus has putative homologues in chemosensitive areas of the ventral medulla in animals. We refer to some of these areas collectively as the rostral ventral medulla (RVM). In the RVM of decerebrate piglets 2-15 days of age, we studied the effects of electrolytic lesions (n=7) or microdialysis of muscimol (n=15), a GABAA receptor agonist, on ventilatory output and the response to hypercapnia. Lesions caused a 66.7+/-17.3% reduction in eupneic phrenic minute activity (MA) and abolished the response to hypercapnia. Muscimol dialysis caused a 32.4+/-10.4% reduction in MA with a significant downward displacement of the response to hypercapnia with no significant effect on the slope. We conclude that the piglet RVM contains neurons of vital importance in the maintenance of normal breathing and the response to systemic CO(2). We hypothesize that dysfunction of homologous regions in the human infant could lead to impaired ability to respond to hypercapnia and could potentially be involved in the pathogenesis of SIDS.

Animals↗