Effect of early embryonic exposure to morphine on defects in the GABAergic system of day-old chicks
Dongmei WangJuan JiangWen ShangJianjun ZhangJiang XiaoFang ShenJing LiangYonghui LiMing LiMengya WangNan Sui
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Muscimol
Laryngeal motoneurons in the nucleus ambiguus were activated antidromically to ipsilateral recurrent nerve stimulation in urethane-chloralose anaesthetized rats. GABAA agonist muscimol and the antagonist bicuculline were applied separately or together with GABA iontophoretically with a multibarrel pipette glued with a recording electrode. The majority of neurons (119/155) which did not respond to the recurrent nerve stimulation exhibited activities mostly related to inspiration. Other 32 neurons were classified as laryngeal motoneurons, according to the criteria. Bicuculline application antagonized GABAA-mediated inhibition while muscimol or GABA reversed this effect significantly. Dose dependent changes were observed for administration of these GABAA-related agents. It can be concluded therefore that laryngeal motoneurons received GABAA-mediated inhibition.
Muscimol
GABA receptor antagonist
Nucleus ambiguus
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GABAA receptors are ligand-gated ion channels that mediate inhibitory synaptic signaling in the CNS. Fluorescent probes with the ability to target these receptors can provide insights into receptor location, distribution and dynamics in live cells, while revealing abnormalities in their distribution and dynamics that could occur in a variety of diseases. We have developed fluorescent probes of GABAA receptors that are composed of a CdSe/ZnS core-shell nanocrystal (quantum dot; qdot) conjugated to pegylated derivatives of the GABA receptor agonists GABA and muscimol (GABA-qdots and muscimol-qdots, respectively). Quantitative fluorescence imaging was used to analyze the binding activity of these conjugates to α1β2γ2 GABAA and ρ1 GABAA receptors expressed in Xenopus oocytes. The selectivity of these conjugates for α1β2γ2 GABAA and ρ1 GABAA receptors was determined by their ability to compete with the antagonists bicuculline and methyl-(1,2,3,6-tetrahydropyridin-4-yl)phosphinic acid (TPMPA). Both GABA- and muscimol-qdots exhibited robust binding to both α1β2γ2 and ρ1 GABAA receptors. At α1β2γ2 receptors, pretreatment with bicuculline reduced conjugate binding by ≥8-fold on average, an extent far exceeding the reduction produced by TPMPA (~30%). Conversely, at ρ1 receptors, pretreatment with TPMPA inhibited binding by ~10-fold, an extent greatly exceeding the change produced by bicuculline (~50% or less). These results indicate specific binding of muscimol-qdots and GABA-qdots to α1β2γ2 GABAA and ρ1 GABAA receptors in a manner that preserves the respective pharmacological sensitivities of these receptors to TPMPA and bicuculline, and encourage the use of qdot-conjugated neurotransmitter analogs as labeling agents at GABAA receptors.
Muscimol
Conjugate
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Muscimol
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Muscimol
Pregnenolone sulfate
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Rats given i.c.v. muscimol overcome a greater number of hypoxic episodes before dying compared with controls whereas animals that receive baclofen (another GABAergic agonist) or GABA itself tolerate fewer episodes than controls. Thus, chloride ions ionophoric site activation appears to be necessary in order to obtain any GABAergic antihypoxic protection whereas GABAergic site activated by both baclofen and GABA would induce an opposite effect.
Muscimol
Baclofen
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Induced activation of the gamma-aminobutyric acidA (GABAA) receptor in the retina of goldfish caused the fish to rotate in the opposite direction to that of the spinning pattern during an optomotor response (OMR) measurement. Muscimol, a GABAA receptor agonist, modified OMR in a concentration-dependent manner. The GABAB receptor agonist baclofen and GABAC receptor agonist CACA did not affect OMR. The observed modifications in OMR included decreased anterograde rotation (0.01∼0.03 μM), coexistence of retrograde rotation and decreased anterograde rotation (0.1∼30 μM) and only retrograde rotation (100 μM∼1 mM). In contrast, the GABAA receptor antagonist bicuculline blocked muscimol-induced retrograde rotation. Based on these results, we inferred that the coding inducing retrograde movement of the goldfish retina is essentially associated with the GABAA receptor-related visual pathway. Furthermore, from our novel approach using observations of goldfish behavior the induced discrete snapshot duration was approximately 573 ms when the fish were under the influence of muscimol.
Muscimol
GABAB receptor
Baclofen
GABA receptor
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Muscimol
Photoaffinity labeling
GABA receptor
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The changes of the GABAA receptor in the brain of phenobarbital (PB)-dependent and -withdrawn rats were investigated using [3H]-muscimol (a potent agonist of GABAA receptor) as the ligand. The dissociation constant for a low affinity binding site (Kd2) of PB-dependent rats significantly increased without affecting the high affinity site (Kd1) and Bmax for both sites. A decrease of specific [3H]-muscimol binding was observed in the whole brain and the cerebellum of the PB-dependent rats, when examined at a fixed drug concentration of 2 nM. Moreover, the specific [3H]-muscimol binding in the withdrawn rats was remarkably lower than that of the dependent rats. These results suggest that the change of the GABAA receptor may be related to the development of PB-dependence and -withdrawal.
Muscimol
Dissociation constant
Phenobarbital
GABA receptor
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Meroterpenoid compounds chrodrimanins produced by Talaromyces sp. YO-2 have been shown to act as competitive antagonists of silkworm larval GABAA receptors using electrophysiology, yet no further evidence has been provided to support such an action. We have investigated the actions of chrodrimanin B on rat brain GABAA receptors by binding assays with non-competitive ligand of GABAA receptors [3H]EBOB and competitive ligands [3H]gabazine and [3H]muscimol. Chrodrimanin B did not significantly affect the binding of [3H]EBOB while reducing the binding of [3H]gabazine and [3H]muscimol to the rat membrane preparations. Chrodrimanin B increased the dissociation constant Kd of [3H]gabazine and [3H]muscimol without significantly affecting the maximum binding, pointing to competitive interactions of chrodrimanin B with rat GABAA receptors in support of our previous observation that the compound acts as a competitive antagonist on the silkworm larval GABA receptor.
Muscimol
Dissociation constant
Competitive antagonist
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Muscimol
Substantia innominata
Ventral pallidum
GABA receptor antagonist
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