The GABAA receptor antagonist picrotoxin induces a ‘pain-like’ behavior when administered into the thalamic reticular nucleus of the behaving rat: a possible model for ‘central’ pain?

1994 ◽  
Vol 179 (1-2) ◽  
pp. 21-24 ◽  
Author(s):  
Jean-Louis Olivéras ◽  
Jacqueline Montagne-Clavel
Keyword(s):  
Receptor Antagonist ◽  
Gabaa Receptor ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Central Pain ◽  
Gabaa Receptor Antagonist

Oscillatory synaptic interactions between ventroposterior and reticular neurons in mouse thalamus in vitro

1994 ◽  
Vol 72 (4) ◽  
pp. 1993-2003 ◽  
Author(s):  
R. A. Warren ◽  
A. Agmon ◽  
E. G. Jones
Keyword(s):  
Receptor Antagonist ◽  
Gabab Receptor ◽  
Initial Response ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Excitatory Postsynaptic Potential ◽  
Postsynaptic Potential ◽  
Synaptic Interactions ◽  
Gabaa Receptor Antagonist

1. The thalamic reticular nucleus (RTN) has reciprocal connections with relay neurons in the dorsal thalamus. We used whole cell recording in a mouse in vitro slice preparation maintained at room temperature to study the synaptic interactions between the RTN and the ventroposterior thalamic nucleus (VP) during evoked low-frequency oscillations. 2. After a single electrical stimulus of the internal capsule, postsynaptic potentials (PSPs) were recorded in all VP and RTN neurons. In 76% of slices, there was an initial response followed by recurrent PSPs lasting for up to 8 s and with a frequency of approximately 2 Hz in both the VP and RTN. 3. In RTN neurons the initial response consisted of a fast excitatory postsynaptic potential (EPSP) that generated a burst of action potentials. Recurrent PSPs consisted of barrages of EPSPs that often reached burst threshold. The structure of subthreshold EPSP barrages in RTN neurons suggested that they were generated by bursting VP neurons. 4. In VP neurons the stimulus usually evoked a small EPSP followed by a large inhibitory postsynaptic potential (IPSP) that was often followed by a rebound burst. This initial response was often followed by a series of recurrent IPSPs presumably generated by RTN bursts, because intrinsic inhibitory neurons are absent in rodent VP. 5. IPSPs in VP neurons and recurrent EPSPs in RTN neurons were completely abolished by application of a gamma-aminobutyric acid-A (GABAA) receptor antagonist. A GABAB receptor antagonist produced no or little change in either the initial or recurrent response. 6. Recurrent IPSPs in VP neurons were abolished by glutamate receptor antagonists before the initial IPSP, which always remained stimulus dependent. 7. The dependency of recurring IPSPs in VP and recurring EPSPs in RTN upon GABA-mediated inhibition and excitatory amino acid-mediated excitation, plus the character of recurring EPSPs in the RTN strongly suggest that the recurring events were generated through reverse-reciprocal synaptic interactions between VP and RTN neurons. These synaptic interactions most likely play an important role in thalamic oscillations in behavior.

scholarly journals Rebound Bursts in GABAergic Neurons of the Thalamic Reticular Nucleus in Postnatal Mice

2010 ◽  
pp. 273-280
Author(s):  
X Wang ◽  
G Yu ◽  
X Hou ◽  
J Zhou ◽  
B Yang ◽  
...  
Keyword(s):  
Patch Clamp ◽  
Receptor Antagonist ◽  
Channel Blocker ◽  
Gabaergic Neurons ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
K Channel ◽  
Whole Cell Patch Clamp ◽  
Gabaa Receptor Antagonist ◽  
Inactive Analog

Whole cell patch-clamp recordings from GABAergic cells of thalamic reticular nucleus (RTN) in thalamocortical slices made from postnatal day 6 (P6) to 10 (P10) were used to investigate the pattern of rebound bursts (RBs) triggered by an injection of hyperpolarizing current into RTN cells. The number of RBs in the RTN and the overlying Na+/K+ spikes changed in an agedependent manner. The generation of RBs depended largely on the amplitude of the after-hyperpolarizations (AHPs). RB patterns in response to hyperpolarizing current injection into relay cells were markedly different from RB patterns in RTN cells with an after-depolarization. GABAA receptor antagonist bicuculline methiodide (BMI) changed burst firing patterns, increasing the duration of RB and decreasing the amplitude of AHP in RTN cells. Furthermore, local puffs of NMDA in the presence of BMI induced RBs. K+ channel blocker 4-aminopyridine partially mimicked the effect of BMI on AHPs. The shapes of RBs were altered by a selective CaMKII inhibitor KN-62, but not by an inactive analog KN-04.

The role of brain acetylcholine in GABAA receptor antagonist-induced blood-pressure changes in rat

1996 ◽  
Vol 317 (2-3) ◽  
pp. 301-307 ◽  
Author(s):  
Tahir Tellioǧlu ◽  
Serap Akin ◽  
Uǧur Özkutlu ◽  
Şule Oktay ◽  
Filiz Onat
Keyword(s):  
Blood Pressure ◽  
Receptor Antagonist ◽  
Gabaa Receptor ◽  
Gabaa Receptor Antagonist ◽  
Pressure Changes ◽  
Brain Acetylcholine

scholarly journals Proteomic and Systems Biology Analysis of Monocytes Exposed to Securinine, a GABAA Receptor Antagonist and Immune Adjuvant

PLoS ONE ◽  
2012 ◽  
Vol 7 (9) ◽  
pp. e41278 ◽  
Author(s):  
Matt Shipman ◽  
Kirk Lubick ◽  
David Fouchard ◽  
Rajani Guram ◽  
Paul Grieco ◽  
...  
Keyword(s):  
Systems Biology ◽  
Receptor Antagonist ◽  
Gabaa Receptor ◽  
Gabaa Receptor Antagonist ◽  
Immune Adjuvant

GABA stimulation of gonadotropin-II release in goldfish: involvement of GABAA receptors, dopamine, and sex steroids

1993 ◽  
Vol 265 (2) ◽  
pp. R348-R355 ◽  
Author(s):  
V. L. Trudeau ◽  
B. D. Sloley ◽  
R. E. Peter
Keyword(s):  
Receptor Antagonist ◽  
Gabaa Receptor ◽  
Receptor Agonist ◽  
Gabab Receptor ◽  
Dependent Manner ◽  
Gamma Aminobutyric Acid ◽  
Turnover Rates ◽  
Pharmacological Agents ◽  
Gabaa Receptor Antagonist ◽  
Gonadotropin Ii

The involvement of gamma-aminobutyric acid (GABA) in regulation of pituitary gonadotropin-II (GTH-II) release was studied in the goldfish. Intraperitoneal injection of GABA (300 micrograms/g) stimulated an increase in serum GTH-II levels at 30 min postinjection. The GABAA receptor agonist muscimol (0.1-10 micrograms/g) stimulated GTH-II in a dose-dependent manner. Baclofen, a GABAB receptor agonist, had a small but significant stimulatory effect at 1 and 10 micrograms/g; the amount of GTH-II released in response to baclofen was significantly less (P < 0.05) than that released by muscimol. Pretreatment of goldfish with bicuculline, a GABAA receptor antagonist, but not saclofen, a GABAB receptor antagonist, blocked the stimulatory effect of GABA on serum GTH-II. Elevation of brain and pituitary GABA levels with the GABA transaminase inhibitor, gamma-vinyl-GABA (GVG), decreased hypothalamic and pituitary dopamine (DA) turnover rates, indicating that GABA may stimulate GTH-II release in the goldfish by decreasing dopaminergic inhibition of GTH-II release. The release of GTH-II stimulated by muscimol and GVG was potentiated by pharmacological agents that decrease inhibitory dopaminergic tone, indicating that DA may also inhibit GABA-stimulated GTH-II release. Based on the linear 24-h accumulation of GABA in brain and pituitary after GVG injection, implantation of testosterone, estradiol, or progesterone, previously shown to regulate the serum GTH-II release response to gonadotropin-releasing hormone and GABA, was also found to modulate GABA synthesis in the brain and pituitary.(ABSTRACT TRUNCATED AT 250 WORDS)

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