Effects of high-affinity GABA B receptor antagonists on active and passive avoidance responding in rodents with gamma-hydroxybutyrolactone-induced absence syndrome

Getova, D.; Bowery, Norman G.

doi:10.1007/s002130100766

Cited by 28 publications

(17 citation statements)

References 10 publications

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“…Low-dose GABA B receptor blockade typically enhanced cognitive task performance (Mondadori et al, 1993;Staubli et al, 1999;Getova and Bowery, 2001;Helm et al, 2005), although decreased spatial performance was also reported (Brucato et al, 1996). GABA B receptors were suggested to alter synaptic plasticity (Brucato et al, 1996;Staubli et al, 1999) or reduce protein binding to the cAMP response element (Helm et al, 2005).…”

Section: Effect Of Gaba B Receptor Blockade and Cognitive Task Enhancmentioning

confidence: 96%

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GABA_B receptor blockade enhances theta and gamma rhythms in the hippocampus of behaving rats

Leung

Shen

2007

Hippocampus

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The participation of GABA(B) receptors in hippocampal EEG generation was studied by intracerebroventricular (icv) and intracerebral infusions of GABA(B) receptor antagonist p-(3-aminopropyl)-p-diethoxymethyl-phosphinic acid (CGP35348) in freely behaving rats. During awake-immobility, icv CGP35348 induced a theta rhythm and increased gamma waves (30-100 Hz) in the hippocampus. The immobility theta peaked at 6-7 Hz and had a theta phase in CA1 stratum radiatum of approximately 160 degrees with reference to the theta at the alveus, when compared with approximately 130 degrees during walking. Immobility theta power peaks at 6-7 Hz was also found in normal rats, and it was detected in 27% of the EEG segments during immobility. Incidence of immobility theta increased to 87.5% after 480 nmol of CGP35348 icv. Muscarinic antagonist scopolamine (5 mg/kg, ip) suppressed the induction of immobility theta and the gamma power increase after icv CGP35348. CGP35348 icv did not significantly change the hippocampal theta power at 7-8 Hz during walking (theta fundamental), but it increased power at 12-15 Hz, at the second harmonic of theta. CGP35348 icv also increased 30-50 Hz gamma power during walking. Medial septal infusion of CGP35348 (12 nmol in 0.4 microl) increased the power and the frequency of the hippocampal theta second harmonic during walking, but did not increase gamma activity. Infusion of CGP35348 (8 nmol in 0.4 microl) in the hippocampus increased the local gamma activity at 30-100 Hz, but did not induce immobility theta or affect the walking theta rhythm. In conclusion, icv GABA(B) receptor blockade increased an atropine-sensitive input that generated an immobility theta rhythm, while GABA(B) receptor blockade of the medial septum increased atropine-resistant theta harmonics possibly generated by apical dendritic spikes. GABA(B) receptor blockade may enhance cognitive task performance by activating hippocampal theta and gamma rhythms in behaving rats.

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Section: Effect Of Gaba B Receptor Blockade and Cognitive Task Enhancmentioning

confidence: 96%

“…In contrast, a low dose of GABA B receptor blockade may enhance LTP induced by unprimed, high-frequency stimulation (Olpe et al, 1993;Staubli et al, 1999). Low-dose GABA B receptor blockade also typically enhanced cognitive task performance (Mondadori et al, 1993;Staubli et al, 1999;Getova and Bowery, 2001;Helm et al, 2005).…”

Section: Introductionmentioning

confidence: 91%

GABA_B receptor blockade enhances theta and gamma rhythms in the hippocampus of behaving rats

Leung

Shen

2007

Hippocampus

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“…They can either enhance (Getova and Bowery, 1998;Nakagawa et al, 1999;Stäubli et al, 1999;Getova and Bowery, 2001) or attenuate (Brucato et al, 1996) cognitive performance in a variety of learning paradigms in mice and rats. We reported previously that GABA B(1) Ϫ/Ϫ mice exhibit a severe impairment of passive avoidance learning .…”

Section: Gaba B(2)mentioning

confidence: 99%

Redistribution of GABA_B(1)Protein and Atypical GABA_BResponses in GABA_B(2)-Deficient Mice

Gassmann¹

2004

J. Neurosci.

218

155

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GABA B receptors mediate slow synaptic inhibition in the nervous system. In transfected cells, functional GABA B receptors are usually only observed after coexpression of GABA B(1) and GABA B(2) subunits, which established the concept of heteromerization for G-proteincoupled receptors. In the heteromeric receptor, GABA B(1) is responsible for binding of GABA, whereas GABA B(2) is necessary for surface trafficking and G-protein coupling. Consistent with these in vitro observations, the GABA B(1) subunit is also essential for all GABA B signaling in vivo. Mice lacking the GABA B(1) subunit do not exhibit detectable electrophysiological, biochemical, or behavioral responses to GABA B agonists. However, GABA B(1) exhibits a broader cellular expression pattern than GABA B(2) , suggesting that GABA B(1) could be functional in the absence of GABA B(2) . We now generated GABA B(2) -deficient mice to analyze whether GABA B(1) has the potential to signal without GABA B(2) in neurons. We show that GABA B(2) Ϫ/Ϫ mice suffer from spontaneous seizures, hyperalgesia, hyperlocomotor activity, and severe memory impairment, analogous to GABA B(1) Ϫ/Ϫ mice. This clearly demonstrates that the lack of heteromeric GABA B(1,2) receptors underlies these phenotypes. To our surprise and in contrast to GABA B(1) Ϫ/Ϫ mice, we still detect atypical electrophysiological GABA B responses in hippocampal slices of GABA B(2) Ϫ/Ϫ mice. Furthermore, in the absence of GABA B(2) , the GABA B(1) protein relocates from distal neuronal sites to the soma and proximal dendrites. Our data suggest that association of GABA B(2) with GABA B(1) is essential for receptor localization in distal processes but is not absolutely necessary for signaling. It is therefore possible that functional GABA B receptors exist in neurons that naturally lack GABA B(2) subunits.

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“…In these studies, we hypothesize that GABA B receptor ligands by interacting with serotonergic neurotransmission may alter behavior in the modified forced swim test. Thus, we compared the behavioral profile of the two equipotent GABA B receptor antagonists CGP56433A and CGP55845A (Froestl et al, 1995a,b;Pozza et al, 1999;Getova and Bowery, 2001;Macey et al, 2001) and the novel GABA B receptor-positive modulator GS39783 (Urwyler et al, 2003; with that of known serotonergic and noradrenergic antidepressants. Furthermore, we examined the contribution of the serotonergic system to the behavioral effects of GABA B receptor antagonist CGP56433A.…”

mentioning

confidence: 99%

GABA_B Receptor Antagonist-Mediated Antidepressant-Like Behavior Is Serotonin-Dependent

Slattery

Desrayaud²,

Cryan³

2004

J Pharmacol Exp Ther

117

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There is an emerging body of data purporting a role of ␥-aminobutyric acid (GABA) in the pathophysiology of mood disorders. However, the role of metabotropic GABA B receptors in depression is not well defined. The modified forced swim test has recently emerged as an excellent tool to assess behaviorally the role of monoamines in antidepressant action. To assess the role of GABA B receptors in antidepressant-related behavior, we examined a number of selective GABA B receptor ligands (novel positive modulators and antagonists) on behavior in the modified forced swim test. We demonstrate that the selective GABA B receptorphenylmethyl-phosphinic acid hydrochloride; 3-10 mg/kg] had a similar profile to the selective serotonin reuptake inhibitor fluoxetine; they decreased immobility and increased swimming behavior. The tricyclic antidepressant desipramine decreased immobility but increased climbing behavior. In contrast, the novel GABA B receptor-positive modulator GS39783 (10 -40 mg/kg) did not display antidepressant-like activity in the modified forced swim test. To further assess the possible interaction between GABA B receptor antagonism and serotonin, rats were pretreated with the tryptophan hydroxylase inhibitor parachlorophenylalanine. 5-Hydroxytryptamine depletion (Ͼ90%) abolished the antidepressant-like behavior of CGP56433A (10 mg/kg) by attenuating the increase in swimming. Together, these data demonstrate that GABA B receptor antagonists via an interaction with the serotonergic system display antidepressant-like properties and therefore represent a novel approach for the treatment of depression.

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Effects of high-affinity GABA B receptor antagonists on active and passive avoidance responding in rodents with gamma-hydroxybutyrolactone-induced absence syndrome

Abstract: GHBL appeared to influence mice and rats in a different manner - rats learned the active avoidance task better than the GHBL-treated mice. The present study confirms previous data that GABAB antagonists suppress absence behaviour.

Cited by 28 publications

References 10 publications

GABA_B receptor blockade enhances theta and gamma rhythms in the hippocampus of behaving rats

GABA_B receptor blockade enhances theta and gamma rhythms in the hippocampus of behaving rats

Redistribution of GABA_B(1)Protein and Atypical GABA_BResponses in GABA_B(2)-Deficient Mice

GABA_B Receptor Antagonist-Mediated Antidepressant-Like Behavior Is Serotonin-Dependent

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Effects of high-affinity GABA B receptor antagonists on active and passive avoidance responding in rodents with gamma-hydroxybutyrolactone-induced absence syndrome

Abstract: GHBL appeared to influence mice and rats in a different manner - rats learned the active avoidance task better than the GHBL-treated mice. The present study confirms previous data that GABAB antagonists suppress absence behaviour.

Cited by 28 publications

References 10 publications

GABAB receptor blockade enhances theta and gamma rhythms in the hippocampus of behaving rats

GABAB receptor blockade enhances theta and gamma rhythms in the hippocampus of behaving rats

Redistribution of GABAB(1)Protein and Atypical GABABResponses in GABAB(2)-Deficient Mice

GABAB Receptor Antagonist-Mediated Antidepressant-Like Behavior Is Serotonin-Dependent

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Product

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GABA_B receptor blockade enhances theta and gamma rhythms in the hippocampus of behaving rats

GABA_B receptor blockade enhances theta and gamma rhythms in the hippocampus of behaving rats

Redistribution of GABA_B(1)Protein and Atypical GABA_BResponses in GABA_B(2)-Deficient Mice

GABA_B Receptor Antagonist-Mediated Antidepressant-Like Behavior Is Serotonin-Dependent