?9-THC-induced cognitive deficits in mice are reversed by the GABAA antagonist bicuculline

Varvel, Stephen A.; Anum, Emmanuel A.; Niyuhire, Floride; Wise, Laura E.; Lichtman, Aron H.

doi:10.1007/s00213-004-1988-2

Cited by 36 publications

(21 citation statements)

References 30 publications

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“…In agreement, THC produces full tetrad effects in the conditional knockout mice lacking CB1R in GABAergic terminals [102]. Likewise, the GABA-A receptor antagonist bicuculline does not block THCinduced tetrad effects [103]. Interestingly, the effects of cannabinoids on long-term memory and working memory have been associated to CB1R in GABAergic terminals [71] or astrocytes [57], respectively.…”

Section: (D) Cellular and Subcellular Localization Of Cb1r And Its Immentioning

confidence: 86%

Cellular and intracellular mechanisms involved in the cognitive impairment of cannabinoids

Puighermanal

Busquets-García

Maldonado

et al. 2012

Phil. Trans. R. Soc. B

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Exogenous cannabinoids, such as delta9-tetrahydrocannabinol (THC), as well as the modulation of endogenous cannabinoids, affect cognitive function through the activation of cannabinoid receptors. Indeed, these compounds modulate a number of signalling pathways critically implicated in the deleterious effect of cannabinoids on learning and memory. Thus, the involvement of the mammalian target of rapamycin pathway and extracellular signal-regulated kinases, together with their consequent regulation of cellular processes such as protein translation, play a critical role in the amnesic-like effects of cannabinoids. In this study, we summarize the cellular and molecular mechanisms reported in the modulation of cognitive function by the endocannabinoid system.

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Section: (D) Cellular and Subcellular Localization Of Cb1r And Its Immentioning

confidence: 86%

Cellular and intracellular mechanisms involved in the cognitive impairment of cannabinoids

Puighermanal

Busquets-García

Maldonado

et al. 2012

Phil. Trans. R. Soc. B

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“…An imbalance in GABAergic transmission resulting from the chronic caffeine-induced alterations of A 1 and CB 1 levels may have occurred, leading to some adaptive changes in the pyramidal cells and/or in the parvalbumin-expressing (PV) GABAergic neurons, which do not express CB 1 receptors (Katona et al, 1999). Interestingly, the blockade of GABAergic transmission was shown to reverse the cognitive effects of acute THC in vivo (Varvel et al, 2005). A critical imbalance in the temporal coordination of pyramidal cell firing could have become evident when THC was administered, if there was an enhanced sensitivity to the fast spiking activity of PV cells; hence, leading to increased inhibition of pyramidal cell firing.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Hippocampal Cannabinoid CB1 Receptor Actions by Adenosine A1 Receptors and Chronic Caffeine Administration: Implications for the Effects of Δ9-Tetrahydrocannabinol on Spatial Memory

Sousa

Assaife-Lopes

Ribeiro

et al. 2010

Neuropsychopharmacol

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The cannabinoid CB 1 receptor-mediated modulation of g-aminobutyric acid (GABA) release from inhibitory interneurons is important for the integrity of hippocampal-dependent spatial memory. Although adenosine A 1 receptors have a central role in fine-tuning excitatory transmission in the hippocampus, A 1 receptors localized in GABAergic cells do not directly influence GABA release. CB 1 and A 1 receptors are the main targets for the effects of two of the most heavily consumed psychoactive substances worldwide: D 9 -tetrahydrocannabinol (THC, a CB 1 receptor agonist) and caffeine (an adenosine receptor antagonist). We first tested the hypothesis that an A 1 -CB 1 interaction influences GABA and glutamate release in the hippocampus. We found that A 1 receptor activation attenuated the CB 1 -mediated inhibition of GABA and glutamate release and this interaction was manifested at the level of G-protein activation. Using in vivo and in vitro approaches, we then investigated the functional implications of the adenosine-cannabinoid interplay that may arise following chronic caffeine consumption. Chronic administration of caffeine in mice (intraperitoneally, 3 mg/kg/day, for 15 days, 412 h before trials) led to an A 1 -mediated enhancement of the CB 1 -dependent acute disruptive effects of THC on a short-term spatial memory task, despite inducing a reduction in cortical and hippocampal CB 1 receptor number and an attenuation of CB 1 coupling with G protein. A 1 receptor levels were increased following chronic caffeine administration. This study shows that A 1 receptors exert a negative modulatory effect on CB 1 -mediated inhibition of GABA and glutamate release, and provides the first evidence of chronic caffeine-induced alterations on the cannabinoid system in the cortex and hippocampus, with functional implications in spatial memory.

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“…In addition, a probe trial (60-s duration, no platform present) was given before the first acquisition session and again before the eighth acquisition session. The other training procedures were identical to those previously reported (Varvel et al 2004;Varvel and Lichtman 2002).…”

Section: Methodsmentioning

confidence: 95%

Disruption of CB1 receptor signaling impairs extinction of spatial memory in mice

2004

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?9-THC-induced cognitive deficits in mice are reversed by the GABAA antagonist bicuculline

Abstract: This is the first demonstration of which we are aware showing that GABA(A) receptors may play a necessary role in Delta(9)-THC-induced memory impairment in whole animals.

Cited by 36 publications

References 30 publications

Cellular and intracellular mechanisms involved in the cognitive impairment of cannabinoids

Cellular and intracellular mechanisms involved in the cognitive impairment of cannabinoids

Regulation of Hippocampal Cannabinoid CB1 Receptor Actions by Adenosine A1 Receptors and Chronic Caffeine Administration: Implications for the Effects of Δ9-Tetrahydrocannabinol on Spatial Memory

Disruption of CB1 receptor signaling impairs extinction of spatial memory in mice

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