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Lack of interaction of endocannabinoids and 5-HT3 neurotransmission in associative fear circuits of the amygdala: Evidence from electrophysiological and behavioural experiments
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Rok publikování | 2013 |
Druh | Článek v odborném periodiku |
Časopis / Zdroj | Brain Research |
Fakulta / Pracoviště MU | |
Citace | |
www | http://www.sciencedirect.com/science/article/pii/S0006899313008627# |
Doi | http://dx.doi.org/10.1016/j.brainres.2013.06.011 |
Obor | Neurologie, neurochirurgie, neurovědy |
Klíčová slova | CB1; 5-HT3; Amygdala; Fear conditioning; Slice; IPSC |
Popis | Both the serotonergic and the endocannabinoid system play a major role in mediating fear and anxiety. In the basolateral amygdala (BLA) it has been shown that the cannabinoid receptor 1 (CB1) is highly co-expressed with 5-HT3 receptors on GABAergic intemeurons suggesting that 5-HT3 receptor activity modulates CB1-mediated effects on inhibitory synaptic transmission. In the present study, we investigated the possible interactions of CB1 and 5-HT3-mediated neuronal processes in the BLA using electrophysiological and behavioural approaches. Whole-cell patch-clamp recordings were performed in coronal brain slices of mice. Electric stimuli were delivered to the lateral amygdala to evoke GABA(A) receptor-mediated inhibitory postsynaptic currents (GABA(A)-eIPSCs) in the BLA. The induction of LTDi, a CB1-mediated depression of inhibitory synaptic transmission, was neither affected by the 5-HT3 antagonists ondansetron (OND; 20 mu M) and tropisetron (Trop; 50 nM) nor by the 5-HT3 agonists SR57227A (10 mu M). In auditory fear conditioning tests, mice treated with SR57227A (3.0 mg/kg i.p.) showed sustained freezing, whereas treatment with Trop (1.0 mg/kg i.p.) decreased the expression of conditioned fear. These effects were overruled by the CB1 antagonist rimonabant (RIM; 3.0 mg/kg), which caused increased freezing with or without co-treatment with Trop. In summary, these experiments do not support a functional interaction between CB1 and 5-HT3 receptors at the level of GABA neurotransmission in the BLA nor in terms of fear regulation. (C) 2013 Elsevier B.V. All rights reserved. |
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