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Abstract Activation of adrenoreceptors modulates synaptic transmission in the basolateral amygdala. Here, we investigated the effects of α2 -adrenoreceptor activation on long-term depression and long-term potentiation in an in vitro slice preparation of the mouse basolateral amygdala. Field potentials and excitatory postsynaptic currents were evoked in the basolateral amygdala by stimulating the lateral amygdala. Norepinephrine (20 µm) reduced synaptic transmission and completely blocked the induction of long-term potentiation and long-term depression. The α2 -adrenoreceptor antagonist yohimbine (2 µm) reversed this effect. The α2 -adrenoreceptor agonist clonidine (10 µm) mimicked the effects of norepinephrine. The Gi/o -protein inhibitor pertussis toxin (5 µg/mL) reversed the effect of clonidine. Long-term depression was blocked in the presence of ω-conotoxin GVIA, but not ω-agatoxin IVA. Clonidine inhibited voltage-activated Ca2+ currents mediated via N- or P/Q-type Ca2+ -channels. The inhibitory action of clonidine on long-term depression was reversed when inwardly rectifying K+ -channels were blocked by Ba2+ (300 µm). The present data suggest that α2 -adrenoreceptor activation impairs the induction of long-term depression in the basolateral amygdala by a Gi/o -protein-mediated inhibition of presynaptic N-type Ca2+ -channels and activation of inwardly-rectifying K+ -channels. [ABSTRACT FROM AUTHOR]

Attempts have been made to attribute the particular features of general anaesthesia such as hypnosis, analgesia, amnesia and autonomic stability to certain brain regions. In the present study, we examined the effects of the commonplace volatile anaesthetic isoflurane on synaptic transmission in an in vitro slice preparation of the murine amygdala. Despite the established role of this limbic structure in the formation of aversive memories, conditioned fear and anxiety, as well as pain processing and regulation of sympathetic tone, the influence of volatile anaesthetics on synaptic signalling has not yet been investigated in this region of the brain. Evoked postsynaptic currents were monitored from principal neurons in the basolateral nucleus of the amygdala by means of patch-clamp recording. The mixed postsynaptic currents were mediated by non-NMDA, NMDA, GABA A and GABA B receptors. Isoflurane added to the perfusion medium reduced the strength of synaptic signalling following the activation of non-NMDA, NMDA, and GABA B receptors, whereas the GABA A receptor-mediated responses were enhanced. The overall reduction of neuronal excitability was also reflected in a reduction of field potential amplitudes. Isoflurane neither changed the membrane resting potential nor the input resistance of principal neurons in the amygdala. The present results may contribute to the understanding of how stress reactions and long-lasting neuroplastic processes are suppressed under general anaesthesia.

Activation of adrenoreceptors modulates synaptic transmission in the basolateral amygdala. Here, we investigated the effects of alpha2-adrenoreceptor activation on long-term depression and long-term potentiation in an in vitro slice preparation of the mouse basolateral amygdala. Field potentials and excitatory postsynaptic currents were evoked in the basolateral amygdala by stimulating the lateral amygdala. Norepinephrine (20 micro m) reduced synaptic transmission and completely blocked the induction of long-term potentiation and long-term depression. The alpha2-adrenoreceptor antagonist yohimbine (2 micro m) reversed this effect. The alpha2-adrenoreceptor agonist clonidine (10 micro m) mimicked the effects of norepinephrine. The Gi/o-protein inhibitor pertussis toxin (5 micro g/mL) reversed the effect of clonidine. Long-term depression was blocked in the presence of omega-conotoxin GVIA, but not omega-agatoxin IVA. Clonidine inhibited voltage-activated Ca2+ currents mediated via N- or P/Q-type Ca2+-channels. The inhibitory action of clonidine on long-term depression was reversed when inwardly rectifying K+-channels were blocked by Ba2+ (300 micro m). The present data suggest that alpha2-adrenoreceptor activation impairs the induction of long-term depression in the basolateral amygdala by a Gi/o-protein-mediated inhibition of presynaptic N-type Ca2+-channels and activation of inwardly-rectifying K+-channels.