Abstract
The central amygdala is critical for the acquisition and expression of fear memories. This region receives a dense innervation from brainstem noradrenergic cell groups and has a high level of α2-adrenoceptor expression. Using whole-cell electrophysiological recordings from rat brain slices, we characterise the role of pre-synaptic α2-adrenoceptor in modulating discrete inhibitory and excitatory connections within both the lateral and medial division of the central amygdala. The selective α2-adrenoceptor agonist clonidine blocked the excitatory input from the pontine parabrachial neurons onto neurons of the lateral central amygdala. In addition, clonidine blocked inhibitory connections from the medial paracapsular intercalated cell mass onto both lateral and medial central amygdala neurons. To examine the behavioural consequence of α2-adrenoceptor-mediated inhibition of these inputs, we infused clonidine into the central amygdala prior to contextual fear-conditioning. In contrast to vehicle-infused rats, clonidine-infused animals displayed reduced levels of freezing 24 hours after training, despite showing no difference in freezing during the training session. These results reveal a role for α2-adrenoceptors within the central amygdala in the modulation of synaptic transmission and the formation of fear-memories. In addition, they provide further evidence for a role of the central amygdala in fear-memory formation.
Highlights
The central amygdala (CeA) receives processed and unprocessed sensory input carrying information about both the conditioned stimulus and unconditioned stimulus needed for fear conditioning
Clonidine administration had no effect on the input resistance, action potential threshold or action potential half-width displayed by the two cells types in the central amygdala (CeAL) or the adapting neurons of the central amygdala (CeAM) (Table 1)
It is likely that any change in frequency or amplitude of spontaneous release events from this single parabrachial nucleus (PBr)-CeAL connection was undetectable within the background of spontaneous release from unaffected excitatory connections to the CeAL neurons
Summary
The central amygdala (CeA) receives processed and unprocessed sensory input carrying information about both the conditioned stimulus and unconditioned stimulus needed for fear conditioning. It is extensively connected (via inhibitory projections) to the brainstem and hypothalamic nuclei responsible for the behavioural, hormonal and autonomic changes that comprise the conditioned response[1]. The medial division of the central amygdala (CeAM) receives dense noradrenergic projections[4] and we have previously demonstrated noradrenergic terminal labelling in close proximity to PBr terminals within the CeAL3 Consistent with this dense innervation, noradrenaline is released into the CeA in rats in response to stressors[5,6]. Action potential width (ms) how α2-adrenoceptor activation alters excitatory and inhibitory synaptic activity within the CeAM and CeAL, and whether activation of α2-adrenoceptor within the CeA influences the acquisition of fear-conditioning in rats
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