Abstract
10+3 sec vs 250+20 sec; P 0.05). Microdialysis of the glutamate NMDA receptor antagonist AP5 (100 μM) into the ACC before but not after conditioning (CPD), blocked the acquisition of CPA learning (-2+0.5 sec vs 200+5 sec sham control; P<0.05). We used ACC field potentials elicited by electrical stimulation of the medial thalamus (MT) as a quantitative measure of synaptic strength. Following CRD training, MT (6V stimulation) evoked a peak long-term potentiation (LTP) response of 270+30% of basal compared to 162+10%, P<0.05 before conditioning. The strengthened synaptic activity persisted for up to 5 wks. In conclusion these results show that neurons in ACC are critical for mediating the affective pain component. Using the glutamatergic pathways, ACC neurons encode and transmit information related to the aversiveness of noxious stimuli and provide teaching signal required for conditioned aversion acquisition. This is mediated by induction and maintenance of LTP in the ACC. In contrast ACC is not required for the expression or retrieval of information related to prediction of aversive stimuli by contextual cue.
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