An alternative explanation for the occlusion of ATPA-induced plasticity during CIE and WD would be that these treatments have down-regulated or blocked the mechanisms required for the expression of this type of ‘pharmacological LTP’. If this were the case, we would expect that the mechanisms associated with the expression of plasticity (e.g. AMPA receptors) would not be engaged by the treatments. However, our previous work has shown dramatic increases in AMPA receptor function after CIE and WD (Lack et al., 2007). Alternatively, the responses of BLA neurons themselves might be reduced during CIE and WD such that the increased AMPA receptor function was negated by reduced neuronal excitability. However, fEPSP responses measured following activation of the EC/BLA synapses were increased after CIE and WD. Thus, both glutamatergic synaptic transmission and the neurophysiological responses of BLA neurons to that transmission are increased during CIE and WD. These findings are inconsistent with any treatment-dependent inhibition of the mechanisms responsible for the expression of APTA-related plasticity.
