In vivo kindling does not alter afterhyperpolarizations (AHPs) following action potential firing in vitro in basolateral amygdala neurons.

Kindling in vivo results in enhanced glutamatergic synaptic transmission and epileptiform bursting in vitro in neurons of the basolateral amygdala (BLA). We tested the hypothesis that reduction of intrinsic inhibitory mechanisms, such as the slow- and medium-afterhyperpolarizations (s-AHPs, m-AHPs), contributes to the enhanced neuronal excitability observed in kindling-induced epileptogenesis using intracellular recording methodology. In these studies, neurons were recorded from the BLA contralateral to the kindling site. AHPs following depolarizing current-induced (100 ms, 1 nA) action potentials were recorded from BLA neurons of control and kindled animals. We found no difference in the amplitude of the s-AHP and m-AHP, or the duration of the s-AHP between control and kindled neurons. In addition, kindling did not alter the distribution of accommodating/non-accommodating BLA neurons (as assessed from neuronal responses during long (500 ms) depolarizing current injection). It is concluded that an alteration in the neuronal network within the BLA rather than a blockade of an intrinsic inhibitory mechanism underlies the enhanced excitability recorded in BLA neurons following kindling.