Kindling causes persistent in vivo changes in firing rates and glutamate sensitivity of central piriform cortex neurons in rats

The present experiments were undertaken to study whether amygdala kindling induces persistent alterations in the functional status of neurons of the central piriform cortex, a subregion of the piriform cortex identified previously as a site involved in the kindling process. Extracellular, single-unit recordings of piriform cortex neurons were made in anesthetized fully kindled rats at an interval of at least five weeks after the last seizure. Electrode implanted but not kindled rats served as sham controls. An additional group of non-implanted rats was used as naive controls. Spontaneously firing piriform cortex neurons were characterized in all groups by smooth, sharp, biphasic (i.e. positive/negative) action potentials with a duration of 0.8-1.8 ms, and were primarily located at the border between piriform cortex layers II and III. In kindled rats, neurons in the central piriform cortex exhibited a significantly higher firing rate compared to controls. Based on median group values, the increase in basal activity in kindled rats averaged about 90%. The responsiveness of piriform cortex neurons to neurotransmitters was tested by microiontophoretic application of glutamate, N-methyl-D-aspartate and GABA. Piriform cortex neurons of kindled rats exhibited a significantly lower responsiveness to the excitatory effect of glutamate than naive controls. A lowered glutamate responsiveness was also seen in sham controls. No significantly altered transmitter sensitivities of piriform cortex neurons from kindled rats were seen with N-methyl-D-aspartate or GABA.The data indicate that amygdala kindling causes persistent interictal changes in both basal activity and glutamate responsiveness of central piriform cortex neurons which could contribute to the abnormal hyperexcitability characteristic of kindling.