Ghotbeddin Z, Mirnajafi-Zadeh J, Semnanian S, Janahmadi M. Electrophysiological study of amygdale-induced changes in the excitability of CA1 hippocampal pyramidal neurons in male adult rats. Physiol Pharmacol 2012; 16 (1) :33-43
URL:
http://ppj.phypha.ir/article-1-801-en.html
Abstract: (13402 Views)
Introduction: Many studies have shown that amygdala kindling produces synaptic potentiation by induction of
changes in the neuronal electrophysiological properties and inward currents both in epileptic focus and in the areas
which are in connection with the epileptic focus and have important role in seizure development and progression such
as hippocampal CA1 region. However, cellular mechanisms of these processes are not clear. In the present study,
changes in the electrophysiological properties of hippocampal CA1 pyramidal neurons following amygdala kindling
were examined in rat.
Methods: Animals were rapidly kindled by stimulation of right amygdala (12 stimulation per day, 1 ms pulse
duration at 50Hz). Twenty-four hours after amygdala kindling, electrophysiological properties and inward currents of
CA1 pyramidal neurons were assessed by using whole-cell patch clamp technique.
Results: Amygdala kindling findings show that percentage broadening of the last spike compared to the first spike
during a trains of action potentials was significantly increased in kindled rats (p<0.05). The number of rebound action
potential was significantly increased from 1±1 in control rats to 6±1 in kindled rats (p<0.01). The amplitude of post
stimulus afterhyperpolarization potential (Post AHP) following a trains of action potential was also significantly
(p<0.05) increased in kindled group (-5±2mV) compared to normal rats (-3±1mV). Under voltage clamp condition,
amygdala kindling produced a significantly larger inward current (-5344.25±33.19 pA, p<0.001) in CA1 pyramidal
neurons compared to normal cells (-9203.6±44.99pA).
Conclusion: The present findings show that amygdala kindling resulted in neuronal hyperexcitability through
alteration of the electrophysiological characteristics possibly by increasing the inward currents in hippocampal CA1
pyramidal neurons.