Institute of Higher Nervous Activity and Neurophysiology RAS, Moscow, Russia, email@example.com
Inhibition of paired-pulse plasticity of CA3-CA1 field EPSPs was studied in relation to natural calpain activity in the hippocampal slices of Wistar rats. Paired-pulse stimulation was performed with the set of different stimulus intensity and two interpulse intervals – 70 ms and 15 ms. After electrophysiological recording calpain activity was measured in each slice separately. It is well established that residual Ca2+ activates transmitter release in response to repeated stimulation shortly after the first one, underlying postsynaptic EPSP facilitation (PPF). However IPSP generated immediately after EPSP in response to the first stimulus is superimposed to synaptic facilitation, decreasing PPF at the shortest interpulse intervals or even producing paired-pulse depression. We used this effect to measure the efficacy of inhibitory transmission. Since the validity of PPF test for estimation of presynaptic plasticity is highly responsive to inappropriate stimulus intensity, we control this factor by new method approximating fEPSPs upon presynaptic fiber values for the first and second responses separately. The ratio of gradients (PPGR) was taken as an index of paired-pulse plasticity. Comparing PPGRs at 15 ms and 70 ms interpulse intervals we calculated the value of inhibition. This criterion revealed that short-term PPGR inhibition was significantly increased in accordance with calpain activation. Calpain activity correlated negatively with PPGR at 15 ms and positively with PPGRs ratio (PPGR15ms/PPGR70ms). This relation may be explained by calpain-dependent proteolysis of glutamate decarboxylase and its participation in phosphorylation of GABAA receptors.
This study was supported by Russian Basic Research Foundation. ЭПИГЕНЕТИЧЕСКИЕ И МОЛЕКУЛЯРНЫЕ ОСОБЕННОСТИ ПРИ СИНДРОМЕ ЛУИ-БАР (АТАКСИЯ-ТЕЛЕАНГИЭКТАЗИЯ)