SR2-INDUCED SUPPRESSION OF INHIBITION AND PROVIDES NEW EVIDENCE FOR APRESYNAPTIC EXPRESSION MECHANISM IN RAT HIPPOCAMPAL SLICES( SUPPORTS DEPOLARIZATION)
W. Morishita et Be. Alger, SR2-INDUCED SUPPRESSION OF INHIBITION AND PROVIDES NEW EVIDENCE FOR APRESYNAPTIC EXPRESSION MECHANISM IN RAT HIPPOCAMPAL SLICES( SUPPORTS DEPOLARIZATION), Journal of physiology, 505(2), 1997, pp. 307-317
1. We studied the transient suppression of evoked GABA(A)ergic inhibit
ory postsynaptic currents (eIPSCs) that follows brief membrane depolar
ization in rat CA1 hippocampal pyramidal cells, a process called depol
arization-induced suppression of inhibition (DSI). We used whole-cell
patch electrodes filled with a CsCl-based solution to voltage clamp th
e currents. All experiments were done in the presence of 50 mu M 2-ami
no-5-phosphonovaleric acid (APV) and 20 mu M 8-cyano-'7-nitroquinoxali
ne-2,3-dione (CNQX) to block ionotropic glutamate-induced currents and
polysynaptic transmission in the slice preparation. 0 2. Substituting
strontium (Sr2+) for extracellular calcium (Ca2+) led to the appearan
ce of numerous 'asynchronous' small IPSCs following an eIPSC. These as
ynchronous IPSCs were indistinguishable from TTX-insensitive quantal I
PSCs. 3. Although somewhat less effective than Ca2+, Sr2+ was capable
of supporting DSI, and both asynchronous and synchronous IPSCs were bl
ocked by the DSI process. 4. During DSI, quantal content of eIPSCs, bu
t not quantal size, was significantly reduced. 5. Sr2+ converted paire
d-pulse depression (PPD) of eIPSCs to a paired-pulse facilitation (PPF
), presumably br altering the probability of release at inhibitory ner
ve terminals. DSI had no effect on either PPD or PPF. 6. The results s
how that Sr2+ induces asynchronous release of GABA as it does of other
neurotransmitters and changes the probability of release at GABA(A)er
gic terminals as well. Most importantly, the results support the hypot
hesis that, despite being induced postsynaptically, DSI is expressed p
resynaptically as a decrease in GABA release, possibly by acting at a
site other than the Ca2+-dependent release step.