Hi Bill!
Thanks for your answer. I observed (while in current clamp) after a
certain delay the onset of sustained spiking activity.
But! Since PFC brain slices are usually silent, there shoudn't be much
inhibitory activity to block. Hence i would expect that application of
bicuculline should only have neglible effects on the network activity.
So I wonder what causes this spike activity???
My interpretation would be, that in a system with excitatory and
inhibitory inputs (EPSPs and IPSPs), blocking of IPSPs leads to a
slightly increase of the relative excitatory input (a shift of the
ratio EPSP/IPSP). This might lead to a slightly depolarisation which
subsequentily leads to a further increase of EPSPs (via voltage gated
mechanisms) and so on... until finally neurons become superthreshold.
Does this make any sense?
I highly appreciate any comments.
Regards,
Thomas
