Abstract
In electrophysiological terms, experimental
models of durable information storage in the
brain include long-term potentiation (LTP),
long-term depression, and kindling. Protein
synthesis correlates with these enduring
processes. We propose a fourth example of
long-lasting information storage in the brain,
which we call the GABA-withdrawal syndrome
(GWS). In rats, withdrawal of a chronic
intracortical infusion of GABA, a ubiquitous
inhibitory neurotransmitter, induced epileptogenesis
at the infusion site. This overt GWS lasted
for days. Anisomycin, a protein synthesis
inhibitor, prevented the appearance of GWS
in vivo. Hippocampal and neocortical slices
showed a similar post-GABA hyperexcitability
in vitro and an enhanced susceptibility to LTP
induction. One to four months after the epileptic
behavior disappeared, systemic administration
of a subconvulsant dose of pentylenetetrazol
produced the reappearance of paroxysmal
activity. The long-lasting effects of tonic