Abstract:
Increasing the impulse activity of neurons in vivo over 3 or more days
causes a reduction in transmitter release that persists for days or weeks (eg.
Mercier and Atwood, 1989). This effect is usually accompanied by decreased
synaptic fatigue. These two changes involve presynaptic mechanisms and
indicate "long-term adaptation" (LTA) of nerve terminals. Previous
experiments have shown that LTA requires extracellular calcium and protein
synthesis (eg. Hong and Lnenicka, Soc. Neurosci. Abstr. 17:1322) and appears
to involve communication between the cell body and the nerve terminals. The
present study examines the possibility that the reduction in transmitter release
is caused by an -increase in the calcium buffering ability within the nerve
terminals. It examines the responses of adapted and control nerve terminals
to exogenously applied calcium buffer, BAPTA-AM, which decreases
transmitter release (Robitialle and Charlton, 1992). If LTA increases intrinsic
Ca2+-buffering, the membrane permeant form of BAPTA should have less
effect on adapted nerve terminals than on controls.
Experiments are performed on the phasic abdominal extensor motor
neurons of the crayfish, Procambarns clarkii. BAPTA-AM decreases excitatory
postsynaptic potentials (EPSP's) of the phasic extensor muscles in a dosedependent
manner between 5 and 50 JLM. LTA is elicited by in vivo
stimulation at 2.5 Hz for 2-4 h per day over 3 days, which reduces EPSP's by
over 50%. Experiments indicate that BAPTA-AM produces no significant
change in EPSP reduction in adapted neurons when compared to controls.
These results do not support the hypothesis that increased daily activity alters
rapid intrinsic calcium buffers, that are able to reduce transmitter output in the
same manner as BAPTA.
