Zy. Sun et S. Schacher, TETANIC STIMULATION AND CYCLIC ADENOSINE-MONOPHOSPHATE REGULATE SEGREGATION OF PRESYNAPTIC INPUTS ON A COMMON POSTSYNAPTIC TARGET NEURON IN-VITRO, Journal of neurobiology, 29(2), 1996, pp. 183-201
Previous studies indicated that Aplysia sensory neurons (SNs) compete
when reestablishing synapses with a motor cell target (L7) in vitro. T
he competition is characterized by a cell number-dependent decrease in
the efficacy of each connection, an increase in the elimination of SN
varicosities, a reduction in the formation of new SN varicosities, an
d the segregation of varicosities of each SN to restricted portions of
the target axons. The changes do not require spike activity, since bo
th the SNs and L7 do not fire spontaneously. Here, we examined whether
adding activity to SNs during the early stages of synapse formation w
ith stimuli known to evoke facilitatory responses in stable SN-L7 conn
ections-tetanic stimulation or increase in intracellular cyclic adenos
ine monophosphate (cAMP)-would modulate the intrinsic segregatory proc
ess. Tetanic stimulation to one SN increased synapse efficacy and the
number of varicosities of the stimulated SNs while reducing the functi
onal changes by the nonstimulated SNs in the same cultures. An increas
e in the stability of preexisting varicosities contributed to the over
all increase in varicosities evoked by tetanus. The functional changes
evoked by tetanus were not expressed when the same tetanic stimulatio
n was also given to the other SN, or when L7 was hyperpolarized during
the tetanus to the SN. Raising cAMP levels in one SN increased synaps
e efficacy and the rate of new varicosity formation by the injected SN
s without affecting the development of the connections formed by the n
oninjected SNs. These results suggest that different forms of presynap
tic and postsynaptic activities in neurons can regulate specific aspec
ts of the competitive process associated with the fine-tuning of conne
ctions formed by converging presynaptic inputs. (C) 1996 John Wiley &
Sons, Inc.