Nj. Emptage et al., THRESHOLD SEROTONIN CONCENTRATION REQUIRED TO PRODUCE SYNAPTIC FACILITATION DIFFERS FOR DEPRESSED AND NONDEPRESSED SYNAPSES IN APLYSIA SENSORY NEURONS, Journal of neurophysiology, 75(2), 1996, pp. 843-854
1. The modulatory actions produced by the neurotransmitter serotonin (
5HT) in Aplysia sensory neurons (SNs) can be distinguished on the basi
s of their concentration requirement for 5HT, their activation and rec
overy kinetics, and their dependence on the relative contribution of d
ifferent second messenger pathways. In addition, some of the facilitat
ory mechanisms activated by 5HT appear to be different depending upon
the recent activation history of synaptic transmission from the SNs. I
n this study, we examined the concentration requirements of 5HT-induce
d facilitation of depressed and nondepressed synapses. 2. In isolated
pleural-pedal ganglia, we produced facilitation of monosynaptic connec
tions between tail SNs and motor neurons (MNs), using different concen
trations of 5HT. As a measure of each preparation's greatest sensitivi
ty to 5HT, we first determined the lowest 5HT concentration that produ
ced increased excitability in the SNs ( ''threshold'' 5HT). Then, in o
ne series of experiments, we applied 5HT sequentially to the same syna
pse, first in the nondepressed and then in the depressed state. In a s
econd series, we applied 5HT simultaneously to two SNs connecting to t
he same MN; one synapse was depressed, the other nondepressed. 3. In b
oth series of experiments, we found that the 5HT concentration require
d to produce facilitation of depressed excitatory postsynaptic potenti
als (EPSPs) was invariably lower than the 5HT concentration that produ
ced facilitation of nondepressed EPSPs. In the first series, 'threshol
d' 5HT (1.6 mu M) was sufficient to facilitate the synapse in the depr
essed state, but not the nondepressed state. However, the nondepressed
synapse could still be facilitated by higher concentrations of 5HT (1
0 mu M). In the second series, increased excitability of SNs, facilita
tion of depressed synapses, and facilitation of nondepressed synapses
were progressively recruited as a function of increasing 5HT concentra
tion (4.1, 6.7, and 10-15 mu M, respectively). 4. These data are consi
stent with previous studies suggesting that different cellular mechani
sms contribute to the facilitation of depressed and nondepressed synap
ses. In addition, our results provide a way to experimentally separate
the two processes and to analyze them simultaneously and independentl
y. Taking advantage of this dissociation, in future experiments it may
be possible to directly compare the relative contributions of differe
nt intracellular mechanisms to synaptic facilitation and to relate the
m to the degree of recent synaptic activation.