gated this problem. Imaging of neuronal cell bod- 
ies, growth cones, or neurites of sensory neurons 
in culture consistently shows an increase in the size 
of the intracellular calcium transient in response to 
5-HT and a decrease in the calcium transient in re- 
sponse to FMRFamide. The Ca^^ transient in re- 
sponse to action potentials is not uniform through- 
out the cell; there appear to be local hot spots of 
calcium. Moreover, the increase in the calcium tran- 
sient with 5-HT is also not uniform. Some areas of 
the cell show significantly larger increases in cal- 
cium than others. What is most surprising is that 
the hot spots of Ca^"*" do not necessarily coincide 
with the regions that show the largest response to 
5-HT 
The modulation of the calcium transients by 5- 
HT and FMRFamide could be due to a modulation 
of calcium influx and/or calcium buffering. To as- 
sess the latter possibility, the effects of 5-HT were 
studied on the calcium transient produced in re- 
PUBLICATIONS 
sponse to intracellular injection of inositol tris- 
phosphate (IP^), a second messenger that releases 
calcium from intracellular stores. IP^ causes a signif- 
icant calcium transient in the sensory neurons that 
is independent of external calcium. 5-HT has no ef- 
fect on the IPj-induced calcium transient, in con- 
trast to its consistent potentiation of the action po- 
tential-induced calcium transient, which does 
depend on external calcium. Therefore the increase 
in the calcium transient with 5-HT is probably due 
to a modulation of calcium influx. Whether this re- 
sults from a direct modulation of calcium channels 
or is an indirect effect of action potential broaden- 
ing due to S channel closure by 5-HT is under 
study. 
Dr. Siegelbaum is also Associate Professor of 
Pharmacology in the Center for Neurobiology and 
Behavior at the Columbia University College of Phy- 
sicians and Surgeons. 
Books and Chapters of Books 
Volterra, A., Siegelbaum, S.A., Sweatt, J.D., and Kandel, E.R. 1989. Presynaptic inhibition, presynaptic facilita- 
tion, and the molecular logic of second-messenger systems. In Molecular and Cellular Aspects of the Drug 
Addictions (Goldstein, A., Ed.). New York: Springer-Verlag, pp 159-197. 
Articles 
Berman, M.F., Camardo, J.S., Robinson, R.B., and Siegelbaum, S.A. 1989. Single sodium channel currents 
from canine ventricular myocytes: voltage-dependence and relative rates of activation and inactivation. 
J Physiol 415:50^-551. 
Lotan, I. , Volterra, A. , Dash, R , Siegelbaum, S.A. , and Goelet, E 1988. Blockade of ion channel expression in 
Xenopus oocytes with complementary DNA probes to Na"*" and K"*" channel mRNAs. Neuron 1:963-971. 
Volterra, A., and Siegelbaum, S.A. 1988. Role of two different guanine nucleotide-binding proteins in the an- 
tagonistic modulation of the S-type K"*" channel by cAMP and arachidonic acid metabolites in Aplysia sen- 
sory neurons. Proc Natl Acad Sci USA 85:7810-7814. 
Volterra, A., and Siegelbaum, S.A. 1989. Antagonistic modulation of S-K"*" channel activity by cyclic AMP and 
arachidonic acid metabolites. Role for two G proteins. Ann NY Acad Sci 559:219-236. 
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