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Next Article 
The Journal of Neuroscience, May 15, 1998, 18(10):3489-3500
Galanin Receptor-Mediated Inhibition of Glutamate Release in the
Arcuate Nucleus of the Hypothalamus
Gregory A.
Kinney,
Paul J.
Emmerson, and
Richard J.
Miller
Department of Pharmacological and Physiological Sciences, The
University of Chicago, Chicago Illinois, 60637
It is thought that galanin, a 29 amino acid neuropeptide, is
involved in various neuronal functions, including the regulation of
food intake and hormone release. Consistent with this idea, galanin
receptors have been demonstrated throughout the brain, with high levels
being observed in the hypothalamus. However, little is known about the
mechanisms by which galanin elicits its actions in the brain.
Therefore, we studied the effects of galanin and its analogs on
synaptic transmission using an in vitro slice
preparation of rat hypothalamus. In arcuate nucleus neurons, application of galanin resulted in an inhibition of evoked
glutamatergic EPSCs and a decrease in paired-pulse depression,
indicating a presynaptic action. The fragments galanin 1-16 and 1-15
produced a robust depression of synaptic transmission, whereas the
fragment 3-29 produced a lesser degree of depression. The chimeric
peptides C7, M15, M32, and M40, which have been reported to antagonize some actions of galanin, all produced varying degrees of depression of
evoked EPSCs. In a minority of cases, C7, M15, and M40 antagonized the
actions of galanin. Analysis of mEPSCs in the presence of TTX and
Cd2+, or after application of  -latrotoxin,
indicated a site of action for galanin downstream of
Ca2+ entry. Thus, our data suggest that galanin acts
via several subtypes of presynaptic receptors to depress synaptic
transmission in the rat arcuate nucleus.
Key words:
galanin; galanin receptors; transmitter release; presynaptic; depression; EPSC; mEPSC
Copyright © 1998 Society for Neuroscience 0270-6474/98/18103489-12$05.00/0
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