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Galanin‐immunoreactive synaptic terminals on basal forebrain cholinergic neurons in the rat
Author(s) -
Henderson Z.,
Morris N.
Publication year - 1997
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/(sici)1096-9861(19970623)383:1<82::aid-cne7>3.0.co;2-h
Subject(s) - galanin , basal forebrain , nucleus basalis , choline acetyltransferase , cholinergic neuron , biology , cholinergic , neuroscience , forebrain , diagonal band of broca , nucleus , colocalization , neuropeptide , medicine , central nervous system , biochemistry , receptor
Previous studies have indicated that galanin is one of the most abundant peptides in the basal forebrain and that it has a significant modulatory influence on cholinergic transmission. The aim of the present study was to use a light electron microscopic correlation technique to determine whether galanin‐immunoreactive terminals form synaptic contacts with basal forebrain cholinergic cells of the rat. Sections from fixed‐perfused brains were stained at the light and electron microscopic levels for galanin and choline acetyltransferase immunoreactivity in the same section by using a dual‐colour immunohistochemical method. The results showed that galanin‐immunoreactive axonal terminals are unevenly distributed in the medial septal nucleus, the diagonal band, and the nucleus basalis. Galanin‐positive synapses were most prominent on choline acetyltransferase‐positive neurons in the lateral parts of the nucleus of the diagonal band and in the posterior half of the nucleus basalis, which is where there was the greatest overlap between the distribution of galanin‐immunoreactive terminals and choline acetyltransferase‐positive neurons. The origins of these galanin‐positive terminals are not known, but the results confirm that the basal forebrain galaninergic system has a synaptic influence on basal forebrain cholinergic neurons in the rat. J. Comp. Neurol. 383:82–93, 1997. © 1997 Wiley‐Liss,Inc.