MORPHOLOGY AND FOS IMMUNOREACTIVITY REVEAL 2 SUBPOPULATIONS OF STRIATAL NEUROTENSIN NEURONS FOLLOWING ACUTE 6-HYDROXYDOPAMINE LESIONS AND RESERPINE ADMINISTRATION

Authors
Citation
Js. Brog et Ds. Zahm, MORPHOLOGY AND FOS IMMUNOREACTIVITY REVEAL 2 SUBPOPULATIONS OF STRIATAL NEUROTENSIN NEURONS FOLLOWING ACUTE 6-HYDROXYDOPAMINE LESIONS AND RESERPINE ADMINISTRATION, Neuroscience, 65(1), 1995, pp. 71-86
Citations number
53
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03064522
Volume
65
Issue
1
Year of publication
1995
Pages
71 - 86
Database
ISI
SICI code
0306-4522(1995)65:1<71:MAFIR2>2.0.ZU;2-5
Abstract
It was previously reported that following striatal dopamine depletion or pharmacological blockade of dopamine neurotransmission, neurotensin immunoreactivity is elicited in at least two distinct subpopulations of striatal neurons (Neuroscience Vol. 46, pp. 335-350, 1992). Recentl y it was shown that Fos immunoreactivity, interpreted as an indicator of enhanced neuronal activity, is appreciably co-localized in only one of the subpopulations of neurotensin-immunoreactive neurons observed following blockade of the dopamine D-2 receptor (Neuroscience Vol. 57, pp. 649-660, 1993). In the present study, similar methods were used t o determine the degree of co-localization of Fos and neurotensin immun oreactivity in striatal neurons in response to the dopamine-depleting effects of 6-hydroxydopamine lesions and reserpine administration. It was observed that following these treatments, a subpopulation of neuro ns at the small end of the medium size range exhibited light neurotens in immunoreactivity and frequent co-localization with Fos immunoreacti vity. This population was predominant after reserpine administration i n the dorsolateral quadrant of the striatum. Another subpopulation com prised larger neurons that exhibited intense neurotensin immunoreactiv ity in perikarya and proximal processes that was rarely co-localized w ith Fos immunoreactivity. This type of neuron was observed following a ll the drug treatments but was present almost to the exclusion of the smaller type of cells three days following ventral midbrain 6-hydroxyd opamine lesions, being mainly located in the dorsomedial and ventrolat eral portions of the striatum. The present data support the results of the preceding studies in being consistent with the existence of two s ubpopulations of striatal neurons that accumulate neurotensin followin g dopamine depletion. The possibility is considered that one subpopula tion accumulates neurotensin in response to co-ordinate increases in n euronal activity and neurotensin synthesis, and the other as a result of decreased release.