Abstract:
:Deficits in experimentally induced drinking and pressor responses after administration of 6-hydroxydopamine (6-OHDA) into the lateral cerebral ventricle (LCV) have been reported. Questions have arisen, however, as to whether these effects are due to non-specific actions of the neurotoxin and, if specific, whether the depletion of dopamine (DA) or of norepinephrine (NE) is the critical factor for producing the impairments. In the present report methods to deplete brain catecholamine (CA) differentially were employed in order to test the hypothesis that central 6-OHDA injections act on brain CA substrates per se to produce behavioral and physiological response deficits to angiotensin II (ANG II) challenges. The findings support the interpretation that forebrain dopamine is essential for the mediation of sensorimotor integration involved in response to acute homeostatic stressors. In addition, the outcome identifies an important role for forebrain noradrenergic systems in the mediation of ANG II-elicited drinking and blood pressure responses.
journal_name
Brain Resjournal_title
Brain researchauthors
Bellin SI,Bhatnagar RK,Johnson AKdoi
10.1016/0006-8993(87)90128-4subject
Has Abstractpub_date
1987-02-10 00:00:00pages
105-12issue
1eissn
0006-8993issn
1872-6240pii
0006-8993(87)90128-4journal_volume
403pub_type
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