Barton G. Weick

Office of Extramural Research

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Judith R. Walters

National Institute of Neurological Disorders and Stroke

Sue Ritter

Washington State University

Joanne H. Carlson

University of California, San Diego

Thomas N. Chase

MacEwan University

Thomas M. Engber

Eli Lilly (United States)

Debra A. Bergstrom

National Institute of Neurological Disorders and Stroke

Raymond M. Quock

Washington State University

Zvi Susel

Weatherford College

Philip G. Pearson

National Institute of Neurological Disorders and Stroke

Sanford P. Markey

National Institute of Mental Health

Cooperative Institutions

National Institutes of Health

National Institute of Neurological Disorders and Stroke

National Institute of Mental Health

George Washington University

Washington State University

University of Washington

University of Illinois Chicago

Purdue University West Lafayette

University of Idaho

Merck & Co., Inc., Rahway, NJ, USA (United States)

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Effects of chronic Levodopa on D1 and D2 receptor-mediated striatal output

Neurochemistry International (1992)

Thomas M. Engber Zvi Susel Barton G. Weick Judith R. Walters Thomas N. Chase

10.1016/0197-0186(92)90248-p

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Citations (5)

Neurophysiological Examination of the Role of D-1 Dopamine Receptors in the Regulation of Neuronal Activity in the Basal Ganglia

Advances in experimental medicine and biology (1988)

Judith R. Walters Joanne H. Carlson Barton G. Weick Debra A. Bergstrom

Autoreceptor

10.1007/978-1-4899-2723-1_10

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Citations (2)

Electrophysiological Investigation of D-1/D-2 Receptor Interactions in the Substantia Nigra and Basal Ganglia

Palgrave Macmillan UK eBooks (1988)

Judith R. Walters D. A. Bergstrom Joanne H. Carlson Barton G. Weick Helen S. Pan

Autoreceptor

D1-like receptor

Neurotransmitter receptor

10.1007/978-1-349-10047-7_15

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Citations (4)

Stimulation of insulin release and suppression of feeding by hepatic portal glucagon infusion in rats

Physiology & Behavior (1986)

Barton G. Weick Sue Ritter

Hyperinsulinemia

10.1016/0031-9384(86)90421-x

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Citations (9)

p-Chloroamphetamine-induced hyperthermia pharmacologically distinct from fenfluramine-induced hyperthermia

Journal of Pharmacy and Pharmacology (1979)

Raymond M. Quock Barton G. Weick

The influence of various drug pretreatments upon the responses of rabbits to the putative indirect 5-hydroxytryptaminergic agonists p-chloroamphetamine (PCA) and fenfluramine were examined. In naive rabbits PCA evoked hyperthermia, behavioural excitation and prominent forepaw clonic activity, while fenfluramine produced only hyperthermia and behavioural stimulation. The hyperthermic and behavioural responses of both agents were reduced by the 5-hydroxytryptamine (5-HT) uptake inhibitor, fluoxetine, potentiated by the monoamine oxidase inhibitor, pheniprazine, and unaltered by the dopaminergic antagonist, haloperidol. Pretreatment with the 5-hydroxytryptaminergic receptor blockers cinanserin, cyproheptadine or D-2-bromolysergic acid diethylamide markedly attenuated the effects of fenfluramine but only slightly influenced the responses to PCA. Depeletion of central 5-HT stores with p-chlorophenylalanine also affected responses to fenfluramine more than responses to PCA. The tryptaminergic receptor blocker methergoline abolished both PCA-induced hyperthermia and forepaw clonus--but not behavioural stimulation--while the effects of flenfluramine were only partly reduced. We interpret these data to mean that PCA- and fenfluramine-induced drug effects have different underlying mechanisms, the PCA responses relying possibly upon tryptamine while the fenfluramine responses are 5-hydroxytryptaminergic.

Quipazine

Cyproheptadine

Metergoline

P-Chloroamphetamine

10.1111/j.2042-7158.1979.tb13416.x

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Citations (15)

AJP Regulatory Integrative and Comparative Physiology (1986)

Barton G. Weick Sue Ritter

Continuous intraportal infusion of pancreatic glucagon during a feeding test conducted in the dark phase of the circadian photoperiod produced a dose-related suppression of feeding in rats. At the end of the 30 min of infusion, food intake was suppressed 10% at the infusion rate of 0.33 micrograms X kg-1 X min-1 and 45% at the highest infusion rate studied (100 micrograms X kg-1 X min-1). At infusion rates of 33 and 100 micrograms X kg-1 X min-1, the suppression of cumulative intake persisted for 30 min after the termination of the infusion, but no effect on 24-h intake was observed. Glucagon's glycemic effects were measured for two glucagon doses (1 and 10 micrograms X kg-1 X min-1) in the absence of food using a paradigm similar to that used for the feeding tests. In contrast to the suppression of food intake, the hyperglycemic effects of glucagon were not dose related for the two doses tested. The hyperglycemia was similar in magnitude 5 min after the start of the infusion at both infusion rates. Subsequently, plasma glucose concentrations declined more rapidly at the higher than at the lower glucagon dose. This difference in the effect of glucagon on glucose disposal may be important for glucagon's satiating effect.

10.1152/ajpregu.1986.250.4.r676

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Citations (23)

Plasma catecholamines in fasted and sucrose supplemented rats

Physiology & Behavior (1983)

Barton G. Weick Sue Ritter Richard McCarty

Turnover

10.1016/0031-9384(83)90014-8

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Citations (24)

Fasting reduces cardiac beta-adrenergic receptor concentration and ornithine decarboxylase activity in rats

Journal of the Autonomic Nervous System (1983)