Central integration of cardiovascular and drinking responses elicited by central administration of angiotensin II: divergence of regulation by the ventral tegmental area and nucleus accumbens

1986 ◽  
Vol 64 (7) ◽  
pp. 1011-1016 ◽  
Author(s):  
D. L. Jones
Keyword(s):  
Angiotensin Ii ◽  
Nucleus Accumbens ◽  
Ventral Tegmental Area ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Dopamine Antagonist ◽  
Central Administration ◽  
Pressor Responses ◽  
Ventral Tegmental ◽  
Goal Directed Behavior

Previous studies had implicated the involvement of the ventral tegmental area and its dopamine projections to the nucleus accumbens in goal-directed behavior. This study investigated whether or not the GABAergic inputs to the ventral tegmental area and, in turn, dopaminergic input to the nucleus accumbens from the ventral tegmental area modify drinking and cardiovascular responses elicited by central administration of angiotensin II. Injections of 25 ng of angiotensin II into a lateral cerebral ventricle of the rat elicited water intakes averaging 7–8 mL in 15 min with latencies usually less than 3 min. Pretreatment of the nucleus accumbens with spiperone, a dopamine antagonist, or the ventral tegmental area with γ-amino butyric acid (GABA) produced dose-dependent reductions in water intake and number of laps taken while increasing the latency to drink. The spiperone injection did not alter the pressor response. On the other hand, the GABA injections attenuated the pressor responses to central angiotensin II administration. These findings suggest that GABA input to the ventral tegmental area modifies both the cardiovascular and drinking responses elicited following central administration of angiotensin II. However, the dopamine projections to the nucleus accumbens appear to be involved only in the drinking responses elicited by central injections of angiotensin II. Divergence for the coordination of the skeletal motor behavioral component and the cardiovascular component elicited by central administration of angiotensin II must occur before the involvement of these dopamine pathways.

Central injections of spiperone and GABA: attenuation of angiotensin II stimulated thirst

1982 ◽  
Vol 60 (5) ◽  
pp. 720-726 ◽  
Author(s):  
D. L. Jones ◽  
G. J. Mogenson
Keyword(s):  
Angiotensin Ii ◽  
Nucleus Accumbens ◽  
Ventral Tegmental Area ◽  
Globus Pallidus ◽  
Water Intake ◽  
Dopamine Antagonist ◽  
Neuronal Circuit ◽  
Ventral Tegmental ◽  
Reduced Drinking ◽  
Dose Dependent

This study investigated the effects of injecting spiperone or γ-aminobutyric acid (GABA) into the brain on drinking induced by angiotensin II injected into a lateral cerebral ventricle of the rat. Injections of 12.5 pM of angiotensin II elicited water intakes averaging 10 mL in 15 min with latencies of less than 3 min. Spiperone, a dopamine antagonist injected into the nucleus accumbens produced dose-dependent reductions in water intake and number of laps while increasing the latency to drink. Injections of GABA into the ventral tegmental area produced dose-dependent reductions in water intake and number of laps without altering latency to drink or lap volume. GABA injected into the globus pallidus reduced drinking in a manner similar to that described for spiperone injected into the nucleus accumbens when angiotensin II was the dipsogenic agent but was totally without effect on drinking induced by carbachol injections. These results indicate that a proposed neuronal circuit composed of GABA input to ventral tegmental area neurons, dopamine input from the ventral tegmental area to nucleus accumbens neurons, and subsequent GABA input from the nucleus accumbens to globus pallidus neurons may interact with the goal-directed behaviour, drinking, elicited by central angiotensin II administration. Further, they provide evidence that this neuronal circuit may be part of a functional interface for response initiation.

Endogenous enkephalin modulation of dopamine neurons in ventral tegmental area

1986 ◽  
Vol 251 (2) ◽  
pp. R243-R249 ◽  
Author(s):  
P. W. Kalivas ◽  
R. Richardson-Carlson
Keyword(s):  
Nucleus Accumbens ◽  
Motor Activity ◽  
Ventral Tegmental Area ◽  
Physiological Role ◽  
Dopamine Metabolism ◽  
Dopamine Neurons ◽  
Spontaneous Motor Activity ◽  
Opioid Antagonist ◽  
Dopamine Antagonist ◽  
Ventral Tegmental

Many lines of evidence support the possibility that the opioid pentapeptides Met- and Leu-enkephalin can modulate dopamine neurons in the ventral tegmental area (VTA). Thus microinjection of enkephalin analogues into the VTA of rats produces a dopamine-dependent increase in spontaneous motor activity and an increase in dopamine metabolism in certain mesolimbic dopamine terminal fields, such as the nucleus accumbens. To determine if these effects can be produced by endogenous enkephalins, an enkephalinase A inhibitor, thiorphan, was microinjected into the VTA to inhibit enkephalin metabolism. Thiorphan produced a dose-dependent (0.3-3.33 micrograms) increase in spontaneous motor activity that was blocked by pretreatment with the opioid antagonist naloxone (2.0 mg/kg ip) or the dopamine antagonist haloperidol (0.1 mg/kg ip). Thiorphan injection into the VTA increased dopamine metabolism in the nucleus accumbens, prefrontal cortex, and septum but not in the striatum. In all brain regions the increase in dopamine metabolism was blocked by pretreatment with naloxone. These data demonstrate that endogenous enkephalin in the VTA can increase the activity of A10 dopamine neurons, supporting a physiological role for enkephalin in mesolimbic and mesocortical dopamine-mediated behaviors.

Kainic acid lesions of the median preoptic nucleus: effects on angiotensin II induced drinking and pressor responses in the conscious rat

1988 ◽  
Vol 66 (8) ◽  
pp. 1082-1086 ◽  
Author(s):  
D. L. Jones
Keyword(s):  
Angiotensin Ii ◽  
Kainic Acid ◽  
Pressor Response ◽  
Cerebral Ventricle ◽  
Central Administration ◽  
Preoptic Region ◽  
Conscious Rat ◽  
Drinking Response ◽  
Pressor Responses ◽  
Lateral Cerebral Ventricle

Input to the nucleus medianus of the preoptic region has been suggested to be involved in both the drinking and pressor responses elicited by the central administration of angiotensin II. Evidence in support of this suggestion has been gained principally from electrical lesion experiments. This lesion procedure does not differentiate between the cells of the region and fibers coursing through the region. To test the hypothesis that cells in this region are involved in both the pressor and drinking responses elicited by central administration of angiotensin II, injections of kainic acid were made to induce lesions of the cells, while sparing fibers of passage. Drinking and blood pressure responses were determined pre- and post-lesion in the chronically instrumented awake rat. Injections of 50 ng angiotensin II in a 2-μL volume into a lateral cerebral ventricle of the conscious rat elicited pronounced drinking and pressor responses with a latency of 3–5 min. Lesions of the median preoptic region produced by injecting 1.0 μg of kainic acid in 0.25 μL for 15 s attenuated or blocked the drinking response and increased the latency to drink induced by central injections of angiotensin II. However, kainic acid lesions did not significantly alter the pressor responses produced by angiotensin II administration. These results suggest that cells in the median preoptic region are involved in the drinking response but do not participate in the pressor response elicited by angiotensin II administration into a lateral cerebral ventricle of the conscious rat.

Cardiovascular depressor responses to stimulation of substantia nigra and ventral tegmental area

1997 ◽  
Vol 273 (6) ◽  
pp. H2549-H2557 ◽  
Author(s):  
Gilbert J. Kirouac ◽  
John Ciriello
Keyword(s):  
Substantia Nigra ◽  
Ventral Tegmental Area ◽  
Intravenous Administration ◽  
Dopaminergic Neurons ◽  
Cardiovascular Responses ◽  
Receptor Blocker ◽  
Transitional Region ◽  
Pars Lateralis ◽  
Ventral Tegmental ◽  
Stimulation Of

Experiments were done in α-chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect ofl-glutamate (Glu) stimulation of the substantia nigra (SN) and ventral tegmental area (VTA) on arterial pressure (AP) and heart rate (HR). Glu stimulation of the SN pars compacta (SNC) elicited decreases in both mean AP (MAP; −18.9 ± 1.3 mmHg; n = 52) and HR (−26.1 ± 1.6 beats/min; n = 46) at 81% of the sites stimulated. On the other hand, stimulation of the SN pars lateralis or pars reticulata did not elicit cardiovascular responses. Stimulation of the adjacent VTA region elicited similar decreases in MAP (−18.0 ± 2.6 mmHg; n = 20) and HR (−25.4 ± 3.8 beats/min; n = 17) at ∼74% of the sites stimulated. Intravenous administration of the dopamine D2-receptor antagonist raclopride significantly attenuated both the MAP (70%) and the HR (54%) responses elicited by stimulation of the transitional region where the SNC merges with the lateral VTA (SNC-VTA region). Intravenous administration of the muscarinic receptor blocker atropine methyl bromide had no effect on the magnitude of the MAP and HR responses to stimulation of the SNC-VTA region, whereas administration of the nicotinic receptor blocker hexamethonium bromide significantly attenuated both the depressor and the bradycardic responses. These data suggest that dopaminergic neurons in the SNC-VTA region activate a central pathway that exerts cardiovascular depressor effects that are mediated by the inhibition of sympathetic vasoconstrictor fibers to the vasculature and cardioacceleratory fibers to the heart.

Mechanisms of centrally administered ET-1-induced increases in systemic arterial pressure and AVP secretion

1997 ◽  
Vol 272 (1) ◽  
pp. E126-E132 ◽  
Author(s):  
N. F. Rossi ◽  
D. S. O'Leary ◽  
H. Chen
Keyword(s):  
Arterial Pressure ◽  
Peak Plasma ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Fold Increase ◽  
Systemic Arterial Pressure ◽  
Sympathetic Outflow ◽  
Central Administration ◽  
Eta Receptor ◽  
The Central Nervous System

Endothelins (ET) within the central nervous system (CNS) alter systemic cardiovascular responses and arginine vasopressin (AVP) secretion. These experiments were designed to ascertain whether the rise in systemic arterial pressure after central administration of ET-1 is mediated by enhancing sympathetic outflow and/or circulating AVP. In Long-Evans (LE/LE) rats, intracerebroventricular injection of 1-10 pmol ET-1 dose dependently increased mean arterial pressure (MAP). Peak response occurred 7-12 min after ET-1 and was inhibited by ETA receptor antagonism. Systemic vasopressin (V1) receptor blockade did not inhibit the pressor response, and rats with central diabetes insipidus (DI/DI) displayed an identical rise in MAP. Ganglionic blockade prevented ET-1-induced hemodynamic effects. Peak plasma AVP levels occurred 60 min after ET-1, as the pressor response began to wane. In sinoaortic-denervated LE/LE rats, ET-1 elicited a 10-fold increase in AVP secretion that coincided with the hemodynamic changes and was blocked by BQ-123. Thus ET-1 via ETA receptors within the CNS induced a concentration-dependent increase in systemic arterial pressure mediated by enhanced sympathetic outflow but not by circulating AVP. Reflex baroreceptor activation attenuated AVP release.

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