Acute effect of intracerebroventricular administration of lead on the drinking behavior of rats induced by dehydration or central cholinergic and angiotensinergic stimulation

Stereotaxic lesions were placed in several parasagittal planes of the lateral hypothalamus of rats at the level of the ventromedial nuclei. Both far- and mid-laterally lesioned animals developed adipsia and aphagia, with the far-lateral syndrome being more drastic in nature. The qualitatively different nature of the "failures" seen between the two groups correlated well with the additional damage to the pallidofugal fiber systems in the far-lateral lesioned group. Bilateral lesions directed to the origins of the pallidofugal fibers reproduced faithfully the far-lateral hypothalamic syndrome, histological studies in these animals revealing degeneration along the pallidofugal trajectories. It appears that the feeding and/or drinking "centers" are only convergence sites for critical fiber systems which are disjoined by far-lateral hypothalamic lesions. Thus, the medial part of the "feeding center" seems to be primarily a "motivational" system, whereas the lateral "feeding" system is more basic and depends essentially on pallidofugal circuitry. When this latter is disjoined, the failure is more than "motivational," since it is not compensated for by merely delivering food and water to the gastrointestinal tract.

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Arterial baroreceptors mediate the inhibitory effect of acute increases in arterial blood pressure on thirst

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00651.2001 ◽

2002 ◽

Vol 282 (6) ◽

pp. R1718-R1729 ◽

Cited By ~ 23

Author(s):

Sean D. Stocker ◽

Edward M. Stricker ◽

Alan F. Sved

Keyword(s):

Blood Pressure ◽

Arterial Blood Pressure ◽

Drinking Behavior ◽

Plasma Osmolality ◽

Inhibitory Effect ◽

Ang Ii ◽

Arterial Blood ◽

Acute Increase ◽

Behavior Of Rats ◽

Arterial Baroreceptor

The present study sought to determine whether arterial baroreceptor afferents mediate the inhibitory effect of an acute increase in arterial blood pressure (AP) on thirst stimulated by systemically administered ANG II or by hyperosmolality. Approximately 2 wk after sinoaortic denervation, one of four doses of ANG II (10, 40, 100, or 250 ng · kg−1 · min−1) was infused intravenously in control and complete sinoaortic-denervated (SAD) rats. Complete SAD rats ingested more water than control rats when infused with 40, 100, or 250 ng · kg−1 · min−1 ANG II. Furthermore, complete SAD rats displayed significantly shorter latencies to drink compared with control rats. In a separate group of rats, drinking behavior was stimulated by increases in plasma osmolality, and mean AP was raised by an infusion of phenylephrine (PE). The infusion of PE significantly reduced water intake and lengthened the latencies to drink in control rats but not in complete SAD rats. In all experiments, drinking behavior of rats that were subjected to sinoaortic denervation surgery but had residual baroreceptor reflex function (partial SAD rats) was similar to that of control rats. Thus it appears that arterial baroreceptor afferents mediate the inhibitory effect of an acute increase in AP on thirst stimulated by ANG II or hyperosmolality.

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Impaired drinking responses of rats with lesions of nucleus medianus: circadian dependence

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1985.248.2.r224 ◽

1985 ◽

Vol 248 (2) ◽

pp. R224-R230 ◽

Cited By ~ 4

Author(s):

T. W. Gardiner ◽

E. M. Stricker

Keyword(s):

Systemic Treatment ◽

Drinking Behavior ◽

Organ Support ◽

Sensory Receptors ◽

Stimulant Drug ◽

Electrolytic Lesions ◽

Ventral Nucleus ◽

Glycol Solution ◽

The Brain ◽

Behavior Of Rats

The drinking behavior of rats with electrolytic lesions of ventral nucleus medianus (vNM) was examined during acute hyperosmolality and hypovolemia. The brain-damaged animals were impaired in their drinking responses to systemic treatment with hypertonic saline or polyethylene glycol solution when they were tested during the day. However, apparently normal drinking responses to both dipsogenic challenges were observed when the same animals were pretreated with the stimulant drug, caffeine, or when they were tested at night. These results suggest that lesions of vNM may produce complex alterations in the control of drinking behavior rather than the destruction of sensory receptors. The lesions appear to disrupt both circadian influences on drinking and activational components of drinking that normally serve to facilitate the behavioral response. The present results, together with similar findings for rats given lesions of the subfornical organ, support recent proposals that periventricular tissue bordering the rostral wall of the third cerebral ventricle plays an important role in the central control of drinking.

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