Linda L. Walsh

Zona incerta lesions: Disruption of regulatory water intake

Abstract Bilateral lesions in the anterior aspects of the zona incerta of male rats produced adipsia. When tested under ad lib access to dry laboratory chow and water, only a small, although statistically reliable, decrease in water intake occurred. However, water intake promptly fell to zero when food was removed, suggesting that drinking occurred not in response to physiological signals which regulate water intake, but only as a means of facilitating the ingestion of dry food.

Loss of feeding in response to 2-deoxy-D-glucose but not insulin after zona incerta lesions in the rat

Abstract Bilateral lesions in the anterior aspects of the zona incerta of male rats reliably reduced the feeding response to systemically administered 2-deoxy-D-glucose. Insulin-induced feeding remained intact. Zona incerta lesions may interrupt central vagal projections important for the feeding response to cellular glucoprivation.

Zona incerta lesions impair osmotic but not hypovolemic thirst

Abstract Male albino rats with bilateral lesions of the anterior zona incerta are hypodipsic when dry food is available and show little or no regulatory drinking when food deprived. They do, however, drink normal quantities of water in response to subcutaneous injections of polyethylene glycol that produce extracellular hypovolemia. In contrast, they show a markedly reduced response to intracellular dehydration produced by intraperitoneal injections of hypertonic saline. The osmotic thirst deficit is not due to an increased latency of response to the injections.

Electrolytic lesions and knife cuts in the region of the zona incerta impair sodium appetite.

Abstract Bilateral lesions in the anterior zona incerta of male rats produced reliable impairments of need-related sodium appetite which were more severe than those seen after bilateral lesions in the thalamic gustatory nucleus. Horizontal knife cuts dorsal to the zona incerta, separating it from the ventral thalamus, seemed to reproduce the effects of thalamic lesions on sodium appetite. Horizontal knife cuts ventral to the zona incerta, separating it from the hypothalamus, produced a greater reduction in sodium intake than did the dorsal knife cuts. Neural pathways that might mediate regulatory sodium intake were discussed.

Dissociation of responses to extracellular thirst stimuli following zona incerta lesions

In male albino rats, bilateral lesions in the anterior zona incerta which decrease ad lib and food-deprivation water intake and osmotic thirst but leave hypovolemic thirst intact, severely impaired or abolished drinking in response to systemic injections of isoproterenol or central administration of angiotensin II. Water intake following water deprivation was reduced by one-fourth. Reasons for the dissociation of responses to hypovolemia, water deprivation, isoproterenol and angiotensin were suggested.

Some biochemical effects of zona incerta lesions that interfere with the regulation of water intake

The concentration of NE, DA and 5-HT in forebrain, striatum, and hypothalamus was measured after zona incerta (ZI) lesions that have been shown to result in general hypodipsia; adipsia during periods of food deprivation; impaired or abolished drinking in response to osmotic challenges (but not polyethylene glycol); impaired drinking after systemic isoproterenol or central angiotensin; and impaired or abolished feeding in response to 2-deoxy-D-glucose. The lesions produced a significant (40-50%) depletion of forebrain NE but a correlational analysis of the behavioral and biochemical effects of the lesions failed to indicate a causal relationship. The lesions did not reliably affect (a) forebrain DA or 5-HT; (b) striatal DA or 5-HT; (c) hypothalamic DA, NE or 5-HT. The results of these experiments indicate that significant impairments in ingestive behavior can be demonstrated in animals with diencephalic lesions that do not result in striatal (or forebrain) DA depletions. This confirms previous behavioral analyses showing that ZI lesions which interfere with ingestive behavior do not produce the debilitating sensory or motor dysfunctions typical of the rat with lateral hypothalamic lesions.