Date of Award:


Document Type:


Degree Name:

Doctor of Philosophy (PhD)




Heber Sharp


Because of inconsistencies in the research literature following Grossman's (1960) demonstration that drinking behavior (thirst) could be modulated by intrahypothalamic injections of adrenergic and cholinergic chemicals, a series of studies were undertaken to clarify the relation between introducing chemicals into the brain and drinking behaviors.

The first study attempted to determine the effect of water deprivation on post-deprivation drink sequencing. It has been demonstrated that 75% - 90% of the water consumed by normal rats is taken during the evening hours (Fitzsimmons, 1957; Stellar & Hill, 1952). Grossman's (1960; 1962a) studies failed to consider normal drinking rhythms and consequently modulated increased or decreased drinking around baseline levels that were well below volumes consumed following water deprivation or during peak nocturnal drinking periods. Because subsequent studies were planned using water deprivation as a "booster stimulus" to increase total output of drinking it was thought important to determine the effects of deprivation on "normal drinking."

The results of Experiment I indicate that with the exception of the increased consumption levels of Ss which had been deprived of water, the circadian patterns of drinking did not differ from normal, nondeprived Ss.

Experiment II considered Crow's (1964) suggestion that implantation procedures might physically alter the organism and these effects might overshadow future manipulations such as chemical injections. This experiment compared the volumes of water consumed by cannula implanted rats with normal nonimplanted Ss. All Ss were maintained on a 23 hour water deprivation schedule for the duration of the experiment./p>

Although the implanted Ss did not differ significantly from the controls, all Ss showed systematic variations in drinking that had a phase of approximately four days. The differences in high volume intake days and low volume intake days were significantly different from each other. There was no apparent systematic relation with changes in climate, and it was hypothesized that the rhythmicity might be endogeneous.

Experiment III, the first experiment of the series using chemical intervention in the drinking cycle, was a systematic replication of Grossman's (1960; 1962) original studies. Four implanted rats from Experiment II, following a period of twenty-four hour water deprivation, were injected daily over a period of 25 day s with a placebo, cholinergic or adrenergic chemical on a random basis. Following chemical injection the Ss were given access to water for one hour.

Under the conditions of this experiment it was found that all chemicals had a slight depressive effect on consumption levels over baseline and placebo levels. The depressive effects of the adrenergic chemicals was significantly greater (p < .05) than the placebo or cholinergic chemicals.

The sequence of drug injection was analyzed to determine if the differences were due to residual effects of previous injections. With the exception of methacholine no residual effects were obtained.

A fourth experiment replicated Experiment III except in requiring the S to obtain their daily water rations by drinking from a drinkometer on a Mult. FR 50; FI 2 min. schedule of reinforcement. The results indicate that prior to chemical intervention the implanted animals responded significantly slower than the non-implanted controls in both the FR and FI components (p < .001). As in Experiment III a11 chemicals produced drinking rates lower than those for the placebo condition. However, in this experiment the differences between cholinergic and adrenergic chemicals were not significant.

These data and data from other laboratories (Fisher & Coury, 1962; Valenstein, e t. al., 1970) indicate that Grossman's chemical specificity of drives hypothesis needs to be modified to include the data on psychogenic drinking, rhythmicity of drinking, additivity of thirst stimuli and the effects of behavioral prepotency.

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