Publication Date


Document Type


First Advisor

Lints, Carlton E.

Degree Name

M.A. (Master of Arts)


Department of Psychology




Many studies have shown that electrical stimulation of similar anatomical loci in the lateral hypothalamus may elicit such behaviors as eating, drinking, and gnawing (Margules & Olds, 1962; Mendelson & Chorover, 1965; Mogenson & Stevenson, 1967; and Roberts & Carey, 1965). These behaviors are labeled "stimulus bound" in that a completely satiated animal will exhibit them only during periods of intracranial stimulation (ICS). Implicit in these studies is the idea that the hypothalamus contains some type of neural circuits for eating and drinking. Chemical stimulation (Grossman, 1960) of identical loci in the lateral hypothalamus of the rat has revealed the existence of a chemical specificity for eating and drinking. Grossman thus proposed that eating was mediated by adrenergic synapses and drinking by cholinergic synapses. The idea of the existence of fixed and specific neural circuits subserving eating and drinking has recently been challenged by evidence showing that for electrical ICS additional types of "stimulus bound" behaviors may be elicited by stimulation delivered through the same electrode (Valenstein, Cox & Kakolewski, 1968). These researchers found that animals which typically exhibited only one type of "stimulus bound" behavior, for example eating, could be made to elicit an additional "stimulus bound" behavior, for example gnawing or drinking, by placing the animal on an overnight schedule of stimulation in the presence of only the nondominant goal object (a wooden block or water). Valenstein et al. interpreted this modifiability of "stimulus bound" behaviors as indicating that the neural circuits subserving eating and drinking were not fixed and specific as previously supposed. The problem investigated by the present study dealt with the modification of "stimulus bound" behaviors elicited by chemical rather than electrical ICS. Double cannulae apparatus, Which allowed repeated stimulation of subcortical structures, were implanted in the lateral hypothalamus of female hooded rats. Stimulation with norepinephrine caused no significant effect on either food or water consumption. Carbachol stimulation at the same location, however, did elicit significant increases in water consumption. In the second phase of this study stimulations with norepinephrine were discontinued, and carbachol stimulations were given sequentially in the presence of both dominant (water) and nondominant (food) goal objects. This paradigm of stimulation was scheduled to be analogous to that used by Valenstein et al. for electrical stimulation. An analysis of variance revealed that food consumption increased as a result of the repeated stimulations with carbachol. Water consumption was also significant but remained constant throughout the experiment. The type of goal object present during the carbachol stimulations had no significant effect on either food or water consumption. To account for both the results of the present study and the contradictory results of Grossman (I960), a two-stage model of the neural anatomical substrate for eating and drinking was proposed. The first stage of this model is concerned with the general activation of the organism, which is mediated by cholinergic (nicotinic) synapses in one hypothalamic location. The second stage of the model is concerned with the specific consummatory behaviors, with drinking mediated by cholinergic (muscarinic) synapses and eating by adrenergic synapses. It is pointed out that further research is necessary before any of the theoretical proposals presented in this study can be verified.


Includes bibliographical references.||Includes illustrations.


vii, 55 pages




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