Changes in self-stimulation at stimulation-bound eating and drinking sites in the lateral hypothalamus during food or water deprivation, glucoprivation, and intracellular or extracellular dehydration.

Abstract

These studies were designed to examine the effects of "hunger" induced by food deprivation, 2deoxy-D-glucose (200 mg/kg), or insulin (2 U/kg) and "thirst" induced by water deprivation, sodium chloride (4 M), or polyethylene glycol (5 ml of 30% w/w) on lateral hypothalamic selfstimulation in 40 male Long-Evans rats. Changes in self-stimulation were evaluated at electrodes that produced stimulation-bound eating and/or drinking or neither behavior. Daily 30-min test sessions consisted of three 5-min periods of self-stimulation alternated with three 5-min periods when bar presses resulted in a 5-s time-out from experimenter-delivered stimulation (stimulation escape). Food deprivation significantly increased self-stimulation; insulin, 2-deoxy-r>-glucose, and sodium chloride significantly suppressed self-stimulation; water deprivation mildly inhibited selfstimulation; and polyethylene glycol had no effect. This pattern of findings was noted at electrodes that did and those that did not elicit eating and/or drinking. These findings argue against the hypothesis that the magnitude of lateral hypothalamic self-stimulation is differentially and predictably controlled by specific drive mechanisms indexed by the consummatory behaviors also elicited bv the stimulation.Many models of brain stimulation reinforcement have proposed that the reinforcing effect of lateral hypothalamic stimulation is directly related to the activation of neuronal circuits that mediate, at least in part, natural eating or drinking behavior (Hoebel, 1976;J. Olds, 1977;Rolls, 1975). These models are consistent with the following observations: (a) Many procedures that decrease food intake also decrease the rate of self-stimulation at lateral hypothalamic sites (

Prefrontal cortex self-stimulation and energy balance.

“…A final point worth noting from the present data concerns the claims of some investigators (e.g., Blundell & Herberg, 1962;Goldstein, Hill, & Templer, 1970) that the facilitation of LH self-stimulation by food deprivation occurs only at sites that produce stimulation-bound eating. Other investigators have failed to find such a relation (e.g., Atrens et al, 1982;Frutiger, 1986). To test this hypothesis with respect to SPC self-stimulation, a Pearson correlation coefficient was computed between the amount of induced eating (grams) in each rat in Experiment 1 and the (%) increase in response rate seen after 48 hr of food deprivation.…”

“…This first experiment also demonstrates that the eating induced by SPC stimulation is not simply an oral stereotypy because block gnawing was not induced by SPC self-stimulation. This distinguishes the effects of SPC stimulation from those of hypothalamic stimulation, for which gnawing as well as eating are often seen (e.g., Frutiger, 1986). The feeding seen with SPC stimulation also differs from that seen with stimulation of the lateral hypothalamus (LH) because eating from the latter site is stimulus-bound, that is, locked to the presence of stimulation.…”

“…This point has been illustrated with reference to LH self-stimulation. It has been repeatedly shown that LH self-stimulation is facilitated by food deprivation (Atrens, Williams, Brady, & Hunt, 1982; Carey et al, 1975; Frutiger, 1986; Margules & Olds, 1962; Olds, 1958). However, when self-stimulation testing occurs under a fixed-interval schedule of reinforcement, only longer periods (48 hr) of food deprivation facilitate LH self-stimulation (Atrens et al, 1982).…”

“…This reasoning has been applied to various studies of LH self-stimulation in which the effects of hunger on self-stimulation have been compared with those of the glucoprivic substances insulin and 2-DG. Such studies have produced contradictory results (e.g., Balagura & Hoebel, 1967; Frutiger, 1986; Hernandez & Briese, 1971; Hoebel, 1979; Russek, 1979). This may be due to the different doses of drugs used across studies in addition to the widely different self-stimulation methodologies used.…”

“Jello® Shots” and Cocktails as Ethanol Vehicles: Parametric Studies with High- and Low-Saccharin-Consuming Rats

“…To be sure, no bright line separates eating from drinking, especially in omnivores such as rats and humans: Foods can be drunk (blood, milk, other liquid diets) and water can be eaten (in prey, fruit, ice), and diverse consummatory behaviors share some associative learning and motivational mechanisms [44,45,46,47]. Nonetheless, eating and drinking are different behaviors that have been shaped by selective pressures related predominantly to, respectively, nutrients and hydration, and they have dissociable motoric, motivational, and neural mechanisms [48,49,50]. For instance, mammals’ need for water is less elastic than is the need for calories and, given the greater range of edibles in most environments relative to liquids, pressure to choose well among foods likely has been greater than choosing among fluids, especially for omnivores [51].…”