David Quartermain

Food motivated behavior in genetically obese and hypothalamic-hyperphagic rats and mice☆

Abstract The food-associated behavior of genetically obese Zucker rats, fa/fa and yellow obese mice, aAy, was studied using classic operant procedures. When obese Zucker rats and yellow mice are compared to their lean littermates and lean littermates made obese by electrolytic lesions and chemical lesions, respectively, the naturally obese animals do not display the behavioral patterns associated with rodents made obese by hypothalamic damage. These experiments point out the necessity for careful selection of animal models in studying behaviors associated with regulatory disturbances of normal food intake.

Amnesic effects of cycloheximide on two strains of mice with different memory characteristics.

Abstract The amnesic effects of the protein synthesis inhibitor cycloheximide were studied in two strains of mice ( C57BL 6J ; DBA 2J ) which have opposite temporal gradients of retention for single trial passive avoidance learning. Mice were given a single trial in a passive avoidance apparatus 30 min after a saline or a cycloheximide injection and tested for retention at seven intervals from 1 min to 72 hr following. Saline-injected C57BL 6J mice showed poor initial retention followed by progressive improvement which was sustained for 72 hr. In contrast, saline-injected DBA 2J mice showed good retention shortly after training followed by absence of retention 6 hr after training. A 3-mg dose of cycloheximide produced significant amnesia in both strains but the memory impairment was greater in the C57BL 6J strain when tested at 5 min. Increased early amnesia occurred when DBA 2J mice were given 5 mg of cycloheximide even though this dose did not significantly increase degree of protein synthesis inhibition. These results indicate that cyclohexamide can disrupt short-term as well as long-term memory and, in addition, raise the question whether the amnesic effect is due exclusively to inhibition of protein synthesis.

Motivational depression associated with norepinephrine-induced eating from the hypothalamus: Resemblance to the ventromedial hyperphagic syndrome ☆

Abstract Rats with lateral hypothalamic cannulae were injected with norepinephrine and tested when both hungry and satiated on appetitive tasks of varying difficulty. On a simple consummatory test norepinephrine produced more eating than saline at both 0 and 24 hr of deprivation, and performance at 24 hr was more potentiated than that at 0 hr. On a continuously reinforced lever-pressing task, norepinephrine potentiated pressing only at 0-hr deprivation. When pressing was reinforced on a 30-sec variable interval schedule, norepinephrine potentiated pressing at 0 hr of deprivation, but after 24 hr of deprivation norepinephrine-injected rats pressed significantly less than saline-injected controls. These data suggest that norepinephrine produced a motivational depression in a rats willingness to work for food which is similar to that seen following ventromedial lesions of the hypothalamus.

Effect of electroconvulsive shock duration on the gradient of retrograde amnesia

Abstract Rats trained in a one trial passive avoidance task received a single 100 mA electroconvulsive shock (ECS) of either 200 msec or 800 msec duration at various intervals following footshock. The resultant amnesic gradient was not significantly altered by the four-fold increase in ECS duration. The results confirm earlier findings that (a) the ECS susceptible phase of memory fixation lasts but a few sec and (b) the maximal effective punishment-ECS interval to produce retrograde amnesia cannot be extended by increasing the intensity of ECS. The data support a previous conclusion that the different amnesic gradients produced by ECS and carbon dioxide gas, in the same learning situation, probably reflect effects on different phases of short term memory fixation.

Extinction Following Intracranial Reward: The Effect of Delay between Acquisition and Extinction

Rats trained to press a bar for intracranial reinforcement gave as many responses during extinction as did water-reinforced controls, when extinction came immediately after an acquisition session. However, the experimental animals gave fewer responses in extinction than water-reinforced animals when extinction was delayed for 1 hour after acquisition. The activity level of the experimental animals was high immediately after acquisition but declined markedly over the delay period, which suggests that resistance to extinction after intracranial reinforcement is primarily a function of activity level.

Relation between medial hypothalamic damage and impairments in regulation of sodium intake

Abstract Lesions of various sizes were placed in the medial hypothalamus of rats to determine the extent and locus of damage sufficient to produce impairments of sodium appetite. Lesions confined to the ventromedial nucleus had no effect on sodium intake after sodium depletion but larger lesions which included the major extent of the medial hypothalamic zone resulted in significant decrements.

Drive properties of mineralocorticoid-induced sodium appetite

Abstract The strength of the sodium drive of desoxycorticosterone-treated rats was compared with that of adrenalectomized (sodium deficient) rats by bar pressing and “quinine tolerance” tests. When rats of the 2 groups were matched for amount of NaCl solution ingested during daily drinking sessions, they bar pressed for NaCl reinforcement at approximately equal rates and manifested the same resistance to extinction of the bar pressing response. Saline intake of desoxycorticosterone-treated rats was not as greatly suppressed by adulteration with quinine as was that of adrenalectomized rats. This difference was probably not due to a difference in drive but to a general intolerance of adrenalectomized rats for aversive tasting substances.

Prevention of ECS-induced amnesia by reestablishing continuity with the training situation

Abstract Retrograde amnesia for a passive avoidance task was produced in rats by electroconvulsive shock (ECS). However, if rats were left to recover for 15 min in the training apparatus after receiving a foot shock-ECS combination, they showed no sign of amnesia at testing 24-hr later. ECS alone without training had no effect on the step-out latencies. Amnesia did occur when the place of training was different from the place of recovery. The results suggest that a core memory survives ECS treatment and that this surviving trace is retrievable at the retest trial if continuity with the preceding experimental events is established upon recovery from the black-out produced by ECS.