Effects of Bilateral Septal Lesions on Lever Pressing for Food Reward in the Rabbit

1975 ◽  
Vol 37 (1-3) ◽  
pp. 249-255
Author(s):  
T. Sakamoto ◽  
R. Kwak ◽  
Y. Okudaira ◽  
J. Suzuki
1979 ◽  
Vol 31 (4) ◽  
pp. 675-690 ◽  
Author(s):  
J. Feldon ◽  
J. A. Gray

Rats sustained electrolytic lesions either in the medial septal (MS) area (of a kind known to eliminate the hippocampal theta rhythm) or in the dorso-lateral septal (LS) area (of a kind known to spare theta) and were compared to sham-operated controls in three experiments in the straight alley with food reward on continuous (CRF) or partial (PRF) reinforcement and inter-trial intervals of 3-8 min. With 6 acquisition trials MS lesions increased resistance to extinction and enhanced the partial reinforcement extinction effect (PREE). With 48 acquisition trials MS lesions did not alter resistance to extinction after either CRF or PRF training, but LS lesions abolished the PREE by increasing resistance to extinction in rats trained with CRF and decreasing it in rats trained with PRF. With 96 acquisition trials LS lesions were without effect on resistance to extinction after either CRF or PRF training, as previously reported by Henke (1974) using total septal lesions. Thus the impairment in the PREE previously shown after large septal lesions is due to damage to the lateral, not the medial, septal area.


1983 ◽  
Vol 35 (1b) ◽  
pp. 53-65 ◽  
Author(s):  
Roger M. Tarpy ◽  
Stephen E. G. Lea ◽  
Marie Midgley

Rats pressed levers for food reward which was delivered, when appropriate, 0·4 s after the response. For one group, the delay interval was filled by a light cue; for the other group, the same number of lights was given but they were not correlated with food delivery. In Experiment I, all lever presses were reinforced and there were no differences in response rate between groups. In Experiments II and III, lever pressing was rewarded according to a VI and VR schedule respectively. Group differences were observed in Experiment II but they disappeared in Experiment III. The results of Experiments I and II show that a reward-related stimulus does not overshadow a lever response unless the stimulus is a better predictor of reward. Differences in salience or competition from sign-tracking behaviors were ruled out as causes of this phenomenon. Experiment III demonstrated, however, that a weak response-reward correlation is not a sufficient condition for the overshadowing effect. A fourth experiment replicated the results of Experiment III using naive animals. The results of these last two experiments are not consistent with an information theory approach unless (a) a response-units concept is adopted or (b) the cue involved in overshadowing is not the pre-food light but the end of a temporal interval, whose salience is enhanced by the light.


1961 ◽  
Vol 201 (5) ◽  
pp. 838-844 ◽  
Author(s):  
P. J. Morgane

Bipolar stimulating electrodes were implanted in the hypothalamus of rats to study the neural organization of the feeding and satiety "centers." Far-lateral hypothalamic stimulation provoked feeding in satiated animals and "motivated" crossing of electrical barriers to lever-press for food reward on several reinforcement schedules. Midlateral hypothalamic stimulation resulted in feeding in sated animals but never motivated grid crossing to lever-press. Medial forebrain bundle (MFB) lesions or stimulations anterior and posterior to the level of the feeding centers did not alter basic feeding behavior. Following MFB lesions, however, far-lateral hypothalamic stimulation never resulted in animals crossing an electrified grid to lever-press for food reward. Concomitant far-lateral hypothalamic and posterior periventricular stimulation inhibited grid crossing to lever-press, and, instantly suppressed this activity if already in progress. Simultaneous far-lateral hypothalamic and ventromedial (VM) hypothalamic stimulation only provoked basic feeding in sated animals. In animals feeding or lever-pressing in response to far-lateral stimulation, addition of VM stimulation slowed but did not completely suppress either activity. VM stimulation alone never provoked feeding or grid crossing, but "rebound" feeding in the sated state and nonelectrified grid crossing to lever-press resulted when this stimulation was turned off.


1965 ◽  
Vol 17 (2) ◽  
pp. 607-618 ◽  
Author(s):  
S. Thomas Elder ◽  
James G. May ◽  
Merrill M. Rye

13 rats were prepared with chronically indwelling electrodes, the exposed tips of which were in the vicinity of median forebrain bundle. In addition, 7 of these received septal lesions, 2 were inflicted with unilateral hippocampal lesions, and 2 sustained unilateral lesions of the anterior neocortex. The remaining two Ss received no further surgery beyond the electrode implant. All were trained to bar press for brain stimulation at crf, FI 10-sec., FI 20-sec., FI 40-sec., FI 60-sec., FI 90-sec., and FI 120-sec. reinforcement contingencies, respectively. Although the major outcome of the study was that bar pressing could be developed and maintained by FI ICSS in a manner similar to FI food reinforcement, there were several characteristics of the FI ICSS-controlled behavior which distinguished it from bar pressing controlled by FI food reward. (1) Even when an S had been exposed to FI ICSS for as many as 28 hr., it was necessary at the beginning of each daily session to “prime” and “retrain” S. (2) For FI 60 sec. to FI 120 sec. the over-all rate and coarse grain of the cumulative record of the ICSS sustained behavior was less pronounced than that characteristic of food-controlled fixed-interval. (3) The lesions situated in the septum, hippocampus, and cortex did not alter the FI performance to a noticeable extent.


2012 ◽  
Vol 303 (3) ◽  
pp. R259-R269 ◽  
Author(s):  
Joost Overduin ◽  
Dianne P. Figlewicz ◽  
Jennifer Bennett-Jay ◽  
Sepideh Kittleson ◽  
David E. Cummings

Homeostatic eating cannot explain overconsumption of food and pathological weight gain. A more likely factor promoting excessive eating is food reward and its representation in the central nervous system (CNS). The anorectic hormones leptin and insulin reduce food reward and inhibit related CNS reward pathways. Conversely, the orexigenic gastrointestinal hormone ghrelin activates both homeostatic and reward-related neurocircuits. The current studies were conducted to identify in rats the effects of intracerebroventricular ghrelin infusions on two distinct aspects of food reward: hedonic valuation (i.e., “liking”) and the motivation to self-administer (i.e., “wanting”) food. To assess hedonic valuation of liquid food, lick motor patterns were recorded using lickometry. Although ghrelin administration increased energy intake, it did not alter the avidity of licking (initial lick rates or lick-cluster size). Several positive-control conditions ruled out lick-rate ceiling effects. Similarly, when the liquid diet was hedonically devalued with quinine supplementation, ghrelin failed to reverse the quinine-associated reduction of energy intake and avidity of licking. The effects of ghrelin on rats' motivation to eat were assessed using lever pressing to self-administer food in a progressive-ratio paradigm. Ghrelin markedly increased motivation to eat, to levels comparable to or greater than those seen following 24 h of food deprivation. Pretreatment with the dopamine D1 receptor antagonist SCH-23390 eliminated ghrelin-induced increases in lever pressing, without compromising generalized licking motor control, indicating a role for D1 signaling in ghrelin's motivational feeding effects. These results indicate that ghrelin increases the motivation to eat via D1 receptor-dependent mechanisms, without affecting perceived food palatability.


1979 ◽  
Vol 31 (4) ◽  
pp. 653-674 ◽  
Author(s):  
J. Feldon ◽  
J. A. Gray

Rats sustained electrolytic lesions of either the medial septal (MS) area (of a kind known to eliminate the hippocampal theta rhythm) or the dorso-lateral septal (LS) area (of a kind known to spare theta) or both (a “total septal”, TS, lesion). They were compared to sham-operated controls in three experiments in the straight alley with food reward on continuous (CRF) or partial (PRF) reinforcement at one trial a day. MS lesions either left the partial reinforcement extinction effect (PREE) unchanged or enhanced it; LS lesions substantially reduced the PREE. The latter effect was due to a fall in resistance to extinction in PRF animals with no change in CRF animals. MS lesions greatly increased resistance to extinction in both CRF and PRF animals in one experiment but increased resistance to extinction only marginally and only in PRF animals in a second experiment. The TS lesion acted like the LS lesion. These results demonstrate a clear double dissociation between the effects of MS and LS lesions, especially in the PRF condition (LS lesions reduce resistance to extinction, MS lesions increase it).


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