Establishment and Control of a Bar-Pressing Habit by Means of Fixed Interval ICSS Reinforcement

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.

1965 ◽  
Vol 16 (3_suppl) ◽  
pp. 1277-1290 ◽  
Author(s):  
Daniel R. Snyder ◽  
Robert L. Isaacson

Ten rats with large bilateral hippocampectomies, 10 rats with smaller amounts of damage of the dorsal hippocampus, 10 rats with destruction of postero-lateral neocortex, and 15 normal animals were trained in two types of passive-avoidance situations. One passive-avoidance task required inhibition of drinking while thirsty, the other required an animal to refrain from entering a small compartment after i: had been trained to enter, while hungry, for a food reward. Animals with the largest amounts of hippocampal destruction were impaired in both types of problems. Animals with smaller degrees of hippocampal damage were not different from normal animals in their ability to inhibit licking but were impaired in the other task. Animals with neocortical destruction showed impairment only in the licking situation.


2020 ◽  
Vol 71 (1) ◽  
pp. 139-164 ◽  
Author(s):  
Ivan E. de Araujo ◽  
Mark Schatzker ◽  
Dana M. Small

The conscious perception of the hedonic sensory properties of caloric foods is commonly believed to guide our dietary choices. Current and traditional models implicate the consciously perceived hedonic qualities of food as driving overeating, whereas subliminal signals arising from the gut would curb our uncontrolled desire for calories. Here we review recent animal and human studies that support a markedly different model for food reward. These findings reveal in particular the existence of subcortical body-to-brain neural pathways linking gastrointestinal nutrient sensors to the brain's reward regions. Unexpectedly, consciously perceptible hedonic qualities appear to play a less relevant, and mostly transient, role in food reinforcement. In this model, gut-brain reward pathways bypass cranial taste and aroma sensory receptors and the cortical networks that give rise to flavor perception. They instead reinforce behaviors independently of the cognitive processes that support overt insights into the nature of our dietary decisions.


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.


1975 ◽  
Vol 37 (1-3) ◽  
pp. 249-255
Author(s):  
T. Sakamoto ◽  
R. Kwak ◽  
Y. Okudaira ◽  
J. Suzuki

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