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Biomedical subjects

B Kolb

Publications and source records attributed to B Kolb.

At least 145 records · Page 8Linked to original sources
PubMed1978

Sparing of function in rats with early prefrontal cortex lesions.

Previous work has shown that medial frontal lesions in adult rats produce deficits on spatial reversals, delayed responses, and active avoidance, whereas more ventrolateral (orbital) lesions have little effect on these tasks. These findings were confirmed. However, when lesions were made at 2, 5 or 9 days of age, rats tested as adults showed dramatic sparing of function on all these tasks, whereas similar lesions inflicted at 35 or 40 days of age produced deficits on delayed responses and spatial reversals. Orbital frontal lesions failed to significantly alter behavior on any task at any age. The effects of the neonatal lesions are in striking contrast to the effects of juvenile or adult lesions, even though the infant lesions were considerably larger. Histological analysis revealed no retrograde degeneration in the dorsomedial thalamic nucleus of the rats operated in infancy unless the lesions were so large that the adjacent caudate-putamen was also damaged. The contrast between these results, and results obtained after similar lesions in adults may indicate the growth of sustaining collaterals after the infant lesions which might be involved in the observed behavioral sparing.

Age Factors↗
PubMed1978

Behavior of the rat after removal of the neocortex and hippocampal formation.

After surgical removal of the neocortex and hippocampal formation, rats retained most of the movement patterns of locomotion, climbing, grooming, feeding, and fighting. However, forepaw immobility during swimming was abolished. Feeding behavior was suppressed temporarily but recovered partially. The distinctive postures of sleep and walking and a circadian rhythm of motor activity were retained. However, behaviors were often not performed at the appropriate time and place. The normal sequence of grooming behavior was disrupted; food hoarding and social behavior were essentially abolished. Removal of the neocortex alone had much the same effect as removal of neocortex and hippocampus together. Removal of hippocampus alone produced only a mild disruption of behavior. It is suggested that ascending nonspecific projections to the cerebral cortex play an important role in the moment-to-moment control of behavior but are not essential for the sleep-waking cycle.

Aggression↗
PubMed1977

Aphagia, behavior sequencing and body weight set point following orbital frontal lesions in rats.

Discrete lesions were made in the orbital frontal neocortex of rats and eating, drinking, sensorimotor responsiveness, and sequencing of motor acts were studied. Duration of aphagia was related to palatability/texture of food. Rats were aphagic for a mean of two days to palatable cookie mash presented on a spatula, six days to a high fat diet mash presented in a 4 cm high dish and for seven days to dry laboratory food. Water drinking was resumed with injestion of dry food. Rats presurgically fattened to 120% of body weight appeared stuporous and akinetic for 2-3 postoperative days, and the period for acceptance of food in tall tests was protracted. Rats presurgically dieted to 80% of normal body weight did not show accelerated recovery of feeding. Preoperatively normal, fattened and dieted rats assumed a chronic postoperative body weight level 25% lower than control rats. Rats with lesions showed sensorimotor neglect when tested on an open table top, but did not show neglect when tested in their home cages. In grooming tests, rats with lesions showed all of the components of normal grooming, but failed to exhibit the long chains of grooming characteristics of control rats. They also showed attenuated tongue extension and had difficulty manipulating food with the forepaws. The experiments suggest that following orbital frontal lesions, motor impairments, motor sequencing dysfunctions, change in body weight set point, and depending upon the test situation, sensorimotor neglect, may all be contributing factors to aphagia. The orbital frontal cortex may influence feeding and other behaviors via descending neural projections to the hypothalamus and branistem.

Animals↗
PubMed1976

Functional development of prefrontal cortex in rats continues into adolescence.

Bilateral removal of the sulcal prefrontal cortex in rats at 60 days of age and older results in aphagia and adipsia, but removal of this area before 60 days of age does not affect food or water regulation. Apparently the development of the role of this neocortical region in feeding and drinking continues well beyond the time of weaning in the rat.

Age Factors↗
PubMed1975

Prefrontal cortex and the regulation of food intake in the rat.

The postoperative regulation of food and water intake was studied in rats with aspiration lesions to either the medial frontal or orbital frontal projection fields of thalamic nucleus medialis dorsalis (prefrontal cortex). These projection fields proved functionally dissociable in that orbital frontal lesions impaired immediate postoperative regulation of food and water intake for up to 2 wk., while medial frontal lesions produced finickiness. Neither lesion affected response to cellular dehydration or recovery from extended deprivation. These data are consistent with data from rhesus monkeys with prefrontal lesions and differ from animals with lateral hypothalamic lesions.

Animals↗