Alterations of conditioned taste aversion after microiontophoretically applied neurotoxins in the medial prefrontal cortex of the rat.
The prefrontal cortex (PFC) has been reported to be essential in neural control of feeding. In the present study, we aimed to provide a complex characterization of behavioral consequences of PFC microlesions in CFY rats. Kainic acid (KA) was microiontophoretically applied into the mediodorsal division of PFC to damage intrinsic neurons, whereas in another group of rats, 6-hydroxydopamine (6-OHDA) was microiontophoretized into the same region to destroy catecholaminergic (CA) projection fiber terminals. Body weights, food and fluid intake of both lesioned and (sham-operated or intact) control animals were daily measured. Effects of intracellular dehydration and water deprivation were also studied. Open field activity, stereotyped behaviors, and orientation towards visual and somesthetic stimuli were pre- and postoperatively tested. To examine hypothesized consequences of mPFC microlesions on central taste information processing, the acquisition and retention of saccharine conditioned taste aversion (CTA) were studied. No major changes were recorded in body weights, food and water consumption. Dehydration or deprivation similarly increased water intake in all animals. Scores of open field activity and stereotyped behaviors in the 6-OHDA group were significantly higher than those of the other groups. As the main findings of the present studies, both KA and 6-OHDA lesioned rats displayed significant deficits in CTA acquisition and retention tests. These results suggest that the medial PFC has a substantial role in both the formation and the retrieval of CTA. Furthermore, the present findings also indicate the general significance of prefrontal CA mechanisms in the organization of goal-directed, adaptive behaviors.
Hernádi
I
I
Neurobiology and Comparative Physiology Group, Department of General Zoology and Neurobiology, Faculty of Natural Sciences, Janus Pannonius University, Pécs, Hungary.
Karádi
Z
Z
Vígh
J
J
Petykó
Z
Z
Egyed
R
R
Berta
B
B
Lénárd
L
L
D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects* / Q000502:physiology; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D003213:Conditioning, Psychological / Q000187:drug effects* / Q000502:physiology; D004326:Drinking / Q000187:drug effects / Q000502:physiology; D004435:Eating / Q000187:drug effects / Q000502:physiology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D007478:Iontophoresis; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D009498:Neurotoxins / Q000494:pharmacology*; D016627:Oxidopamine / Q000494:pharmacology; D017397:Prefrontal Cortex / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D011597:Psychomotor Performance / Q000187:drug effects / Q000502:physiology; D051381:Rats; D012462:Saline Solution, Hypertonic / Q000494:pharmacology; D013565:Sympatholytics / Q000494:pharmacology; D013649:Taste / Q000187:drug effects* / Q000502:physiology
D018690:Excitatory Amino Acid Agonists; D009498:Neurotoxins; D012462:Saline Solution, Hypertonic; D013565:Sympatholytics; D016627:Oxidopamine; D007608:Kainic Acid