title: Insular cortex lesions impair the acquisition of conditioned immunosuppression.
abstract: Conditioned immunosuppression can be readily obtained in animals by associating a taste with an immunosuppressive drug. On subsequent exposure to the conditioned taste, the animals show an attenuated immune response and also exhibit a conditioned taste aversion. It has been established that insular cortex lesions disrupt the acquisition of conditioned taste aversion. The effect of NMDA-induced lesions in either the insular cortex or the parietal cortex of male Wistar rats was evaluated in the acquisition of conditioned immunosuppression in two experiments. Unlesioned control rats showed the conditioned immunosuppressive response after reexposure to the taste, as indicated by lower hemagglutinating titers to sheep red blood cells in the first experiment and by a decreased IgM production to ovalbumin, measured by ELISA, in the second experiment. Insular cortex-lesioned rats did not show the conditioned immunosuppression in either experiment, while parietal cortex lesions and the sham-lesioned animals presented a clear decrease of hemagglutinating titer and a low IgM production. The insular cortex lesions did not affect the normal immune response, showing normal hemagglutinating titers and IgM production when compared to nonconditioned controls. The immunosuppressive action of cyclophosphamide also remained unaltered. In conclusion, these results show that the insular cortex is essential for the acquisition of conditioned immunosuppression.
authors.affiliation: Departamento de Neurociencias, Universidad Nacional Autónoma de México, México, D.F., 04510, México.
authors.forename: V
authors.initials: V
authors.lastname: Ramírez-Amaya
authors.forename: B
authors.initials: B
authors.lastname: Alvarez-Borda
authors.forename: C E
authors.initials: CE
authors.lastname: Ormsby
authors.forename: R D
authors.initials: RD
authors.lastname: Martínez
authors.forename: R
authors.initials: R
authors.lastname: Pérez-Montfort
authors.forename: F
authors.initials: F
authors.lastname: Bermúdez-Rattoni
mesh_terms: D000818:Animals; D001362:Avoidance Learning / Q000502:physiology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000502:physiology*; D003216:Conditioning, Operant / Q000502:physiology*; D003520:Cyclophosphamide / Q000494:pharmacology*; D006388:Hemagglutinins / Q000096:biosynthesis; D007114:Immunization; D007075:Immunoglobulin M / Q000096:biosynthesis; D007165:Immunosuppression Therapy; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D008297:Male; D016202:N-Methylaspartate / Q000633:toxicity*; D015213:Neuroimmunomodulation / Q000502:physiology*; D009498:Neurotoxins / Q000633:toxicity*; D010047:Ovalbumin / Q000276:immunology; D010296:Parietal Lobe / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000502:physiology; D012439:Saccharin / Q000494:pharmacology*; D012756:Sheep / Q000097:blood; D013649:Taste
chemical_list: D006388:Hemagglutinins; D007075:Immunoglobulin M; D007166:Immunosuppressive Agents; D009498:Neurotoxins; D016194:Receptors, N-Methyl-D-Aspartate; D016202:N-Methylaspartate; D003520:Cyclophosphamide; D010047:Ovalbumin; D012439:Saccharin