MODULATION OF WORKING, SHORT- AND LONG-TERM MEMORY BY NICOTINIC RECEPTORS IN THE BASOLATERAL AMYGDALA IN RATS.

BARROS DM, RAMIREZ MR, IZQUIERDO I.

NEUROBIOLOGY OF LEARNING AND MEMORY

ACADEMIC PRESS INC ELSEVIER SCIENCE

Año: 2005 vol. 83 p. 113 - 118

1074-7427

<!-- /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin:0cm; margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-fareast-font-family:"Times New Roman"; mso-bidi-font-family:"Times New Roman"; mso-ansi-language:PT-BR; mso-fareast-language:PT-BR; mso-bidi-language:AR-SA;} @page Section1 {size:595.3pt 841.9pt; margin:70.85pt 3.0cm 70.85pt 3.0cm; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> Male Wistar rats were exposed to one-trial step-down inhibitory avoidance training using a 0.5mA footshock. Through bilaterally implanted indwelling cannulae, they received bilateral 0.5 _L infusions of saline, mecamylamine (1.0 or 10.0 _g/side), or nicotine (0.6 or 3.0 _g/side) into the basolateral complex of the amygdaloid nucleus (BLA). Infusions were either 10 min before training (Experiment 1) or 4min after training (Experiment 2). In Experiment 1, the animals were tested three times: Wrst for working memory (WM) 5 s after training, then for short-term memory (STM) 90 min later, and Wnally for long-term memory (LTM) 24 h later. Mecamylamine depressed and nicotine enhanced WM, STM, and LTM. In Experiment 2, the treatments were given after WM was presumably over. Again, mecamylamine inhibited and nicotine enhanced STM and LTM. The results indicate that nAChRs in BLA participate in the regulation of WM formation and STM and LTM acquisition and consolidation.