Molecular pharmacological dissection of short- and long-term memory

• Autor(a) principal: Izquierdo, Luciana Adriana
• Data de Publicação: 2002
• Outros Autores: Barros, Daniela Marti, Vianna, Mônica Ryff Moreira Roca, Coitinho, Adriana Simon, Silva, Tiago Luís de Dedavid e, Choi, Humberto Kukhyun, Moletta, Beatriz, Medina, Jorge Horacio, Izquierdo, Ivan Antônio
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da FURG (RI FURG)
• Texto Completo: http://repositorio.furg.br/handle/1/2993
• topic: Short-term memory; Long-term memory; Memory types

It has been discussed for over 100 years whether short-term memory (STM) is separate from, or just an early phase of, long-term memory (LTM). The only way to solve this dilemma is to find out at least one treatment that blocks STM while keeping LTMintact for the same task in the same animal. The effect of a large number of treatments infused into the hippocampus, amygdala, and entorhinal, posterior parietal or prefrontal cortex on STM and LTMof a one-trial stepdown inhibitory avoidance task was studied. The animals were tested at 1.5 h for STM, and again at 24 h for LTM. The treatments were given after training. Eleven different treatments blocked STM without affecting LTM. Eighteen treatments affected the two memory types differentially, either blocking or enhancing LTM alone. Thus, STM is separate from, and parallel to the first hours of processing of, LTM of that task. The mechanisms ofSTMare different from those of LTM. The former do not include gene expression or protein synthesis; the latter include a double peak of cAMP-dependent protein kinase activity, accompanied by the phosphorylation of CREB, and both gene expression and protein synthesis. Possible cellular and molecular events that do not requiremRNAor protein synthesis should account for STM. These might include a hyperactivation of glutamate AMPA receptors, ribosome changes, or the exocytosis of glycoproteins that participate in cell addition.