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É possível concluir que dentre os mecanismos candidatos de plasticidade sináptica para o processo de consolidação da memória de longa duração, a LTP na região CA1 do hipocampo é considerado favorito. Porém não é possível afirmar que a LTP seja sinônimo de memória, pois apesar de várias características em comum, as evidências mostram que não são totalmente idênticas.

É certo que a NA liberada por neurônios do LC, modula a LTP hipocampal, atuando através dos receptores β-adrenérgicos, podendo melhorar ou prejudicar a formação de memórias, dependendo da frequência de estimulação. A ativação dos receptores β-adrenérgicos resulta na formação da PKA. Como essa quinase é ativada também durante a ocorrência da LTP, isso sugere que o mecanismo pelo qual a via noradrenérgica melhora ou prejudica a formação de memórias no hipocampo ocorre através dessa via de sinalização em comum entre a LTP hipocampal o mecanismo de ação da NA.

Isso está estreitamente relacionado com o estresse, pois durante o período de excitação emocional a NA é liberado no cérebro em maiores quantidades que em um estado normal, alterando a plasticidade hipocampal, em especial a LTP. Como a NA modula a plasticidade sináptica em CA1 durante a baixa frequência de estimulação e melhora a LTP nessa região é possível inferir que o estresse leve ou moderado, que resulta numa liberação de baixa quantidade de NA, pode melhorar a LTP e a formação de memórias, enquanto que o estresse excessivo e intenso pode prejudicar a formação de memórias. Mas esse efeito não depende apenas da liberação de NA no hipocampo.

A modulação da consolidação da LTP hipocampal é dada pela interação do hipocampo com o BLA. Nessa região os efeitos da NA sobre os receptores β-adrenérgicos são mediados via interação com receptores α1-β-adrenérgicos, que por sua vez, são influenciados pelos glicocorticóides também liberados durante a situação estressante. Sendo assim, os efeitos do estresse sobre a memória hipocampal para estímulos emocionais não dependem unicamente da ativação dos receptores β-adrenérgicos, mas sim de interações complexas entre diferentes neuromoduladores e

estruturas cerebrais. Mas a via de receptores β-adrenérgicos é necessária para que os outros fatores, como os glicocorticóides ou a ativação dos receptores α1-adrenérgicos sejam capazes de influenciar a consolidação das memórias.

Porém, os mecanismos envolvidos durante todos esses processos ainda não estão completamente elucidados e exigem novos estudos para compreensão. Além disso, a maneira como o estresse influencia na memória depende das características dos agentes estressores, o contexto em que a experiência estressante ocorre e sua intensidade. Dessa forma, o estresse pode prejudicar ou melhorar a formação das memórias, pois a forma como todo esse mecanismo se expressa pode ser alterada, por exemplo, através da liberação de mais ou menos glicocorticóides.

Como os dados da literatura indicaram, as consequência à exposição crônica a altos níveis de catecolaminas ou cortisol pode levar a alteração da função dos receptores β-adrenérgicos. Tendo em vista a incidência dos distúrbios de ansiedade e estresse que acometem a população humana, seria possível através de novos estudos sobre o mecanismo pelo qual o estresse altera a formação das memórias estabelecer tratamentos adequados, mas para isso é necessário o entendimento completo da via e dos fatores que levam a alterar as funções cognitivas durante as experiências emocionais.

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