Calcineurin as a regulator of memory formation: Mechanisms Involved

DE LA FUENTE V; FEDERMAN N; FUSTIÑANA MS; ROMANO A

Huerta Grande, Córdoba

Congreso; XXVII Congreso Sociedad Argentina de Investigación en Neurociencia; 2012

Sociedad Argentina de Investigación en Neurociencias

Many studies on synaptic signaling in neural plasticity support that synaptic strengthening is induced by altering the balance between protein kinases and protein phosphatases towards the side of the kinases. Conversely, synaptic depression is mediated by phosphatase activation. The phosphatase calcineurin CaN was particularly studied due to the fact that it is activated directly by Ca2+/Calmodulin signals and that it is highly present in synaptic spines. Some studies support its role as a memory constraint in consolidation in different paradigms. On the other hand, it is well known that the transcription factor NF-_B is necessary for memory formation. In the present work we studied the effect of CaN pharmacological inhibition during fear conditioning consolidation. We found that hippocampal CaN inhibition by means of the drug FK506 improved contextual fear memory. If NF-_B was also inhibited, facilitation of memory was not observed. Thus, our next studies were aimed to see if CaN acts as a negative constraint by inhibiting NF-_B signaling pathway. Preliminary results show that FK506-induced memory enhancement produced an increment in the activity of NF-_B. We discuss possible mechanisms of CaN signaling as a constraint regulator of memory formation.