Classical conditioning
Neural basis of learning and memory

Fear and eyeblink conditioning involve generally non overlapping neural circuitry, but share molecular mechanisms. Fear conditioning occurs in the basolateral amygdala, which receives glutaminergic input directly from thalamic afferents, as well as indirectly from prefrontal projections. The direct projections are sufficient for delay conditioning, but in the case of trace conditioning, where the CS needs to be internally represented despite a lack of external stimulus, indirect pathways are necessary. The anterior cingulate is one candidate for intermediate trace conditioning, but the hippocampus may also play a major role. Presynaptic activation of protein kinase A and postsynaptic activation of NMDA receptors and its signal transduction pathway are necessary for conditioning related plasticity. CREB is also necessary for conditioning related plasticity, and it may induce downstream synthesis of proteins necessary for this to occur. As NMDA receptors are only activated after an increase in presynaptic calcium(thereby releasing the Mg2+ block), they are a potential coincidence detector that could mediate spike timing dependent plasticity. STDP constrains LTP to situations where the CS predicts the US, and LTD to the reverse.
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