Synaptic plasticity plays an important role in mediating the behavior of neuronal networks including learning and memory. However, not much is understood about how it is implemented in vivo, especially in the complex dendritic trees of neurons in the mammalian fear circuit. Neuromodulation is very important in such circuits and its impact on plasticity has not been characterized adequately. We will consider the calcium-based plasticity mechanisms implemented in recently reported models, and study how neuromodulation and dendritic morphology impact plasticity.

Norepinephrine and dopamine are the key neurotransmitters that modulate the neurons in the mammalian amygdala during Pavlovian fear conditioning. We will consider their impact on long-term potentiation (LTP) and long-term depression (LTD) using the NMDAR-based calcium learning rule implemented in the post-synapse. The calcium based learning rule requires depolarization of local membrane potentials in dendrites to relieve the Mg2+ block of NMDA receptors. A high level depolarization produces LTP, while LTD is caused by lower levels of depolarization. Hebbian pairing typically requires both dendritic spiking and back-propagating action potentials to achieve LTP. However, biological reports show that a certain level of dendritic spiking may by itself be sufficient to cause LTP/LTD. We will investigate all these mechanisms comprehensively using compartmental models of different complexity.

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