Nitric oxide synthesis in the basolateral complex of the amygdala is required for the consolidation and expression of fear potentiated startle but not shock sensitization of the acoustic startle.

Nitric oxide (NO) is synthesized as a result of N-methyl-d-asparate (NMDA) receptor activation, it acts as an retrograde neurotransmitter freely diffusing across cell membranes interacting with its targets in a non-synaptic manner. Consequently, NO has been described as an extension of NMDA receptor activation. The targets of NO include cellular components within the basolateral complex of the amygdala (BLA) that are necessary for the consolidation of conditioned fear as well as targets that can significantly modulate neurotransmission associated with its expression. Given that both are NMDA receptor associated processes, this implies that NO may be an important intermediary of NMDA receptor activation and both fear memory consolidation and expression. The current study sought to examine this using visual fear conditioning and fear potentiated startle. Three experiments were conducted, rats received intra-BLA microinfusions of the global nitric oxide synthase inhibitor l-NAME either prior to fear conditioning, or expression of learned fear. Furthermore, NO's ability to modulate a NMDA receptor independent fear process was assessed by microinfusing l-NAME into the BLA prior to examination of the shock sensitization of the acoustic startle affect. The results indicated that NO was, indeed, required for both the consolidation and expression of learned fear, whereas it was not required for NMDA independent shock enhanced startle responding. This study illustrates that NO plays a pivotal role in the examined NMDA associated fear processes.