The way network activity is coordinated in the basolateral amygdala (BLA) plays a critical role in the expression of fear. While neuromodulatory systems are known to regulate shifts between behavioral states, the underlying mechanisms largely remain a mystery. Dr. Tasker joins us in this episode to discuss his recent findings which shed light on this enigmatic process.

His team used a mouse model to explore the effects of chemogenetic Gq activation and α1 adrenoreceptor activation in BLA parvalbumin (PV) interneurons. The results revealed a stereotyped phasic bursting in PV neurons and time-locked synchronized bursts of inhibitory postsynaptic currents and phasic firing in BLA principal neurons. Interestingly, this activation in PV neurons was found to suppress gamma oscillations in vivo and in an ex vivo slice model, facilitating fear memory recall. This phenomenon aligns with the observed suppression of BLA gamma during the expression of conditioned fear.

Dr. Tasker's research identifies a key neuromodulatory mechanism in PV inhibitory interneurons of the BLA, offering new insights into the regulation of BLA network oscillations and fear memory recall. Tune in as we delve into this exciting area of neuroscience research.

Keywords: Dr. Tasker, Fear Memory Recall, Network Oscillations, Basolateral Amygdala, Neuromodulatory Systems, Parvalbumin Interneurons, Gamma Suppression.

Gq neuromodulation of BLA parvalbumin interneurons induces burst firing and mediates fear-associated network and behavioral state transition in mice. (2022). https://doi.org/10.1038/s41467-022-28928-y