Biology subjects

Yau, J. O. Y.

Publications and source records attributed to Yau, J. O. Y..

2 recordsLinked to original sources

bioRxiv2025

Instrumental Punishment Learning Enhances the Intrinsic Excitability of Basolateral Amygdala Neurons

The basolateral amygdala (BLA) is a structure that is critical for forming Pavlovian and instrumental emotional associations. Previous studies have established that Pavlovian fear conditioning increases the intrinsic excitability of BLA projection neurons. Learning-associated increases in excitability are hypothesised to facilitate the induction of synaptic plasticity and integration of neurons into functional learning circuits. Here, we examined whether instrumental learning produces similar changes in intrinsic excitability. Male and Female Long Evans rats were trained to lever press for a food reward and subsequently split into 3 behavioural groups; punished, yoked, and reward. Punished rats received response-contingent footshocks, yoked rats received response-independent footshocks, and reward rats received no shock. Intrinsic excitability was measured as the number of action potentials (APs) evoked by a series of depolarising current injections during whole-cell patch clamp recordings. Reward learning increased the intrinsic excitability of BLA projection neurons compared to naive controls. Punishment training maintained excitability and excitability was correlated with performance on the punishment task. Response-independent footshocks arrested reward-associated increases in excitability, reverting the BLA neurons to a naive state. Group differences were observed in AP half-width and the current underlying the post-burst AHP. Together, these findings show that instrumental reward learning enhances the intrinsic excitability of BLA projection neurons, potentially supporting action-outcome encoding by promoting synaptic plasticity and circuit integration. The results also suggest that different forms of learning engage distinct biophysical adaptations. A mechanistic understanding of the neurobiology underlying instrumental association learning may help inform the development of treatments for psychiatric disorders characterized by deficits in this process, such as major depressive disorder and conduct disorder.

neuroscience↗

bioRxiv2017

Basolateral amygdala glutamatergic neurons maintain aversive emotional salience

Basolateral amygdala (BLA) glutamatergic neurons serve a well-accepted role in fear conditioning and fear extinction. However, the specific learning processes related to their activity at different times during learning remain poorly understood. We addressed this using behavioral tasks isolating distinct aspects of fear learning in rats. We show that brief optogenetic inhibition of BLA glutamatergic neurons around moments of aversive reinforcement or non-reinforcement causes reductions in the salience of conditioned stimuli, rendering these stimuli less able to be learned about and less able to control fear or safety behaviours. This salience reduction was stimulus-specific, long-lasting, and specific to aversive emotional states - precisely the goals of therapeutic interventions in human anxiety disorders. Our findings identify a core learning process disrupted by brief BLA optogenetic inhibition. They show that a primary function of BLA glutamatergic neurons is to maintain the salience of conditioned stimuli. This is a necessary precursor for these stimuli to gain and maintain control over fear and safety behavior.\n\nSignificance statementThe amygdala is essential for learning to fear and learning to reduce fear. However, the specific roles served by activity of different amygdala neurons at different times during learning is poorly understood. We used behavioral tasks isolating distinct aspects of learning in rats to show that brief optogenetic inhibition of BLA glutamatergic neurons around moments of reinforcement or non-reinforcement disrupts maintenance of conditioned stimulus (CS) salience. This causes a stimulus-specific, long-lasting, and aversive emotion specific deficit in the ability of the CS to be learned about or control fear responses. These consequences are the precisely goals of therapeutic interventions in human anxiety disorders. Our findings identify a core learning process disrupted by brief BLA optogenetic inhibition.

neuroscience↗