Abstract
Homeostatic plasticity maintains balance in the cortical circuit through mechanisms of integrating new changes to the system while keeping the system at a baseline. Neuronal firing rates in the visual cortex remain stable despite disruptions like monocular deprivation (MD). Initially, during MD, activity in the deprived hemisphere drops but returns to baseline within six days through homeostatic plasticity mechanisms. Utilizing more naturalistic paradigms, such as cricket hunting, cortical activity can be perturbed using ethologically-relevant stimuli, rather than coarse adjustments of cortical input. It remains unclear how prior induction of homeostatic plasticity may affect long-term cortical activity or future learning capacity. To explore this, we chemogenetically disrupted activity in the visual cortex (V1) of juvenile Long Evans rats to first induce homeostatic plasticity mechanisms, allowed activity to normalize, and then measured hunting performance and neuronal activity levels one week later. As expected, both cohorts of animals learned prey capture learning, but rats that underwent a perturbation of V1 activity exhibited slight improvements in hunting performance compared to control rats, along with decreased cFos activity. These preliminary findings may indicate that the prior recruitment of homeostatic plasticity mechanisms may predispose neural circuits to encode learning-induced plasticity more efficiently and enable faster learning.