Alejandro Torrado Pacheco
“Sleep drives downward firing rate homeostasis in V1 neurons”
The brain prefers to be in a state of functional balance, known as homeostasis. Mechanisms are in plance to return the activity of a neuron to a set level once it has been excited. But what are these mechanisms? Mr. Torrado Pacheco is examining the question using a rat model, and notes that recovery of homeostasis is associated with sleep but not particular behavioral states.Homeostatic plasticity mechanisms act to keep the activity of individual neurons within a target set-point, a process known as firing rate homeostasis (FRH). In earlier work from our lab we first demonstrated upward FRH neurons in primary visual cortex (V1) of rats following monocular deprivation (MD), and that this upward recovery is restricted to periods of wake. This raises important questions about how firing rates (FRs) are homeostatically regulated in the brain, and about the role of sleep and wake in this process. We use chronic electrophysiology in freely behaving rats and perform eye re-opening (ER) after 5 days of MD. This causes activity in V1 to increase above its pre-MD baseline in the first 24 hours, but FRs then recover to their pre-MD baseline within 4 days. Thus, downward FRH happens in vivo, and FRH is bi-directional. Using pharmacology and slice electrophysiology, we show that the FR changes after ER are driven by different plasticity mechanisms. Specifically, we demonstrate that the downward recovery phase is driven by homeostatic mechanisms. Additionally, in contrast to our results on upward FRH, we find that this downward homeostatic recovery of activity is driven by sleep. Finally, analysis of the decrease in FR caused by MD reveals no dependence on behavioral state: FR decreases were instead associated with time spent in light (vs darkness), suggesting an activity-dependent process. These data reveal a complex regulation of FRs in vivo, where plastic changes in different directions are gated by different behavioral states.