October 26, 2017 16:00 - 17:30
BSI Central Building 1F Seminar Room
Neocortical networks must generate and maintain stable activity patterns despite perturbations induced by learning and experience- dependent plasticity, and this stability must be maintained across distinct behavioral states with very different sensory drive and modulatory tone. There is abundant theoretical and experimental evidence that network stability is achieved through homeostatic plasticity mechanisms that adjust synaptic and neuronal properties to stabilize some measure of average activity, and this process has been extensively studied in primary visual cortex (V1), where chronic visual deprivation induces an initial drop in activity and ensemble average firing rates (FRs), but over time activity is restored to baseline despite continued deprivation. Here I discuss recent work from the lab in which we followed FR homeostasis in individual V1 neurons in freely behaving animals during a prolonged visual deprivation paradigm, as animals cycled between natural periods of sleep and wake. We find that - when FRs are perturbed by visual deprivation - over time they returned precisely to a cell-autonomous set-point, and this restoration of firing occurred selectively during periods of active waking and was suppressed by sleep. Longer natural waking periods result in more FR homeostasis, as did artificially extending the length of waking. This exclusion of FR homeostasis from sleep raises the possibility that memory consolidation or some other sleep-dependent process is vulnerable to interference from homeostatic plasticity mechanisms.
- Open to Public
- Taro Toyoizumi [Taro Toyoizumi, Neural Computation and Adaptation ]