Topic: intrinsic excitability

Conventionally, neurons are thought to be cellular units that process synaptic inputs into synaptic spikes. However, it is well known that neurons can also spike spontaneously and display a rich repertoire of firing properties with no apparent functional relevance e.g. in in vitro cortical slice preparations. In this talk, I will propose a hypothesis according to which intrinsic excitability in neurons may be a survival mechanism to minimize toxic byproducts of the cell’s energy metabolism. In neurons, this toxicity can arise when mitochondrial ATP production stalls due to limited ADP. Under t

Can alterations in experience trigger different plastic modifications in neuronal structure and function, and if so, how do they integrate at the cellular level? To address this question, we interrogated circuitry in the mouse olfactory bulb responsible for the earliest steps in odor processing. We induced experience-dependent plasticity in mice of either sex by blocking one nostril for one day, a minimally invasive manipulation that leaves the sensory organ undamaged and is akin to the natural transient blockage suffered during common mild rhinal infections. We found that such brief sensory d

Various working memory (WM) models based on a diverse set of biologically plausible synaptic and neural plasticity mechanisms have been proposed. We show that these proposed short-term plasticity mechanisms may not necessarily be competing explanations, but instead yield interesting functional interactions on a wide set of WM tasks and enhance the biological plausibility of spiking neural network models of WM. While reductionist models (WM explained by one particular mechanism) are theoretically appealing and have increased our understanding of specific mechanisms, they are insufficient. WM mo