Topic: Metabolic spikes

Parkinson's disease (PD), characterized by the absence of dopamine in the striatum[1], is caused by the death of the substantia nigra pars compacta dopamine (SNcDA) neurons in the mid-brain. The cause of this cell loss is attributed to irreparable damage due to a dysregulation cascade originating from excess cytosolic dopamine[2]. However, it is unresolved if dopamine dysregulation in SNcDA neurons themselves is the cause of PD or if it is a mere symptom. Here, we introduce a theory of specialized non-causal action potentials that serve metabolic homeostasis called `metabolic spikes' which can

Neurons spike spontaneously in many experimental settings. Such firing patterns are often characterized by prolonged periods of silence followed by an unknown trigger of spontaneous activity that propagates throughout the slice. These were dubbed `neural avalanches' as they resemble avalanches in which accumulated snow rapidly flows down a mountain slope. Expanding this analogy -- if the network connectivity is equivalent to the mountain slope, what is the 'snow' that accumulates prior to a neural avalanche? Here, we propose that it is the accumulation of ATP in neuronal mitochondria, and that

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

Parkinson's disease (PD), characterized by the absence of dopamine in the striatum[1], is caused by the death of the substantia nigra pars compacta dopamine (SNcDA) neurons in the midbrain. The loss of these autonomously pacemaking[2] neurons is attributed to irreparable damage due to a dysregulation cascade starting from excess cytosolic dopamine and its decomposition into its aldehyde[3]. However, it is unresolved if dopamine dysregulation in SNcDA neurons themselves is the cause of PD or if it is a mere symptom. Here, we applied a recent theory of metabolic spikes[4] to SNcDA neurons, to