Once this cluster of neurons recieves strong enough stimulus for the activation to spread (the stronger the stimulus, often the more neurons become involved), the entire cluster of neurons can easily depolarize at once, creating the characteristic waves of excitation seen in epilepsy.įor example, in photosensitive epilepsy, intense visual stimuli cause a critical mass of neurons in the visual cortex to fire synchronously, initiating a wave of excitation. Genetic factors can cause this, but certain drugs can cause it as well, such as lamotrigine. So, instead of needing to integrate enough excitatory signals to go from -70mv -> -55mV, someone with epilepsy might have a nucleus in the brain (a cluster of cell bodies) that only needs to depolarize from -60mV -> -55mV in order to fire action potentials. Fundamentally, the problem in epilepsy is that some resting membrane potentials in any of the clusters of cells in the brain can move closer to threshold. Of course, it gets much more complicated if you look into it. Those are mostly K+ channels, so the membrane potential is still very close to E_K.Ĭontrary to these other two answers, I think you're spot on with the mechanistic explanation. As they close, the membrane returns to the resting potential, which is set by permeability through the "leak" channels. The membrane is hyperpolarized at the end of the AP because voltage-gated potassium channels have increased the permeability to K+. The E_ion is determined by the concentration gradient set up by the pump. The membrane potential is a function of the relative permeability (through ion channels) of the membrane to each ion, and the equilibrium potential (E_ion) for that ion. This is because membrane potential changes are not determined by concentration changes, but by permeability changes. The pump simply maintains the concentrations gradients over a long time period.īut: When an action potential occurs, only a tiny, tiny amount of ions (<0.001%) need to move across the membrane to change the membrane potential. The pump plays no direct role in returning to resting potential. 2 nd ed.Hi, I'm a neurobio professor, and this is one of the biggest misconceptions in neuroscience. Nelson & Connaughton, Bipolar Cell Pathways in the Vertebrate Retina. There are situations where multiple axons arise, but that occurs only in neurons that have been tinkered around with genetically. Basically, the neuron has still just one axonal output, but collateral regulatory info is sent off back to the cell. The only situation where multiple axons arise from one cell is when the axon bifurcates along the way, sending one or more collaterals from the axon off back to the cell. bipolar cells), others as many as thousands of terminals (Brady et al., 2012). The axon can target neurons along the way ( en passant) and the axon can terminate in multiple terminals contacting various cells. Hence, dependent on the cell type, neurons can have one or as many as 200k dendritic connections.Īs far as I am aware, all neurons have just one axon. Etymology: axon, from Greek xn, meaning axle. Hence they integrate massive amounts of (sensory) information and funnel it into one output signal (Purves et al., 2002). Medicine definition: Axon hillock is an axon nerve fiber that is a long projection of a neuron that carries the outbound neuronal cell signals as opposed to dendrites, which are the short protrusions from the neuronal cell body that brings in the inbound signals to the neuron. These cells have elaborate dendritic trees making 100,000 to 200,000 connections, but still there is just one axon. Multipolar neurons have multiple inputs (dendritic connections), and one output (the axon).There are also bipolar cells in the retina, these have one dendrite (input) and one axon (output) (Nelson & Connaughton, 2012).Ī striking example are the Purkinje cells in the cortex.
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