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On a method of making the wavelength of sodium light the actual and practical standard of length

1887; Yale University; Volume: s3-34; Issue: 204 Linguagem: Inglês

10.2475/ajs.s3-34.204.427

1945-452X

A. A. Michelson, Edward W. Morley,

Advanced Memory and Neural Computing

Abstract Elevated extracellular [K + ] is associated with many disorders including epilepsy, traumatic brain injury, ischemia and kidney failure. Experimentally, elevated [K + ] is used to increase excitability in neurons and networks, by shifting the potassium equilibrium potential (E K ) and consequently, the resting membrane potential. We studied the effects of increased extracellular [K + ] on the well-described pyloric circuit of the crab, Cancer borealis , while recording pyloric network activity extracellularly and the activity of Pyloric Dilator neuron (PD) intracellularly. A 2.5-fold increase in extracellular [K + ] (2.5x[K + ]) depolarized PD neurons and resulted in an unexpected short-term loss of their normal bursting activity. This period of silence was followed by the recovery of spiking and/or bursting activity during the continued superfusion of 2.5x[K + ] saline. In contrast, when PD neurons were pharmacologically isolated from pyloric presynaptic inputs, they exhibited no loss of spiking activity in 2.5x[K + ], suggesting the existence of an acute inhibitory effect mediated by circuit interactions. Action potential threshold in PD neurons decreased markedly over the course of exposure to 2.5x[K + ] concurrent with the recovery of spiking and/or bursting activity. This study illustrates a case of rapid adaptation to a global perturbation that is influenced by local synaptic connections. Moreover, the complex response of pyloric neurons to elevated [K + ] demonstrates that electrophysiological recordings are necessary to determine how neuronal and circuit activity are affected by altered K + concentrations. Significance Statement To characterize the sensitivity of a neuronal circuit to global perturbation, we tested the response of the well-described pyloric circuit of the crab stomatogastric ganglion to saline with elevated [K + ]. Unexpectedly, a 2.5-fold increase in extracellular [K + ] led to a temporary loss of activity in pyloric neurons that is not due to depolarization block. This was followed by a rapid increase in excitability and concurrent recovery of spiking activity within minutes. In contrast, when presynaptic inputs to pyloric neurons were blocked, there was no temporary loss of spiking activity in elevated [K + ]. This is a case of rapid adaptation that restores neuronal activity disrupted by global depolarization.