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Y. Grossman
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Journal Articles
Publisher: Journals Gateway
Neural Computation (2013) 25 (1): 75–100.
Published: 01 January 2013
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We simulate the inhibition of Ia-glutamatergic excitatory postsynaptic potential (EPSP) by preceding it with glycinergic recurrent (REN) and reciprocal (REC) inhibitory postsynaptic potentials (IPSPs). The inhibition is evaluated in the presence of voltage-dependent conductances of sodium, delayed rectifier potassium, and slow potassium in five -motoneurons (MNs). We distribute the channels along the neuronal dendrites using, alternatively, a density function of exponential rise (ER), exponential decay (ED), or a step function (ST). We examine the change in EPSP amplitude, the rate of rise (RR), and the time integral (TI) due to inhibition. The results yield six major conclusions. First, the EPSP peak and the kinetics depending on the time interval are either amplified or depressed by the REC and REN shunting inhibitions. Second, the mean EPSP peak, its TI, and RR inhibition of ST, ER, and ED distributions turn out to be similar for analogous ranges of G. Third, for identical G, the large variations in the parameters’ values can be attributed to the sodium conductance step ( ) and the active dendritic area. We find that small on a few dendrites maintains the EPSP peak, its TI, and RR inhibition similar to the passive state, but high on many dendrites decrease the inhibition and sometimes generates even an excitatory effect. Fourth, the MN's input resistance does not alter the efficacy of EPSP inhibition. Fifth, the REC and REN inhibitions slightly change the EPSP peak and its RR. However, EPSP TI is depressed by the REN inhibition more than the REC inhibition. Finally, only an inhibitory effect shows up during the EPSP TI inhibition, while there are both inhibitory and excitatory impacts on the EPSP peak and its RR.
Journal Articles
Publisher: Journals Gateway
Neural Computation (2010) 22 (7): 1764–1785.
Published: 01 July 2010
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We simulate reconstructed α -motoneurons (MNs) under physiological and morphological realistic parameters and compare the modeled reciprocal (REC) and recurrent (REN) inhibitory postsynaptic potentials (IPSPs) containing voltage-dependent channels on the dendrites with the IPSPs of a passive MN model. Three distribution functions of the voltage-dependent channels on the dendrites are applied: a step function (ST) with uniform spatial dispersion; an exponential decay (ED) function, with channels with high density located proximal to the soma; and an exponential rise (ER) with a higher density of channels located distally. The excitatory and REN inhibitory inputs are located as a gaussian function on the dendrites, while the REC inhibitory synapses are located proximal to the soma. Our simulations generate four key results. (1) The distribution pattern of the voltage-dependent channels does not affect the IPSP peak, its time integral (TI), or its rate of rise (RR). However, the IPSP peak decreased in the presence of the active dendrites, while the EPSP peak increased. (2) Proximally located IPSP conductance produces greater IPSP peak, RR, and TI. (3) Increased duration of the IPSP produces greater RR and moderately increased TI and has a small effect on the peak amplitude. (4) The IPSP of both REC and REN models is specific to each MN: its amplitude is proportional to the MNs' input resistance, R N ; the increase of IPSP at the proximal location of the IPSP synapses is inversely related to R N ; and the effect of the IPSP conductance duration is insensitive to R N .