INHIBITION CAN DISRUPT HYPERSYNCHRONY IN MODEL NEURONAL NETWORKS

Authors
Citation
Sn. Deyo et Ww. Lytton, INHIBITION CAN DISRUPT HYPERSYNCHRONY IN MODEL NEURONAL NETWORKS, Progress in neuro-psychopharmacology & biological psychiatry, 21(5), 1997, pp. 735-750
Citations number
28
Categorie Soggetti
Neurosciences,"Clinical Neurology","Pharmacology & Pharmacy",Psychiatry
ISSN journal
02785846
Volume
21
Issue
5
Year of publication
1997
Pages
735 - 750
Database
ISI
SICI code
0278-5846(1997)21:5<735:ICDHIM>2.0.ZU;2-R
Abstract
1. Model neuronal network simulations were performed using a reduced T raub neuronal network model. In the absence of inhibition the network produced synchronous population bursting. 2. Bursting of individual ne urons was dependent on 1 or more of the following: build-up of charge in the dendritic compartment, prolonged current flow through simulated NMDA associated channels, current flow through T channels. Interburst interval duration and consequent burst frequency was dependent on the density of slow afterhyperpolarizing potassium channels. 3. Addition of an inhibitory interneuron population projecting to GABA(A) receptor s resulted in rapid desynchronization of the population, generally aft er only 1-2 cycles. This effect was found to be due to reduced partici pation in the individual population burst and to the need for multi-sy naptic activation of the individual neuron in the presence of inhibiti on. 4. This desynchronizing effect could be offset by increasing the s trength of interburst hyperpolarization either through increased densi ty of I-AHP, Or through the addition of a separate inhibitory interneu ron pool projected to GABA(B) receptors. 5. These data suggest that th e synchronizing effects of inhibition may vary depending on circumstan ces - with desynchronization being dominant in cases characterized by large population bursts such as those seen in epilepsy.