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
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.