Regulation of the NMDA component of EPSP’s by different components of postsynaptic GABAergic inhibition: computer simulation analysis in piriform cortex. J. Neurophysiol. 78: 2546–2559

Physiological analysis in the companion paper demonstrated that tory postsynaptic currents (IPSCs) are generated in apical g-aminobutyric acid-A (GABAA)-mediated inhibition in piriform dendrites as well as cell bodies, that the neuronal circuitry cortex is generated by circuits that are largely independent in apical that generates IPSCs in distal dendritic and somatic regions dendritic and somatic regions of pyramidal cells and that GABAA- is largely separate, that GABAA inhibition consists of fast mediated inhibitory postsynaptic currents (IPSCs) in distal dendrites and slow components, and that there is a greater proportionhave a slower time course than those in the somatic region. This of the slow component in distal dendrites than cell bodiesstudy used modeling methods to explore these characteristics of (Kapur et al. 1997). Other studies in piriform cortex haveGABAA-mediated inhibition with respect to regulation of the N- demonstrated that GABAB-mediated IPSCs also are gener-methyl-D-aspartate (NMDA) component of excitatory postsynaptic ated in pyramidal cell dendrites (Kanter et al. 1996; Tsengpotentials. Such regulation is relevant to understanding NMDA-dependent long-term potentiation (LTP) and the integration of repet- and Haberly 1988). itive synaptic inputs that can activate the NMDA component as well There is now evidence for piriform cortex (Kanter et al. as pathological processes that can be activated by overexpression of 1996), as originally demonstrated in other cortical areas the NMDA component. A working hypothesis was that the indepen- (Dingledine et al. 1986; Garthwaite and Garthwaite 1989; dence and differing properties of IPSCs in apical dendritic and so- Luhmann and Prince 1990), that the NMDA componen