Previous models of visual cortical ocular dominance (OD) plasticity (e.g., Clothiaux et al., 1991; Miller et al., 1989) are based on afferent excitatory synaptic plasticity alone; these models do not consider the role of lateral interactions and synaptic plasticity in lateral pathways in OD plasticity. Recent models of other cortical properties and functions have emphasized lateral intracortical interactions, however, and long-range lateral pathways develop during the early postnatal stages (Callaway & Katz, 1990). Thus, a biologically plausible model of OD plasticity should consider the development of intracortical pathways and its effects on OD and other cortical properties during early postnatal stages. In this paper, the EXIN model (Marshall, 1995a), which consists of afferent excitatory and lateral inhibitory synaptic plasticity, is used to model OD plasticity during the "classical" rearing paradigms such as normal rearing, monocular deprivation, reverse suture, strabismus, binocu...

Infusion of a GABA agonist (Reiter & Stryker, 1988) and infusion of an NMDA receptor antagonist (Bear et al., 1990), in the primary visual cortex of kittens during monocular deprivation, shifts ocular dominance toward the closed eye, in the cortical region near the infusion site. This reverse ocular dominance shift has been previously modeled by variants of a covariance synaptic plasticity rule (Bear et al., 1990; Clothiaux et al., 1991; Miller et al., 1989; Reiter & Stryker, 1988). Kasamatsu et al. (1997, 1998) showed that infusion of an NMDA receptor antagonist in adult cat primary visual cortex changes ocular dominance distribution, reduces binocularity, and reduces orientation and direction selectivity. This paper presents a novel account of the effects of these pharmacological treatments, based on the EXIN synaptic plasticity rules (Marshall, 1995), which include both an instar afferent excitatory and an outstar lateral inhibitory rule. Functionally, the EXIN plasticity rules enha...

A large variety of synaptic plasticity rules have been used in models of excitatory synaptic plasticity (Brown et al., 1990). These rules are generalizations of the Hebbian rule and have some properties consistent with experimental data on long-term excitatory synaptic plasticity, but they also have some properties inconsistent with experimental data. For example, the BCM rule (Bear et al., 1987; Bienenstock et al., 1982) produces homosynaptic potentiation and depression, which has been observed experimentally (Artola et al., 1990; Dudek & Bear, 1992; Kirkwood et al., 1993; Fr'egnac et al., 1994; Yang & Faber, 1991). But the BCM rule is also inconsistent with some experimental results; e.g., the BCM rule cannot produce heterosynaptic depression (Abraham & Goddard, 1983; Lynch et al., 1977). In addition, long-term synaptic plasticity in inhibitory pathways has been emphasized in some models of cortical function (Marshall, 1990abc, 1995a; Sirosh et al., 1996), but experimental data on in...