DEVELOPMENT OF EXCITATORY AND INHIBITORY POSTSYNAPTIC POTENTIALS IN THE RAT NEOCORTEX

Citation
B. Sutor et Hj. Luhmann, DEVELOPMENT OF EXCITATORY AND INHIBITORY POSTSYNAPTIC POTENTIALS IN THE RAT NEOCORTEX, Perspectives on developmental neurobiology, 2(4), 1995, pp. 409-419
Citations number
74
Categorie Soggetti
Neurosciences
ISSN journal
10640517
Volume
2
Issue
4
Year of publication
1995
Pages
409 - 419
Database
ISI
SICI code
1064-0517(1995)2:4<409:DOEAIP>2.0.ZU;2-G
Abstract
The postnatal development of synaptic potentials in the rat neocortex is characterized by the sequential appearance of functional excitatory and inhibitory synapses. Morphological and electrophysiological studi es provided evidence that at early stages of development, pyramidal ce lls are extensively coupled to each other, presumably via gap junction s. Thus, immature neurons are able to communicate through pathways tha t are not available or only weakly expressed in the mature neocortex. During the very early postnatal period, excitatory synaptic inputs pre vail. Excitatory postsynaptic potentials (EPSPs) are characteristicall y long in duration and show high sensitivity to frequent stimulation. Although spontaneous inhibitory postsynaptic potentials (IPSPs) and ma ture responses to exogenously applied gamma-aminobutyric acid (GABA) h ave been described during the first postnatal week evoked IPSPs do not develop before postnatal day 10 (P10). During the period of maximum s ynaptogenesis (P11 to P20), GABA-mediated synaptic inhibition develops and pyramidal cells respond to afferent activation with efficient EPS Ps and IPSPs. These postsynaptic potentials gradually mature during th e late postnatal period. The delayed development of synaptic inhibitio n in the neocortex simultaneously promotes synaptic plasticity while i ncreasing seizure susceptibility. On the one hand, the functional lack of synaptic inhibition during early stages of development enables a p eriod of enhanced neuronal activity and augmented synaptic plasticity necessary to form proper synaptic connections. On the other hand, the absence of inhibitory control over excitatory processes increases the vulnerability of the developing neocortex to seizure activity during p ostnatal ontogenesis.