Embryonic neural cell adhesion molecule (N-CAM) is elevated in the denervated rat dentate gyrus

Abstract

We evaluated the immunohistological changes in neural cell adhesion molecule (N-CAM) expression in the adult rat dentate gyrus during the period of synaptic degeneration, axonal sprouting, and synaptogenesis following ipsilateral entorhinal cortex (ERC) lesion. This lesion denervates the outer two-thirds of the dentate granule cells dendrites and induces compensatory sprouting from the subjacent inner one-third into the denervated zone, as well as reactive synaptogenesis in the denervated outer molecular layer. In unlesioned adult hippocampus, antibodies to total N-CAM stained the inner molecular layer intensely, and the outer molecular layer (ML) more lightly. After ERC lesion the intense staining of the inner layer widened, the expansion following the known temporal sequence of commissural and associational (C/A) axon sprouting into the denervated zone. In normal unlesioned controls there was very light, uniform staining of the ML with antibodies directed against embryonic N-CAM (eN-CAM). By 2 d post-ERC lesion, the outer two- thirds of the ML stained robustly with antibody to eN-CAM. This area of intense staining receded as the C/A axon collaterals from the inner one- third entered the denervated zone, so that by 30 d the intense eN-CAM staining only occupied the outer half of the ML. The increased expression of eN-CAM remained present at 60 d post-ERC lesion, past the point that synaptic volume density has returned to normal levels in the denervated zone. Ultrastructural studies showed that the newly expressed eN-CAM was located on the surface of dendrites in the denervated zone, but was not found at the synaptic contacts.(ABSTRACT TRUNCATED AT 250 WORDS)

Expression of fetal ALZ-50 reactive clone 1 (FAC1) in dentate gyrus following entorhinal cortex lesion

“…We examined the effect of ERC lesion on FAC1 protein expression and localization in hippocampal dentate gyrus and report that FAC1 protein, like eN-CAM, 1) is rapidly re-expressed in the denervated OML following ERC lesion, 2) is localized to dendrites within the denervated zone, and 3) follows the same temporal and spatial sequence of initial expression and subsequent diminution that we have previously reported for eN-CAM (Miller et al, 1994;Styren et al, 1994a).…”

Temporal and spacial relationships between PSA-NCAM-expressing, newly generated granule cells, and radial glia-like cells in the adult dentate gyrus

“…Because the dendrites of the granule cells receive afferents containing sensory information from the entorhinal cortex in postnatal animals, the new neuronal circuit formed by these two immature elements could be under the influence of sensory input. Moreover, PSA-NCAM has been reported to be essential in neuronal plasticity such as induction of long-term potentiation (Muller et al, 1996), learning (Fox et al, 1995b;Murphy et al, 1996), and reconstruction of neuronal tissue (Theodosis et al, 1991;Le Gal La Salle et al, 1992;Kiss et al, 1993;Miller et al, 1994;Bonfanti et al, 1996). Therefore, it should be interesting to explore what function the PSA-NCAM-expressing granule cells and radial glia-like cells play in sensory input-dependent synapse formation of the dentate gyrus and whether age-dependent changes in PSA-NCAM expression, neurogenesis, and glial environment affect the plasticity including memory and learning function.…”

Different polysialic acid-neural cell adhesion molecule expression patterns in distinct types of mossy fiber boutons in the adult hippocampus

“…Another possibility is that these PSA-expressing boutons contribute to synaptic remodeling and plasticity in the adult hippocampus. In this respect, it should be noted that PSA reexpression is seen in sprouting and synaptic remodeling of the mossy fibers in lesion experiments (Miller et al, 1994;Muller et al, 1994).…”

“…Although, in the adult brain, PSA expression disappears from most of brain regions, persistent PSA expression is found in several restricted regions, including the olfactory bulb, hippocampus, hypothalamus, and spinal cord (Bonfanti et al, 1992;Seki and Arai, 1993a;Theodosis et al, 1998). In the adult hippocampus, PSA-NCAM has been reported to contribute to several phenomena in relation to hippocampal plasticity, such as the induction of long-term potentiation and long-term depression (LTD) (Becker et al, 1996;Muller et al, 1996), learning behavior (Fox et al, 1995b;Becker et al, 1996;Murphy et al, 1996), the formation of aberrant mossy fibers (Mathern et al, 1994;Miller et al, 1994;Seki and Rutishauser, 1998), and axonal regeneration and sprouting after injury (Aubert et al, 1998). However, it is unclear how the expression of PSA in mossy fibers functions in hippocampal plasticity.…”