Exercise increases mRNA levels for adhesion molecules N-CAM and L1 correlating with BDNF response

Macias, Matylda; Fehr, Susanne; Dwornik, A; Sulejczak, Dorota; Wiater, M.; Czarkowska-Bauch, Julita; Skup, M; Schachner, Melitta

doi:10.1097/00001756-200212200-00029

Cited by 23 publications

(25 citation statements)

References 24 publications

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“…Loss of L1 immunoreactivity in chronic sedentary was not significantly different from that in chronic exercised animals (P Յ 0.18). and thus our results differ from those of Macias et al (2002). They recorded an increase in L1 mRNA in normal rats that were allowed 1 km of daily treadmill walking for 4 weeks but noted that the results did not reach statistical significance.…”

Section: E-h) and Ib4 (I-l) A-dcontrasting

confidence: 99%

“…Exercise has been shown to increase neurogenesis in the mouse dentate gyrus (van Praag et al, 1999), to facilitate recovery from spinal cord injury (Barbeau et al, 1998;Edgerton et al, 2004), to increase growth factor expression (Gomez-Pinilla et al, 2002), and to regulate expression of cell adhesion molecules such as L1 (Itoh et al, 1997;Macias et al, 2002). However, the present study did not detect a change in L1 expression following exercise, …”

Section: Effect Of Exercise On L1 Expressioncontrasting

confidence: 88%

“…After a complete spinal transection in neonatal rats L1 expression is upregulated above and below the lesion and continues to be expressed on corticospinal tract axons two months after injury (Kubasak et al, 2005). In addition to its proposed role in axon growth and regeneration, Macias et al (2002) suggested that exercise increases the levels of L1 mRNA expression in adult animals.…”

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L1 CAM expression in the superficial dorsal horn is derived from the dorsal root ganglion

et al. 2005

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The cell adhesion molecule L1 is highly expressed on embryonic axons and may play a role in axonal outgrowth and fasciculation. Generally only low levels of L1 are found in adult spinal cord except for intense labeling in Lissauer's tract, in laminae I-II, and on dorsolateral funicular axons. In this study we determine the source of L1 immunoreactivity in the dorsal spinal cord, the presence of L1 expression on sprouting axons, and the effect of exercise on L1 expression. We determined the source of L1 immunoreactivity in the superficial dorsal horn by performing acute unilateral rhizotomies (T12-L4) in adult rats. This resulted in a marked decrease in L1 expression in Lissauer's tract and laminae I-II on the deafferented side. The peptidergic and nonpeptidergic small-diameter primary afferent markers, calcitonin gene-related peptide (CGRP) and the lectin IB4 respectively, closely correlated with L1 expression and also decreased dramatically after rhizotomy. Considering its developmental role, we asked whether L1 was expressed on sprouting axons following chronic rhizotomy. L1 and CGRP, but not IB4, were detected on sprouting axons. Lastly, we investigated the effect of exercise on L1 expression by giving animals with chronic rhizotomies free access to an exercise wheel. After extensive exercise, L1, CGRP, and IB4 expression levels were unchanged compared with those of sedentary chronic animals. Combined, these data demonstrate that the dorsal root ganglia is a major source of L1-positive axons in the superficial dorsal horn, that both L1 and CGRP identify sprouting axons following rhizotomy, and that exercise does not upregulate L1 expression.

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Section: E-h) and Ib4 (I-l) A-dcontrasting

confidence: 99%

Section: Effect Of Exercise On L1 Expressioncontrasting

confidence: 88%

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confidence: 99%

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L1 CAM expression in the superficial dorsal horn is derived from the dorsal root ganglion

et al. 2005

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“…Images were captured on a Leica DM5000B epifluorescence microscope using nonoverlapping ET series filters (Chroma Technology). For in situ hybridization to detect ALCAM or L1 mRNA, sense and antisense probes were generated from psBluescript SK plasmid containing mouse L1 cDNA (Macias et al, 2002) or a 900 bp fragment of mouse ALCAM cDNA (Weiner et al, 2004), and hybridization was performed using digoxigenin-labeled probes as described previously (Bartsch et al, 1994;Garrett and Weiner, 2009).…”

Section: Methodsmentioning

confidence: 99%

ALCAM Regulates Mediolateral Retinotopic Mapping in the Superior Colliculus

Buhusi

Demyanenko²,

Jannie

et al. 2009

J. Neurosci.

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“…Macias et al [180] showed that rats exposed to long-term moderate locomotor exercise, in addition to showing enhanced levels of BDNF, also presented increased expression of both adhesion molecules, as evaluated in the spinal gray matter. Further studies are needed to establish if similar increases can also be found in specific brain regions.…”

Section: Clinical Evidencementioning

confidence: 99%

A Model for the Involvement of Neural Cell Adhesion Molecules in Stress-Related Mood Disorders

Sandi

Bisaz²

2007

Neuroendocrinology

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Critical interactions between genetic and environmental factors – among which stress is one of the most potent non-genomic factors – are involved in the development of mood disorders. Intensive work during the past decade has led to the proposal of the network hypothesis of depression [Castren E: Nat Rev Neurosci 2005;6:241–246]. In contrast to the earlier chemical hypothesis of depression that emphasized neurochemical imbalance as the cause of depression, the network hypothesis proposes that problems in information processing within relevant neural networks might underlie mood disorders. Clinical and preclinical evidence supporting this hypothesis are mainly based on observations from depressed patients and animal stress models indicating atrophy (with basic research pointing at structural remodeling and decreased neurogenesis as underlying mechanisms) and malfunctioning of the hippocampus and prefrontal cortex, as well as the ability of antidepressant treatments to have the opposite effects. A great research effort is devoted to identify the molecular mechanisms that are responsible for the network effects of depression and antidepressant actions, with a great deal of evidence pointing at a key role of neurotrophins (notably the brain-derived neurotrophic factor) and other growth factors. In this review, we present evidence that implicates alterations in the levels of the neural cell adhesion molecules of the immunoglobulin superfamily, NCAM and L1, among the mechanisms contributing to stress-related mood disorders and, potentially, in antidepressant action.

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Exercise increases mRNA levels for adhesion molecules N-CAM and L1 correlating with BDNF response

Cited by 23 publications

References 24 publications

L1 CAM expression in the superficial dorsal horn is derived from the dorsal root ganglion

L1 CAM expression in the superficial dorsal horn is derived from the dorsal root ganglion

ALCAM Regulates Mediolateral Retinotopic Mapping in the Superior Colliculus

A Model for the Involvement of Neural Cell Adhesion Molecules in Stress-Related Mood Disorders

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