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Alterations in trkB mRNA in the human prefrontal cortex throughout the lifespan
Author(s) -
Romanczyk T. B.,
Weickert C. Shan,
Webster M. J.,
Herman M. M.,
Akil M.,
Kleinman J. E.
Publication year - 2002
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.0953-816x.2001.01858.x
Subject(s) - tropomyosin receptor kinase b , tropomyosin receptor kinase a , neocortex , neurotrophin , biology , prefrontal cortex , dorsolateral prefrontal cortex , brain derived neurotrophic factor , neuroscience , tropomyosin receptor kinase c , in situ hybridization , neurotrophic factors , messenger rna , receptor , gene , genetics , growth factor , cognition , platelet derived growth factor receptor
Signalling through tyrosine kinase receptor B (trkB) influences neuronal survival, differentiation and synaptogenesis. trkB exists in a full‐length form (trkB TK+ ), which contains a catalytic tyrosine kinase (TK) domain, and a truncated form (trkB TK– ), which lacks this domain. In the rodent brain, expression of trkB TK+ decreases and trkB TK– increases during postnatal life. We hypothesized that both forms of trkB receptor mRNA would be present in the human neocortex and that the developmental profile of trkB gene expression in human may be distinct from that in rodent. We detected both trkB TK+ and trkB TK– mRNA in RNA extracted from multiple human brain regions by Northern blot. Using in situ hybridization, we found trkB TK+ mRNA in all cortical layers, with highest expression in layer IV and intermediate‐to‐high expression in layers III and V of the human dorsolateral prefrontal cortex. trkB TK+ mRNA was present in neurons with both pyramidal and nonpyramidal shapes in the dorsolateral prefrontal cortex. trkB TK+ mRNA levels were significantly increased in layer III in young adults as compared with infants and the elderly. In the elderly, trkB TK+ mRNA levels were reduced markedly in all cortical layers. Unlike the mRNA encoding the full‐length form of trkB, trkB TK– mRNA was distributed homogeneously across the grey matter, and trkB TK– mRNA levels increased only slightly during postnatal life. The results suggest that neurons in the human dorsolateral prefrontal cortex are responsive to neurotrophins throughout postnatal life and that this responsiveness may be modulated during the human lifespan.