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Effects of acetyl- l-carnitine treatment and stress exposure on the nerve growth factor receptor (p75 NGFR) mRNA level in the central nervous system of aged rats
1. 1. There is growing evidence that the nerve growth factor protein (NGF), a neurotrophic factor for peripheral and central nervous system (CNS) neurons, may play a role in the modulation of the hypothalamo-pituitary-adrenocortical axis (HPAA). While NGF binding is decreased in rodent CNS after str...
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Published in: | Progress in neuro-psychopharmacology & biological psychiatry 1995, Vol.19 (1), p.117-133 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 1.
1. There is growing evidence that the nerve growth factor protein (NGF), a neurotrophic factor for peripheral and central nervous system (CNS) neurons, may play a role in the modulation of the hypothalamo-pituitary-adrenocortical axis (HPAA). While NGF binding is decreased in rodent CNS after stress exposure, this reduction is prevented by treatment with Acetyl-L-Carnitine (ALCAR), a chemical substance able to prevent some degenerative events associated with aging.
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2. The authors studied the effect of cold stress on the low-affinity NGF receptor (p75
NGFR) mRNA levels in the basal forebrain and cerebellum of aged rats chronically treated with ALCAR.
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3. The present results show that ALCAR abolished the age-associated reduction of p75
NGFR mRNA levels in the basal forebrain of old animals, but did not affect the response to stress stimuli.
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4. Also, treatment with ALCAR mantained p75
NGFR mRNA levels in the cerebellum of old animals at levels almost identical to those observed in young control animals.
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5. These results suggest a neuroprotective effect for ALCAR on central cholinergic neurons exerted at the level of transcription of p75
NGFR. The restoration of p75
NGFR levels could increase trophic support by NGF of these CNS cholinergic neurons which are implicated in degenerative events associated with aging. |
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ISSN: | 0278-5846 1878-4216 |
DOI: | 10.1016/0278-5846(94)00109-U |