Literature DB >> 9789809

TrkA antagonists decrease NGF-induced ChAT activity in vitro and modulate cholinergic synaptic number in vivo.

T Debeir1, H U Saragovi, A C Cuello.   

Abstract

Cholinergic neurons are known to respond in vivo to the administration of nerve growth factor (NGF) by a prominent and selective increase of choline acetyl transferase activity and by cholinergic synaptogenesis in the rat brain. By using a synthetic TrkA antagonist we demonstrated that endogenously produced NGF is involved in the continual re-modeling of cholinergic neuronal connections during adulthood, acting through TrkA receptors.

Entities:  

Mesh:

Substances:

Year:  1998        PMID: 9789809     DOI: 10.1016/s0928-4257(98)80011-9

Source DB:  PubMed          Journal:  J Physiol Paris        ISSN: 0928-4257


  4 in total

1.  Activation of TrkA by nerve growth factor upregulates expression of the cholinergic gene locus but attenuates the response to ciliary neurotrophic growth factor.

Authors:  B Berse; I Lopez-Coviella; J K Blusztajn
Journal:  Biochem J       Date:  1999-09-01       Impact factor: 3.857

2.  Developmental suppression of forebrain trkA receptors and attentional capacities in aging rats: A longitudinal study.

Authors:  Brittney Yegla; Vinay Parikh
Journal:  Behav Brain Res       Date:  2017-08-10       Impact factor: 3.332

3.  Reorganization of cholinergic terminals in the cerebral cortex and hippocampus in transgenic mice carrying mutated presenilin-1 and amyloid precursor protein transgenes.

Authors:  T P Wong; T Debeir; K Duff; A C Cuello
Journal:  J Neurosci       Date:  1999-04-01       Impact factor: 6.167

4.  A new role for matrix metalloproteinase-3 in the NGF metabolic pathway: Proteolysis of mature NGF and sex-specific differences in the continuum of Alzheimer's pathology.

Authors:  Rowan Pentz; M Florencia Iulita; Maya Mikutra-Cencora; Adriana Ducatenzeiler; David A Bennett; A Claudio Cuello
Journal:  Neurobiol Dis       Date:  2020-10-30       Impact factor: 5.996

  4 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.