Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form
As of April 1st VIVO Scientific Profiles will no longer updated for faculty, and the link to VIVO will be removed from the library website. Faculty profile pages will continue to be updated via Interfolio. VIVO will continue being used behind the scenes to update graduate student profiles. Please contact helplib@scripps.edu if you have questions.
How to download citations from VIVO | Alternative profile options

The role of brain-derived neurotrophic factor receptors in the mature hippocampus: modulation of long-term potentiation through a presynaptic mechanism involving TrkB

Academic Article
uri icon
  • Overview
  • Research
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Xu, Baoji
  • Gottschalk, W.
  • Chow, A.
  • Wilson, R. I.
  • Schnell, E.
  • Zang, K.
  • Wang, D.
  • Nicoll, R. A.
  • Lu, B.
  • Reichardt, L. F.

publication date

  • September 2000

journal

  • Journal of Neuroscience  Journal

abstract

  • The neurotrophin BDNF has been shown to modulate long-term potentiation (LTP) at Schaffer collateral-CA1 hippocampal synapses. Mutants in the BDNF receptor gene trkB and antibodies to its second receptor p75NTR have been used to determine the receptors and cells involved in this response. Inhibition of p75NTR does not detectably reduce LTP or affect presynaptic function, but analyses of newly generated trkB mutants implicate TrkB. One mutant has reduced expression in a normal pattern of TrkB throughout the brain. The second mutant was created by cre-loxP-mediated removal of TrkB in CA1 pyramidal neurons of this mouse. Neither mutant detectably impacts survival or morphology of hippocampal neurons. TrkB reduction, however, affects presynaptic function and reduces the ability of tetanic stimulation to induce LTP. Postsynaptic glutamate receptors are not affected by TrkB reduction, indicating that BDNF does not modulate plasticity through postsynaptic TrkB. Consistent with this, elimination of TrkB in postsynaptic neurons does not affect LTP. Moreover, normal LTP is generated in the mutant with reduced TrkB by a depolarization-low-frequency stimulation pairing protocol that puts minimal demands on presynaptic terminal function. Thus, BDNF appears to act through TrkB presynaptically, but not postsynaptically, to modulate LTP.

subject areas

  • Animals
  • Antigens, Differentiation
  • Axons
  • Brain-Derived Neurotrophic Factor
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Hippocampus
  • In Vitro Techniques
  • Long-Term Potentiation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Neuronal Plasticity
  • Patch-Clamp Techniques
  • Presynaptic Terminals
  • Pyramidal Cells
  • RNA, Messenger
  • Receptor, Nerve Growth Factor
  • Receptor, trkB
  • Receptors, Glutamate
  • Signal Transduction
  • Stem Cells
scroll to property group menus

Research

keywords

  • CA1
  • TrkB
  • conditional mutant
  • long-term potentiation
  • neuronal survival
  • presynaptic
scroll to property group menus

Identity

PubMed Central ID

  • PMC2711895

International Standard Serial Number (ISSN)

  • 0270-6474

PubMed ID

  • 10995833
scroll to property group menus

Additional Document Info

start page

  • 6888

end page

  • 6897

volume

  • 20

issue

  • 18

©2022 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support