These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Decline of long-term potentiation (LTP) in the rat auditory cortex in vivo during postnatal life: involvement of NR2B subunits.
    Author: Hogsden JL, Dringenberg HC.
    Journal: Brain Res; 2009 Aug 04; 1283():25-33. PubMed ID: 19520065.
    Abstract:
    A decline in the ability of synapses to express plasticity and long-term potentiation (LTP) during postnatal maturation has been characterized in primary visual and somatosensory cortices. The present study is the first to document changes in the magnitude of LTP in the primary auditory cortex (A1) of rats at different stages of postnatal life. In urethane-anesthetized rats, field postsynaptic potentials (fPSPs) in A1 were elicited by stimulation of the medial geniculate nucleus, and LTP of cortical fPSPs was induced by application of repeated episodes of theta burst stimulation. Rats tested between postnatal day (PD) 30-35 showed the greatest level of LTP, with fPSP amplitude reaching approximately 165% of baseline after delivery of TBS. Levels of LTP decreased with increasing age, with approximately 140% and approximately 120% potentiation in rats aged PD 40-45 and 100-110, respectively. In rats older than 200 days, LTP could no longer be reliably induced ( approximately 105-110% potentiation). Application of an antagonist of NMDA receptor NR2B subunits (Ro 25-6981, 10 mM) in A1 reduced LTP in PD 30-35 rats to levels similar to those in adults without affecting LTP in adults (PD 100-110). Additional pharmacological experiments demonstrated a critical role of AMPA, but not NMDA, receptors in eliciting baseline, non-potentiated fPSPs in A1, an effect not significantly influenced by age. Together, these experiments demonstrate a pronounced, age-related decline in plasticity of synapses in the rodent A1, with elevated levels of plasticity in juvenile animals requiring activation of NR2B subunits, known to facilitate plasticity in other cortical and subcortical circuits.
    [Abstract] [Full Text] [Related] [New Search]