PMID- 9425202
OWN - NLM
STAT- MEDLINE
DCOM- 19980218
LR  - 20171213
IS  - 0022-3077 (Print)
IS  - 0022-3077 (Linking)
VI  - 79
IP  - 1
DP  - 1998 Jan
TI  - Aging differentially alters forms of long-term potentiation in rat hippocampal 
      area CA1.
PG  - 334-41
AB  - Long-term potentiation (LTP) of the Schaffer collateral/commissural inputs to CA1 
      in the hippocampus was shown to consist of N-methyl-D-aspartate receptor (NMDAR) 
      and voltage-dependent calcium channel (VDCC) dependent forms. In this study, the 
      relative contributions of these two forms of LTP in in vitro hippocampal slices 
      from young (2 mo) and old (24 mo) Fischer 344 rats were examined. Excitatory 
      postsynaptic potentials (EPSP) were recorded extracellularly from stratum 
      radiatum before and after a tetanic stimulus consisting of four 200-Hz, 0.5-s 
      trains given 5 s apart. Under control conditions, a compound LTP consisting of 
      both forms was induced and was similar, in both time course and magnitude, in 
      young and old animals. NMDAR-dependent LTP (nmdaLTP), isolated by the application 
      of 10 microM nifedipine (a voltage-dependent calcium channel blocker), was 
      significantly reduced in magnitude in aged animals. The VDCC dependent form 
      (vdccLTP), isolated by the application of 50 microM 
      D,L-2-amino-5-phosphonvalerate (APV), was significantly larger in aged animals. 
      Although both LTP forms reached stable values 40-60 min posttetanus in young 
      animals, in aged animals vdccLTP increased and nmdaLTP decreased during this 
      time. In both young and old animals, the sum of the two isolated LTP forms 
      approximated the magnitude of the compound LTP, and application of APV and 
      nifedipine or genestein (a tyrosine kinase inhibitor) together blocked 
      potentiation. These results suggest that aging causes a shift in synaptic 
      plasticity from NMDAR-dependent mechanisms to VDCC-dependent mechanisms. The data 
      are consistent with previous findings of increased L-type calcium current and 
      decreased NMDAR number in aged CA1 cells and may help explain age-related 
      deficits in learning and memory.
FAU - Shankar, S
AU  - Shankar S
AD  - Department of Neuroscience, Case Western Reserve University School of Medicine, 
      Cleveland 44106, USA.
FAU - Teyler, T J
AU  - Teyler TJ
FAU - Robbins, N
AU  - Robbins N
LA  - eng
GR  - AG-00105-08/AG/NIA NIH HHS/United States
GR  - AG-08886/AG/NIA NIH HHS/United States
GR  - NS-28698/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
RN  - 0 (Calcium Channels)
RN  - 0 (Calcium Channels, N-Type)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (voltage-dependent calcium channel (P-Q type))
RN  - 76726-92-6 (2-Amino-5-phosphonovalerate)
RN  - DH2M523P0H (Genistein)
RN  - I9ZF7L6G2L (Nifedipine)
SB  - IM
MH  - 2-Amino-5-phosphonovalerate/pharmacology
MH  - Aging/*physiology
MH  - Animals
MH  - Calcium Channels/physiology
MH  - *Calcium Channels, N-Type
MH  - Electric Stimulation
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - Genistein/pharmacology
MH  - Hippocampus/growth & development/*physiology
MH  - In Vitro Techniques
MH  - Long-Term Potentiation/drug effects/*physiology
MH  - Male
MH  - Nifedipine/pharmacology
MH  - Pyramidal Cells/drug effects/*physiology
MH  - Rats
MH  - Rats, Inbred F344
MH  - Reaction Time
MH  - Receptors, N-Methyl-D-Aspartate/physiology
EDAT- 1998/02/21 00:00
MHDA- 1998/02/21 00:01
CRDT- 1998/02/21 00:00
PHST- 1998/02/21 00:00 [pubmed]
PHST- 1998/02/21 00:01 [medline]
PHST- 1998/02/21 00:00 [entrez]
AID - 10.1152/jn.1998.79.1.334 [doi]
PST - ppublish
SO  - J Neurophysiol. 1998 Jan;79(1):334-41. doi: 10.1152/jn.1998.79.1.334.