PMID- 9882020
OWN - NLM
STAT- MEDLINE
DCOM- 19990322
LR  - 20190116
IS  - 1050-9631 (Print)
IS  - 1050-9631 (Linking)
VI  - 8
IP  - 6
DP  - 1998
TI  - Alteration of NMDA receptor-mediated synaptic responses in CA1 area of the aged 
      rat hippocampus: contribution of GABAergic and cholinergic deficits.
PG  - 627-37
AB  - Synaptic responses mediated by the N-methyl-D-aspartate receptor (NMDAr) and 
      non-NMDAr activation were compared in CA1 hippocampal region of young (3-4 months 
      old) and aged (25-33 months old) Sprague-Dawley rats with the use of ex vivo 
      extracellular recordings techniques. In aged rats, the amplitude of the 
      NMDAr-mediated field excitatory postsynaptic potentials (fEPSPs) was not altered, 
      whereas their duration was significantly increased. In contrast, the magnitude of 
      non-NMDAr-mediated fEPSPs was significantly smaller. The presynaptic fiber volley 
      was not affected by age. Considering that the depression of non-NMDAr-mediated 
      responses was previously attributed to fewer synaptic contacts between 
      glutamatergic afferent fibers and pyramidal cells in aged animals (see Barnes et 
      al., Hippocampus 1992;2:457-468), the absence of age-related changes in the 
      amplitude of NMDAr-mediated fEPSPs suggests that compensatory mechanisms may 
      occur. The contribution of gamma-aminobutyric acid (GABA) and acetylcholine to 
      these mechanisms was addressed. The NMDAr-mediated fEPSPs were then recorded (1) 
      in young and aged rats before and after blockade of the GABA(B) receptor-mediated 
      inhibition by the specific antagonist CGP 55845 and (2) in young rats after a 
      selective cholinergic denervation of the hippocampus by the immunotoxin 192 
      IgG-saporin. The results did not indicate statistically relevant age-related 
      effects of CGP 55845. In contrast, the loss of the cholinergic innervation by the 
      immunotoxin induced a significant increase in both the amplitude and duration of 
      the NMDAr-mediated fEPSPs. Our results indicate that the functional properties of 
      the ionotropic glutamate receptor subtypes located on CA1 pyramidal cells are 
      differentially affected by aging and suggest that the cholinergic deficit that 
      occurs during aging may be involved in the maintenance of robust NMDAr-mediated 
      synaptic responses.
FAU - Jouvenceau, A
AU  - Jouvenceau A
AD  - Laboratoire de Physiopharmacologie du Systeme Nerveux, Paris, France.
FAU - Dutar, P
AU  - Dutar P
FAU - Billard, J M
AU  - Billard JM
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Hippocampus
JT  - Hippocampus
JID - 9108167
RN  - 0 (192 IgG-saporin)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Cholinergic Agents)
RN  - 0 (GABA-B Receptor Antagonists)
RN  - 0 (Immunotoxins)
RN  - 0 (Phosphinic Acids)
RN  - 0 (Propanolamines)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (Ribosome Inactivating Proteins, Type 1)
RN  - 148056-42-2 (CGP 55845A)
RN  - 56-12-2 (gamma-Aminobutyric Acid)
RN  - EC 3.2.2.- (N-Glycosyl Hydrolases)
RN  - EC 3.2.2.22 (Saporins)
RN  - N9YNS0M02X (Acetylcholine)
SB  - IM
MH  - Acetylcholine/*physiology
MH  - Aging/*physiology
MH  - Animals
MH  - Antibodies, Monoclonal/toxicity
MH  - Cholinergic Agents/toxicity
MH  - Denervation
MH  - Excitatory Postsynaptic Potentials/drug effects/physiology
MH  - GABA-B Receptor Antagonists
MH  - Hippocampus/drug effects/growth & development/*physiology
MH  - Immunotoxins/toxicity
MH  - Male
MH  - N-Glycosyl Hydrolases
MH  - Nerve Fibers/drug effects/physiology
MH  - Phosphinic Acids/*pharmacology
MH  - Presynaptic Terminals/drug effects/*physiology
MH  - Propanolamines/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, N-Methyl-D-Aspartate/*physiology
MH  - Ribosome Inactivating Proteins, Type 1
MH  - Saporins
MH  - Synapses/drug effects/*physiology
MH  - gamma-Aminobutyric Acid/*physiology
EDAT- 1999/01/09 00:00
MHDA- 1999/01/09 00:01
CRDT- 1999/01/09 00:00
PHST- 1999/01/09 00:00 [pubmed]
PHST- 1999/01/09 00:01 [medline]
PHST- 1999/01/09 00:00 [entrez]
AID - 10.1002/(SICI)1098-1063(1998)8:6<627::AID-HIPO5>3.0.CO;2-X [doi]
PST - ppublish
SO  - Hippocampus. 1998;8(6):627-37. doi: 
      10.1002/(SICI)1098-1063(1998)8:6<627::AID-HIPO5>3.0.CO;2-X.