PMID- 10629752
OWN - NLM
STAT- MEDLINE
DCOM- 20000203
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 850
IP  - 1-2
DP  - 1999 Dec 11
TI  - Developmental exposure to a commercial PCB mixture (Aroclor 1254) produces a 
      persistent impairment in long-term potentiation in the rat dentate gyrus in vivo.
PG  - 87-95
AB  - Developmental exposure to polycholorinated biphenyls (PCBs) has been associated 
      with cognitive deficits in humans and laboratory animals. The present study 
      sought to examine synaptic plasticity in the hippocampus, a brain region critical 
      for some types of memory function, in animals exposed to PCBs early in 
      development. Pregnant Long-Evans rats were administered either corn oil (control) 
      or 6 mg/kg/day of a commercial PCB mixture, Aroclor 1254 (A1254) by gavage from 
      gestational day (GD) 6 until pups were weaned on postnatal day (PND) 21. In adult 
      male offspring (3-6 months of age), field potentials evoked by perforant path 
      stimulation were recorded in the dentate gyrus under urethane anesthesia. 
      Input/output (I/O) functions were assessed by averaging the response evoked in 
      the dentate gyrus to stimulus pulses delivered to the perforant path in an 
      ascending intensity series. Long-term potentiation (LTP) was induced by 
      delivering a series of brief high frequency (400 Hz) train bursts to the 
      perforant path at a moderate stimulus intensity and I/O functions were reassessed 
      1 h later. No differences in baseline synaptic population spike (PS) and minor 
      effects on excitatory postsynaptic potential (EPSP) slope amplitudes were 
      discerned between the groups prior to train delivery. Post-train I/O functions, 
      however, revealed a 50% decrement in the magnitude of LTP in PCB-exposed animals. 
      These data are the first to demonstrate persistent decrements in hippocampal 
      synaptic plasticity in the intact animal following developmental exposure to 
      PCBs. Disruption of early brain ontogeny due to developmental PCB exposure may 
      underlie perturbations in the neurological substrates that support synaptic 
      plasticity and contribute to deficits in LTP and learning that persist into 
      adulthood.
FAU - Gilbert, M E
AU  - Gilbert ME
AD  - Neurotoxicology Division, US Environmental Protection Agency, Research Triangle 
      Park, NC 27711, USA. gilbert.mary@epamail.epa.gov
FAU - Crofton, K M
AU  - Crofton KM
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 11097-69-1 (Chlorodiphenyl (54% Chlorine))
SB  - IM
MH  - Action Potentials/drug effects
MH  - Animals
MH  - Chlorodiphenyl (54% Chlorine)/*toxicity
MH  - Dentate Gyrus/*drug effects/growth & development
MH  - Electric Stimulation
MH  - Electrophysiology
MH  - Excitatory Postsynaptic Potentials/drug effects
MH  - Female
MH  - Long-Term Potentiation/*drug effects
MH  - Male
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects
MH  - Rats
MH  - Rats, Long-Evans
MH  - Synaptic Transmission/drug effects/physiology
EDAT- 2000/01/12 00:00
MHDA- 2000/01/12 00:01
CRDT- 2000/01/12 00:00
PHST- 2000/01/12 00:00 [pubmed]
PHST- 2000/01/12 00:01 [medline]
PHST- 2000/01/12 00:00 [entrez]
AID - S0006-8993(99)02107-1 [pii]
AID - 10.1016/s0006-8993(99)02107-1 [doi]
PST - ppublish
SO  - Brain Res. 1999 Dec 11;850(1-2):87-95. doi: 10.1016/s0006-8993(99)02107-1.