PMID- 14637380
OWN - NLM
STAT- MEDLINE
DCOM- 20040130
LR  - 20131121
IS  - 0161-813X (Print)
IS  - 0161-813X (Linking)
VI  - 24
IP  - 6
DP  - 2003 Dec
TI  - Perinatal exposure to polychlorinated biphenyls alters excitatory synaptic 
      transmission and short-term plasticity in the hippocampus of the adult rat.
PG  - 851-60
AB  - Developmental exposure to polychlorinated biphenyls (PCBs) has been associated 
      with cognitive deficits in humans and laboratory animals. Previous work has 
      demonstrated a reduced capacity to support long-term potentiation (LTP) in 
      animals exposed to a PCB mixture, Aroclor 1254 (A1254) via the dam in utero and 
      throughout the preweaning period [Brain Res. 850;1999:87-95; Toxicol. Sci. 
      57;2000:102-11]. Assessment of normalized input/output (I/O) functions collected 
      prior to LTP induction failed to reveal consistent differences in baseline 
      synaptic transmission between control and PCB-exposed groups. The present study 
      was designed to systematically evaluate excitatory and inhibitory synaptic 
      transmission using a more extensive I/O analysis and paired pulse functions to 
      assess short-term plasticity. Pregnant Long-Evans rats were administered either 
      corn oil (control) or 6 mg/kg per day of A1254 by gavage from gestational day 
      (GD) 6 until pups were weaned on postnatal day (PND) 21. In adult male offspring 
      (5-11 months of age), field potentials evoked by perforant path stimulation were 
      recorded in the dentate gyrus under urethane anesthesia. Detailed I/O functions 
      were assessed by averaging the responses evoked in the dentate gyrus to stimulus 
      pulses delivered to the perforant path in an extensive ascending intensity 
      series. Population spike (PS) and postsynaptic potential (PSP) amplitudes 
      recorded in the dentate gyrus were significantly enhanced in PCB-exposed animals 
      relative to controls at midrange intensities. No group differences were observed 
      in EPSP slope amplitudes. Short-term plasticity was assessed by delivering pairs 
      of stimulus pulses at interpulse intervals (IPIs) ranging from 10 to 70 ms. In 
      the dentate gyrus this range of intervals activates both inhibitory and 
      excitatory mechanisms leading to a pattern of depression at brief intervals (<30 
      ms) followed by facilitation as the interval between pulses is extended. Paired 
      pulse depression was decreased at an intermediate IPI (30 ms) with submaximal 
      stimulus intensities. These data augment previous work demonstrating persistent 
      changes in hippocampal plasticity as a result of exposure to PCBs during 
      development. Furthermore, as increases in field potential amplitudes were 
      observed, these findings support previous conclusions that A1254-induced LTP 
      deficits are not readily attributable to reductions in synaptic excitability. 
      Thus, in addition to impairment in use-dependent synaptic plasticity reported 
      previously, the present report reveals that basic components of information 
      processing within the hippocampus are permanently altered as a result of 
      perinatal exposure to PCBs.
FAU - Gilbert, M E
AU  - Gilbert ME
AD  - Neurotoxicology Division (B105-05), National Health and Environmental Effects 
      Research Laboratory, US Environmental Protection Agency, Research Triangle Park, 
      NC 27711, USA. gilbert.mary@epamail.epa.gov
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - Netherlands
TA  - Neurotoxicology
JT  - Neurotoxicology
JID - 7905589
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Animals
MH  - Excitatory Postsynaptic Potentials/*drug effects/physiology
MH  - Female
MH  - Hippocampus/*drug effects/embryology/growth & development
MH  - Male
MH  - Neuronal Plasticity/*drug effects/physiology
MH  - Polychlorinated Biphenyls/*toxicity
MH  - Pregnancy
MH  - *Prenatal Exposure Delayed Effects
MH  - Rats
MH  - Rats, Long-Evans
MH  - Synaptic Transmission/*drug effects/physiology
EDAT- 2003/11/26 05:00
MHDA- 2004/01/31 05:00
CRDT- 2003/11/26 05:00
PHST- 2003/11/26 05:00 [pubmed]
PHST- 2004/01/31 05:00 [medline]
PHST- 2003/11/26 05:00 [entrez]
AID - S0161-813X(03)00073-1 [pii]
AID - 10.1016/S0161-813X(03)00073-1 [doi]
PST - ppublish
SO  - Neurotoxicology. 2003 Dec;24(6):851-60. doi: 10.1016/S0161-813X(03)00073-1.