Perinatal diazepam exposure

Behavioral and neurochemical consequences

Julie A. Lauer, Perrie M. Adams, Kenneth M. Johnson

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

In the present study the effects of perinatal diazepam (DZP) exposure on behavior and benzodiazepine binding site characteristics in offspring were investigated. Pregnant F344 rats were treated during the last trimester of gestation with vehicle or diazepam (3 mg/kg, 5 mg/kg, or 10 mg/kg). Lactating dams were similarly treated on postnatal days 1-7. Both prenatal and postnatal exposure to diazepam resulted in significant effects on the acquisition and extinction of active avoidance behavior measured postweaning. The number of trials to extinction of one-way active avoidance behavior was significantly greater in offspring exposed gestationally to 3 mg/kg and 10 mg/kg diazepam and postnatally to 10 mg/kg diazepam. The mean response latencies for all diazepam treated groups were significantly shorter than those of the vehicle treated rats during the first 15 trials under extinction conditions. In contrast, neither gestational nor postnatal diazepam exposure significantly affected either acquisition or retention of a passive avoidance task. In addition, the binding affinity between the benzodiazepine type I selective ligand, CL218,872, and cortical membranes, as well as the degree to which GABA potentiated 3H-flunitrazepam were significantly altered by perinatal diazepam exposure. No treatment altered the approximate number of benzodiazepine binding sites in either the cortex, hippocampus, or cerebellum. The results of this study further support diazepam as a behavioral teratogen and give new evidence for neurochemical effects following gestational as well as postnatal diazepam exposure.

Original languageEnglish (US)
Pages (from-to)213-219
Number of pages7
JournalNeurotoxicology and Teratology
Volume9
Issue number3
DOIs
StatePublished - 1987

Fingerprint

Diazepam
Benzodiazepines
Avoidance Learning
Rats
Binding Sites
Teratogens
Flunitrazepam
Inbred F344 Rats
Third Pregnancy Trimester
Cerebellum
gamma-Aminobutyric Acid
Dams
Reaction Time
Hippocampus
Ligands
Membranes
Pregnancy

Keywords

  • Active avoidance
  • Benzodiazepine binding site
  • Diazepam
  • Passive avoidance
  • Perinatal exposure
  • Postnatal exposure

ASJC Scopus subject areas

  • Neuroscience(all)
  • Cellular and Molecular Neuroscience
  • Toxicology

Cite this

Perinatal diazepam exposure : Behavioral and neurochemical consequences. / Lauer, Julie A.; Adams, Perrie M.; Johnson, Kenneth M.

In: Neurotoxicology and Teratology, Vol. 9, No. 3, 1987, p. 213-219.

Research output: Contribution to journalArticle

Lauer, Julie A. ; Adams, Perrie M. ; Johnson, Kenneth M. / Perinatal diazepam exposure : Behavioral and neurochemical consequences. In: Neurotoxicology and Teratology. 1987 ; Vol. 9, No. 3. pp. 213-219.
@article{5b08206b30914957a21e14e9583b3cd5,
title = "Perinatal diazepam exposure: Behavioral and neurochemical consequences",
abstract = "In the present study the effects of perinatal diazepam (DZP) exposure on behavior and benzodiazepine binding site characteristics in offspring were investigated. Pregnant F344 rats were treated during the last trimester of gestation with vehicle or diazepam (3 mg/kg, 5 mg/kg, or 10 mg/kg). Lactating dams were similarly treated on postnatal days 1-7. Both prenatal and postnatal exposure to diazepam resulted in significant effects on the acquisition and extinction of active avoidance behavior measured postweaning. The number of trials to extinction of one-way active avoidance behavior was significantly greater in offspring exposed gestationally to 3 mg/kg and 10 mg/kg diazepam and postnatally to 10 mg/kg diazepam. The mean response latencies for all diazepam treated groups were significantly shorter than those of the vehicle treated rats during the first 15 trials under extinction conditions. In contrast, neither gestational nor postnatal diazepam exposure significantly affected either acquisition or retention of a passive avoidance task. In addition, the binding affinity between the benzodiazepine type I selective ligand, CL218,872, and cortical membranes, as well as the degree to which GABA potentiated 3H-flunitrazepam were significantly altered by perinatal diazepam exposure. No treatment altered the approximate number of benzodiazepine binding sites in either the cortex, hippocampus, or cerebellum. The results of this study further support diazepam as a behavioral teratogen and give new evidence for neurochemical effects following gestational as well as postnatal diazepam exposure.",
keywords = "Active avoidance, Benzodiazepine binding site, Diazepam, Passive avoidance, Perinatal exposure, Postnatal exposure",
author = "Lauer, {Julie A.} and Adams, {Perrie M.} and Johnson, {Kenneth M.}",
year = "1987",
doi = "10.1016/0892-0362(87)90005-5",
language = "English (US)",
volume = "9",
pages = "213--219",
journal = "Neurotoxicology and Teratology",
issn = "0892-0362",
publisher = "Elsevier Inc.",
number = "3",

}

TY - JOUR

T1 - Perinatal diazepam exposure

T2 - Behavioral and neurochemical consequences

AU - Lauer, Julie A.

AU - Adams, Perrie M.

AU - Johnson, Kenneth M.

PY - 1987

Y1 - 1987

N2 - In the present study the effects of perinatal diazepam (DZP) exposure on behavior and benzodiazepine binding site characteristics in offspring were investigated. Pregnant F344 rats were treated during the last trimester of gestation with vehicle or diazepam (3 mg/kg, 5 mg/kg, or 10 mg/kg). Lactating dams were similarly treated on postnatal days 1-7. Both prenatal and postnatal exposure to diazepam resulted in significant effects on the acquisition and extinction of active avoidance behavior measured postweaning. The number of trials to extinction of one-way active avoidance behavior was significantly greater in offspring exposed gestationally to 3 mg/kg and 10 mg/kg diazepam and postnatally to 10 mg/kg diazepam. The mean response latencies for all diazepam treated groups were significantly shorter than those of the vehicle treated rats during the first 15 trials under extinction conditions. In contrast, neither gestational nor postnatal diazepam exposure significantly affected either acquisition or retention of a passive avoidance task. In addition, the binding affinity between the benzodiazepine type I selective ligand, CL218,872, and cortical membranes, as well as the degree to which GABA potentiated 3H-flunitrazepam were significantly altered by perinatal diazepam exposure. No treatment altered the approximate number of benzodiazepine binding sites in either the cortex, hippocampus, or cerebellum. The results of this study further support diazepam as a behavioral teratogen and give new evidence for neurochemical effects following gestational as well as postnatal diazepam exposure.

AB - In the present study the effects of perinatal diazepam (DZP) exposure on behavior and benzodiazepine binding site characteristics in offspring were investigated. Pregnant F344 rats were treated during the last trimester of gestation with vehicle or diazepam (3 mg/kg, 5 mg/kg, or 10 mg/kg). Lactating dams were similarly treated on postnatal days 1-7. Both prenatal and postnatal exposure to diazepam resulted in significant effects on the acquisition and extinction of active avoidance behavior measured postweaning. The number of trials to extinction of one-way active avoidance behavior was significantly greater in offspring exposed gestationally to 3 mg/kg and 10 mg/kg diazepam and postnatally to 10 mg/kg diazepam. The mean response latencies for all diazepam treated groups were significantly shorter than those of the vehicle treated rats during the first 15 trials under extinction conditions. In contrast, neither gestational nor postnatal diazepam exposure significantly affected either acquisition or retention of a passive avoidance task. In addition, the binding affinity between the benzodiazepine type I selective ligand, CL218,872, and cortical membranes, as well as the degree to which GABA potentiated 3H-flunitrazepam were significantly altered by perinatal diazepam exposure. No treatment altered the approximate number of benzodiazepine binding sites in either the cortex, hippocampus, or cerebellum. The results of this study further support diazepam as a behavioral teratogen and give new evidence for neurochemical effects following gestational as well as postnatal diazepam exposure.

KW - Active avoidance

KW - Benzodiazepine binding site

KW - Diazepam

KW - Passive avoidance

KW - Perinatal exposure

KW - Postnatal exposure

UR - http://www.scopus.com/inward/record.url?scp=2642711109&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=2642711109&partnerID=8YFLogxK

U2 - 10.1016/0892-0362(87)90005-5

DO - 10.1016/0892-0362(87)90005-5

M3 - Article

VL - 9

SP - 213

EP - 219

JO - Neurotoxicology and Teratology

JF - Neurotoxicology and Teratology

SN - 0892-0362

IS - 3

ER -