Prenatal exposure to diazepam results in enduring reductions in brain receptors and deep slow wave sleep

  title={Prenatal exposure to diazepam results in enduring reductions in brain receptors and deep slow wave sleep},
  author={G. T. Livezey and Miodrag Radulova{\vc}ki and Lawrence Isaac and Thaddeus J. Marczynski},
  journal={Brain Research},

Prenatal Diazepam Exposure Functionally Alters the GABAA Receptor That Modulates [3H]Noradrenaline Release from Rat Hippocampal Synaptosomes

It is demonstrated that prenatal exposure to DZ produces functional modifications of the GABAA receptor subtype, which is located on hippocampal noradrenergic nerve endings and mediates the release of NA, which may be related to the relative contributions of the various protein subunits that compose the G ABAA receptor complex.

Prenatal Diazepam Exposure Affects β‐Adrenergic Receptors in Brain Regions of Adult Rat Offspring

The permanent reduction in number of β‐adrenergic receptors, which depends on the scaling and duration of the drug application period, points to the necessity of a prolonged evaluation of effects of exposure to psychotropic drugs in early stages of brain development.



A benzodiazepine receptor antagonist decreases sleep and reverses the hypnotic actions of flurazepam.

3-hydroxymethyl-beta-carboline blocks sleep induction by a large dose of flurazepam, suggesting that the benzodiazepine receptor may play a role in both the physiological regulation and pharmacological induction of sleep.

Adenosine analogs and sleep in rats.

The results indicate that the effect on sleep of all three adenosine analogs was obtained with nanomolar doses of the drugs and that it diminished or disappeared when the drug dose reached micromolar range (0.9 mumol/kg); it appears, therefore, that activation of A1 rather than A2 receptors contributed to the sleep effects of the Drugs.

beta-Carbolines enhance shock-induced suppression of drinking in rats.

Pentylenetetrazole, which causes convulsions by interacting with a subunit of the gamma-aminobutyric acid receptor that is different from the benzodiazepine recognition site, induces a proconflict action that is antagonized by anxiolytic Benzodiazepines but not by RO 15-1788.

Characterization of the Binding of [3H]Ro 5‐4864, a Convulsant Benzodiazepine, to Guinea Pig Brain

The high density of binding sites for [3H]Ro 5‐4864, coupled with the potency of this compound as a convulsant in the guinea pig, suggest this species will be a valuable model for elucidating putative pharmacologic and physiologic functions of these sites in brain.