Behavioral Toxicity of Nitrous Oxide in Rats Following Prenatal Exposure

Abstract

Nitrous oxide (N2O) exposure has been associated with neurotoxicity, especially peripheral neuropathy, in both humans and animals. The effects of this anesthetic gas on the central nervous system (CNS) and spontaneous behavior, however, have yet to be delineated. Timed-pregnant Sprague-Dawley rats were exposed to 75% N2O/25% O2 on gestational days 14 and 15 or day 15 only for eight hours per day. The offspring were tested at one and five months of age; their spontaneous behavior in a novel environment was recorded in the residential maze and using time-lapse photography. The results indicated that in utero exposure to N2O permanently altered the spontaneous motor output of the CNS. This effect was most prominent in 5 month old animals, and females were affected more than males. Exposures on gestational days 14 and 15 produced an effect that was not only greater but also qualitatively different than that produced by exposure on day 15 only. The two-day exposure induced hyperactivity in both sexes, whereas the one-day exposure induced hyperactivity in the males and slight hypoactivity in the females. These behavioral changes were not accompanied by physical abnormalities but nonetheless were lasting effects in need of further consideration.

Glyphosate Use Predicts ADHD Hospital Discharges in the Healthcare Cost and Utilization Project Net (HCUPnet): A Two-Way Fixed-Effects Analysis

“…That is to say that many of the behavioral phenotypes that are noted in ASD, including anxiety, hyperactivity, stereotypical compulsivity and compromised social interactions, may arise out of a compensating, homeostatic preference to curtail the dominating parasympathetic influences and may not be explicitly indicative of any genuine etiological link to the disorder. A few animal studies on the effect of prenatal N 2 O exposure indicate behavioral differences, although care should be taken to avoid direct human ASD comparisons [ 112 , 113 ].…”

Effects of sevoflurane on primary neuronal cultures of embryonic rats

“…Furthermore, ketamine at nonapoptotic concentrations can impair dendritic arbor development of GABAergic neurons as shown for cultured rat neurons [17]. Another substance that acts mainly via the inhibition of the NMDA receptors, nitrous oxide [18], showed the induction of behavioural changes as well as neurodegenerative effects in different in-vivo settings [19,20].…”

L’anesthésie a-t-elle un impact sur le développement cérébral ?

“…Des expériences récentes montrent que même une exposition modérée à la kétamine , antagoniste non compétitif du récepteur NMDA, pourrait provoquer une apoptose dans le cerveau de souriceaux âgés de 7 jours, et cela dès la 4 e heure suivant une injection unique de kétamine à des doses anesthésiques et sous-anesthésiques [14]. En accord avec les résultats obtenus après l'administration de kétamine, il est maintenant prouvé qu'une exposition de 3 heures au protoxyde d'azote (N2O), un antagoniste puissant des récepteurs glutamatergiques de type NMDA, peut aussi provoquer l'apoptose dans le cerveau en développement [15]. Des effets similaires ont été obtenus en exposant les jeunes rongeurs au midazolam, un potentialisateur du système GABAergique [14] ou au propofol [16].…”