Long-Term Neurobehavioral Consequences of a Single Ketamine Neonatal Exposure in Rats: Effects on Cellular Viability and Glutamate Transport in Frontal Cortex and Hippocampus

Autor:	Tharine Dal-Cim, Wagner C. Martins, Gabriela Godoy Poluceno, Frederico C. Pereira, Fabiana K. Ludka, Rui Daniel Prediger, Ana Paula Costa, Carla I. Tasca, Karen Andrinéia de Oliveira, Tuane Bazanella Sampaio, Laíse Figueiredo de Oliveira, Leandra C. Constantino
Rok vydání:	2018
Předmět:	Male 0301 basic medicine medicine.medical_specialty Amino Acid Transport System X-AG Glutamic Acid Hippocampus In Vitro Techniques Hippocampal formation Tritium Toxicology 03 medical and health sciences 0302 clinical medicine Neurochemical Internal medicine medicine Animals Ketamine Rats Wistar Swimming Behavior Animal business.industry General Neuroscience Glutamate receptor Neurotoxicity Recognition Psychology medicine.disease Frontal Lobe Rats Motor coordination 030104 developmental biology Endocrinology Animals Newborn Exploratory Behavior NMDA receptor Female business Excitatory Amino Acid Antagonists 030217 neurology & neurosurgery medicine.drug
Zdroj:	Neurotoxicity Research. 34:649-659
ISSN:	1476-3524 1029-8428
DOI:	10.1007/s12640-018-9927-x
Popis:	The neonatal exposure to general anesthetics has been associated with neuronal apoptosis and dendritic spines morphologic changes in the developing brain. Ketamine, a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, is widely used in pediatric patients to induce general anesthesia, analgesia, and perioperative sedation. In the present study, we investigated short- and long-term effects of a single ketamine (20 mg/kg, s.c.) neonatal exposure at postnatal day 7 in rats on the hippocampal and frontal cortical cellular viability. Additionally, putative neurochemical alterations and neurobehavioral impairments were evaluated in the adulthood. Ketamine neonatal administration selectively decreased cellular viability in the hippocampus, but not in the frontal cortex, 24 h after the treatment. Interestingly, a single ketamine neonatal exposure prevented the vulnerability to glutamate-induced neurotoxicity in the frontal cortex of adult rats. No short- or long-term damage to cellular membranes, as an indicative of cell death, was observed in hippocampal or cortical slices. However, ketamine induced a long-term increase in hippocampal glutamate uptake. Regarding behavioral analysis, neonatal ketamine exposure did not alter locomotor activity and anxiety-related parameters evaluated in the open-field test. However, ketamine administration disrupted the hippocampal-dependent object recognition ability of adult rats, while improved the motor coordination addressed on the rotarod. These findings indicate that a single neonatal ketamine exposure induces a short-term reduction in the hippocampal, but not in cortical, cellular viability, and long-term alterations in hippocampal glutamate transport, improvement on motor performance, and short-term recognition memory impairment.
Databáze:	OpenAIRE
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