1. Enhancement of parvalbumin interneuron-mediated neurotransmission in the retrosplenial cortex of adolescent mice following third trimester-equivalent ethanol exposure
- Author
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C. Fernando Valenzuela, Glenna J Chavez, Megan J. Barber, and Clark W. Bird
- Subjects
Male ,0301 basic medicine ,Cell death in the nervous system ,Hippocampus ,Ion channels in the nervous system ,Synaptic Transmission ,Mice ,0302 clinical medicine ,Receptor pharmacology ,Retrosplenial cortex ,Pregnancy ,Multidisciplinary ,biology ,GABAA receptor ,Chemistry ,Pyramidal Cells ,Developmental disorders ,Parvalbumins ,medicine.anatomical_structure ,Medicine ,Female ,Rhodopsin ,medicine.medical_specialty ,Interneuron ,Science ,Thalamus ,Mice, Transgenic ,Neurotransmission ,Inhibitory postsynaptic potential ,Gyrus Cinguli ,Article ,03 medical and health sciences ,Interneurons ,Internal medicine ,medicine ,Animals ,Ethanol ,Synaptic development ,Receptors, GABA-A ,030104 developmental biology ,Endocrinology ,Animals, Newborn ,Inhibitory Postsynaptic Potentials ,nervous system ,biology.protein ,Neuroscience ,030217 neurology & neurosurgery ,Parvalbumin - Abstract
Prenatal ethanol exposure causes a variety of cognitive deficits that have a persistent impact on quality of life, some of which may be explained by ethanol-induced alterations in interneuron function. Studies from several laboratories, including our own, have demonstrated that a single binge-like ethanol exposure during the equivalent to the third trimester of human pregnancy leads to acute apoptosis and long-term loss of interneurons in the rodent retrosplenial cortex (RSC). The RSC is interconnected with the hippocampus, thalamus, and other neocortical regions and plays distinct roles in visuospatial processing and storage, as well as retrieval of hippocampal-dependent episodic memories. Here we used slice electrophysiology to characterize the acute effects of ethanol on GABAergic neurotransmission in the RSC of neonatal mice, as well as the long-term effects of neonatal ethanol exposure on parvalbumin-interneuron mediated neurotransmission in adolescent mice. Mice were exposed to ethanol using vapor inhalation chambers. In postnatal day (P) 7 mouse pups, ethanol unexpectedly failed to potentiate GABAA receptor-mediated synaptic transmission. Binge-like ethanol exposure of P7 mice expressing channel rhodopsin in parvalbumin-positive interneurons enhanced the peak amplitudes, asynchronous activity and total charge, while decreasing the rise-times of optically-evoked GABAA receptor-mediated inhibitory postsynaptic currents in adolescent animals. These effects could partially explain the learning and memory deficits that have been documented in adolescent and young adult mice exposed to ethanol during the third trimester-equivalent developmental period.
- Published
- 2021