Long-term Reductions in the Population of GABAergic Interneurons in the Mouse Hippocampus following Developmental Ethanol Exposure

Bird, Clark W.; Taylor, Devin H.; Pinkowski, Natalie J.; Chavez, Glenna J.; Valenzuela, C. Fernando

doi:10.1016/j.neuroscience.2018.05.003

Cited by 35 publications

(38 citation statements)

References 85 publications

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“…Bird et al 13 demonstrated that ethanol vapor exposure during P2-9 (peak BEC = 221 mg/dl) reduces IN numbers in the adult mouse hippocampus; this study also found that a single vapor chamber exposure at P7 (peak BEC = 297 mg/dl) increases the number of INs that express activated caspase-3, suggesting that they are programmed to undergo apoptotic neurodegeneration. Ethanol administration to P7 mice (subcutaneous injection; peak BEC near 500 mg/dl) has been shown to reduce the numbers of PV-INs in the frontal cortex at P82 14 , as well as in the hippocampal formation (at P14 and P90-100) and the pyriform cortex (at P100) 15,16 .…”

Section: Introductionsupporting

confidence: 75%

Enhancement of Parvalbumin Interneuron-Mediated Neurotransmission in the Retrosplenial Cortex of Adolescent Mice Following Third Trimester-Equivalent Ethanol Exposure

Bird

Chavez

Barber

et al. 2020

Preprint

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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 third-trimester equivalent 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 and retrieval of hippocampal-dependent episodic memories. Here we used slice electrophysiology to characterize the acute effects of ethanol on GABAergic neurotransmission in neonates, 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 GABA A receptor-mediated synaptic transmission. Binge-like ethanol exposure of P7 mice expressing channel rhodopsin in parvalbumin-positive interneurons enhanced the peak amplitudes, total charge, decays, and decreased rise-times of optically-evoked GABA A receptor-mediated inhibitory postsynaptic currents in adolescent animals. These effects could partially explain learning and memory deficits caused by developmental ethanol exposure. Experiment 2 AnimalsMice expressing the channel rhodopsin-2 (ChR2) variant ChR2 H134R fused to tdTomato in PV-INs were generated by crossing female heterozygous B6.129P2-Pvalb tm1(cre)Arbr /J (B6 PV cre , Jackson Laboratory, Bar Harbor, ME; stock number 017320) and male heterozygous B6.Cg-Gt(ROSA)26Sor tm27.1(CAG-COP4*H134R/tdTomato)Hze /J (Ai27D, Jackson Laboratory; stock number 012567) mice. After weaning, the offspring (hereafter referred to as B6 PV cre -Ai27D mice) were ear-tagged and tail snips were collected under isoflurane anesthesia. Genotyping was performed by Transnetyx (Cordova, TN). Male and female mice aged between P40 and P60 were used for all subsequent experiments ( Figure 1b). Ethanol vapor chamber exposurePups and dams were exposed to either air or vaporized ethanol (95%, Koptec, King of Prussia, PA) for 4 h (approximately 10 a.m. to 2 p.m.) at P7 in custom-built ethanol vapor chambers 25 . Ethanol vapor concentrations were determined using a breathalyzer (Intoximeters, St. Louis, MO) and were between 8-9 g/dl. This exposure paradigm produces peak BECs in pups near 80 mM and triggers apoptotic neurodegeneration in several brain regions, including the RSC 13,18 . Immunohistochemistry 1 0

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Section: Introductionsupporting

confidence: 75%

Enhancement of Parvalbumin Interneuron-Mediated Neurotransmission in the Retrosplenial Cortex of Adolescent Mice Following Third Trimester-Equivalent Ethanol Exposure

Bird

Chavez

Barber

et al. 2020

Preprint

Self Cite

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“…When a binge drinking pattern of alcohol consumption is used on pregnant rats or newborn pups, there is a reduction in the cell density and number in the CA1, CA3, and DG regions only when alcohol is administered in the period equivalent to the last trimester in humans (P4 to P9 in rats) or all three trimesters (E1 to P9; Livy et al, 2003), and there are no significant effects on the cell number when alcohol is administered to the rats in the period equivalent to the first two trimesters (Maier and West, 2001), suggesting that the third trimester equivalent is the developmental period when the hippocampus is more susceptible to the effects of alcohol. Moreover, ethanol exposure during this developmental stage reduces the number of GABAergic interneurons in adulthood (P90), possibly contributing to cognitive impairment (Bird et al, 2018). Binge-like alcohol administration during the gestation period produces neurodegeneration through an apoptotic mechanism (Ikonomidou et al, 2000), which has also been observed by assessing neuronal death in rat primary hippocampal neurons obtained from fetuses exposed to alcohol during the gestation period (Akbar et al, 2006).…”

Section: Hippocampal Effects Of Alcohol In Prenatal and Neonatal Devementioning

confidence: 99%

Effect of Alcohol on Hippocampal-Dependent Plasticity and Behavior: Role of Glutamatergic Synaptic Transmission

Mira

Lira

Tapia-Rojas

et al. 2020

Front. Behav. Neurosci.

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Problematic alcohol drinking and alcohol dependence are an increasing health problem worldwide. Alcohol abuse is responsible for approximately 5% of the total deaths in the world, but addictive consumption of it has a substantial impact on neurological and memory disabilities throughout the population. One of the better-studied brain areas involved in cognitive functions is the hippocampus, which is also an essential brain region targeted by ethanol. Accumulated evidence in several rodent models has shown that ethanol treatment produces cognitive impairment in hippocampal-dependent tasks. These adverse effects may be related to the fact that ethanol impairs the cellular and synaptic plasticity mechanisms, including adverse changes in neuronal morphology, spine architecture, neuronal communication, and finally an increase in neuronal death. There is evidence that the damage that occurs in the different brain structures is varied according to the stage of development during which the subjects are exposed to ethanol, and even much earlier exposure to it would cause damage in the adult stage. Studies on the cellular and cognitive deficiencies produced by alcohol in the brain are needed in order to search for new strategies to reduce alcohol neuronal toxicity and to understand its consequences on memory and cognitive performance with emphasis on the crucial stages of development, including prenatal events to adulthood.

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“…EtOH is known to directly impact inhibitory cells in the brain; however, only a few studies have examined the impact of perinatal EtOH exposure on these cells in the dentate gyrus (see Table 4). In one study, a transgenic mouse model (Venus‐VGAT) was used that allowed them to directly visualize inhibitory (GABAergic) interneurons (Bird et al, 2018). This paper found a decrease in the number of interneurons in the granule cell layer (GCL) of the dentate gyrus.…”

Section: Resultsmentioning

confidence: 99%

A Systematic Review of the Effects of Perinatal Alcohol Exposure and Perinatal Marijuana Exposure on Adult Neurogenesis in the Dentate Gyrus

Reid

Lysenko‐Martin

Snowden

et al. 2020

Alcoholism Clin & Exp Res

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Background: Marijuana and alcohol are both substances that, when used during pregnancy, may have profound effects on the developing fetus. There is evidence to suggest that both drugs have the capacity to affect working memory, one function of the hippocampal formation; however, there is a paucity of data on how perinatal exposure to alcohol or cannabis impacts the process of adult neurogenesis.Methods: This systematic review examines immunohistochemical data from adult rat and mouse models that assess perinatal alcohol or perinatal marijuana exposure. A comprehensive list of search terms was designed and used to search 3 separate databases. All results were imported to Mendeley and screened by 2 authors. Consensus was reached on a set of final papers that met the inclusion criteria, and their results were summarized.Results: Twelve papers were identified as relevant, 10 of which pertained to the effects of perinatal alcohol on the adult hippocampus, and 2 pertained to the effects of perinatal marijuana on the adult hippocampus. Cellular proliferation in the dentate gyrus was not affected in adult rats and mice exposed to alcohol perinatally. In general, perinatal alcohol exposure did not have a significant and reliable effect on the maturation and survival of adult born granule neurons in the dentate gyrus. In contrast, interneuron numbers appear to be reduced in the dentate gyrus of adult rats and mice exposed perinatally to alcohol. Perinatal marijuana exposure was also found to reduce inhibitory interneuron numbers in the dentate gyrus.Conclusions: Perinatal alcohol exposure and perinatal marijuana exposure both act on inhibitory interneurons in the hippocampal formation of adult rats. These findings suggest simultaneous perinatal alcohol and marijuana exposure (SAM) may have a dramatic impact on inhibitory processes in the dentate gyrus.

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Long-term Reductions in the Population of GABAergic Interneurons in the Mouse Hippocampus following Developmental Ethanol Exposure

Cited by 35 publications

References 85 publications

Enhancement of Parvalbumin Interneuron-Mediated Neurotransmission in the Retrosplenial Cortex of Adolescent Mice Following Third Trimester-Equivalent Ethanol Exposure

Enhancement of Parvalbumin Interneuron-Mediated Neurotransmission in the Retrosplenial Cortex of Adolescent Mice Following Third Trimester-Equivalent Ethanol Exposure

Effect of Alcohol on Hippocampal-Dependent Plasticity and Behavior: Role of Glutamatergic Synaptic Transmission

A Systematic Review of the Effects of Perinatal Alcohol Exposure and Perinatal Marijuana Exposure on Adult Neurogenesis in the Dentate Gyrus

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