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Shiro Nakagawa - One of the best experts on this subject based on the ideXlab platform.
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morphological study of orexin neurons in the hypothalamus of the Long Evans Rat with special reference to co expression of orexin and nadph diaphorase or nitric oxide synthase activities
Neuroscience Research, 2003Co-Authors: Shi-bin Cheng, Satoshi Kuchiiwa, Hong-zhi Gao, Toshiko Kuchiiwa, Shiro NakagawaAbstract:Abstract Orexins, novel neuropeptides, are exclusively localized in the hypothalamus and implicated in the regulation of a variety of activities, including food intake and energy balance. Nitric oxide (NO), an unconventional neurotransmitter, is widely present in numerous brain regions including the hypothalamus, and has similar physiological roles to those of the orexins. The present study was undertaken to examine the distribution of orexin neurons and the presence of neuronal nitric oxide synthase (nNOS) in the orexin neurons to clarify whether NO interacts with the orexins in the neuronal regulation activities in the Long–Evans Rat. We used two double-labeling methods: nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry in combination with orexin immunohistochemistry, and double-labeling fluorescent immunohistochemistry for orexin and nNOS. The majority of the orexin immunoreactive neurons were localized mainly in the areas of the dorsomedial hypothalamic nucleus (DMN), the dorsal part of the perifornical nucleus (PEF) and lateral hypothalamic area. The orexin immunoreactive cell bodies were medium in size, and triangular, round, elliptic, and fusiform in shape. The sizes and shapes of orexin neurons in the different parts were similar. Cell bodies coexpressing the orexin and nNOS or NADPH-d were present in the areas of the DMN and the PEF, and the nerve fibers containing orexin and nNOS were distributed in the DMN and PEF, arcuate nucleus (ARN) and ventromedial hypothalamic nucleus (VMH). These results provide morphological evidence that there exists a population of nNOS- or NADPH-d-/orexin-coexpressing neurons in the orexinergic cell group in the hypothalamus, and taken together with previous findings, suggest that NO may play a role in the mechanisms by which orexin neurons regulate food intake and energy balance.
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Up-regulation of methionine-enkephalin-like immunoreactivity by 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment in the forebrain of the Long-Evans Rat.
Journal of Chemical Neuroanatomy, 2003Co-Authors: Shi-bin Cheng, Satoshi Kuchiiwa, Akio Kawachi, Hong-zhi Gao, Atsushi Gohshi, Tomohiro Kozako, Toshiko Kuchiiwa, Shiro NakagawaAbstract:Abstract 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is considered to be one of the most toxic environmental contaminants, named dioxin. Exposure to TCDD induces a plethora of intoxication symptoms, including anorexia and hypothermia, in several mammals and human. Enkephalin, an endogenous pentapeptide, is an important neuroregulator of autonomic functions, such as food intake and body tempeRature. In this study, we investigated the effects of TCDD gastric administRation on methionine-enkephalin (MEK) immunoreactivity in the brain of the Long-Evans Rat, the species strain considered to be the most TCDD-susceptible, using immunohistochemical staining. A single dose of TCDD (dissolved in olive oil, 50 μg/kg) or olive oil alone was administRated to the Rats by gavage. Compared with the vehicle-treated Rat, a marked increase in the density of MEK immunoreactive cell bodies, fibers and terminals was found 2 weeks after TCDD treatment in the forebrain of the TCDD-treated Rat, i.e. the central amygdaloid nucleus, field CA3 of the hippocampus, paraventricular hypothalamic nucleus, medial preoptic nucleus, interstitial nucleus of the posterior limb of the anterior commissure, lateral globus pallidus, ventral pallidum and lateral division of the bed nucleus of the stria terminalis. These results demonstRated for the first time a site-specific increased enkephalinergic activity in certain brain regions of the Long-Evans Rat. It is suggested that the increased MEK immunoreactivity may act as a compensatory adaptation for the pathophysiological alteRations caused by TCDD exposure.
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2,3,7,8-Tetrachlorodibenzo-p-dioxin treatment induces c-Fos expression in the forebrain of the Long-Evans Rat.
Brain research, 2002Co-Authors: Shi-bin Cheng, Satoshi Kuchiiwa, Toshiko Kuchiiwa, Itsugi Nagatomo, Yasuaki Akasaki, Masahiro Uchida, Masataka Tominaga, Wataru Hashiguchi, Shiro NakagawaAbstract:2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is one of the most toxic environmental pollutants. In the present study, we examined c-Fos expression in the central nervous system (CNS) after administRation of a lethal dose of TCDD to the adult Long-Evans Rat to clarify if the CNS participates in TCDD-induced intoxication. A single dose of TCDD (dissolved in olive oil, 50 microg/kg) or olive oil alone was administered to the Rats by gavage. Animals were allowed to survive for 1 day to 5 weeks. Three days after the administRation, a significantly large number of Fos-immunopositive cells were found in the hypothalamus (i.e. dorsomedial hypothalamic nucleus, paraventricular hypothalamic nucleus, medial preoptic nucleus), central amygdaloid nucleus and bed nucleus of the stria terminalis. These results suggest that some TCDD toxicity may be induced by its direct action on the CNS.
James R Coleman - One of the best experts on this subject based on the ideXlab platform.
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audiogenic seizure activity following hsv 1 gad65 sense or antisense injection into inferior colliculus of Long Evans Rat
Epilepsy & Behavior, 2017Co-Authors: James R Coleman, Karen C Thompson, Marlene A. Wilson, Steven P. WilsonAbstract:Abstract Herpes virus technology involving manipulation of GAD65 was used to study effects on audiogenic seizures (AGS). Audiogenic seizure behaviors were examined following injections of replication-defective herpes simplex virus (HSV-1) vectors incorpoRating sense or antisense toward GAD65 aLong with 10% lac -Z into the central nucleus of inferior colliculus (CNIC) of Long–Evans Rats. In seizure-sensitive animals developmentally primed by intense sound exposure, injection of GAD65 in the sense orientation increased wild running latencies and reduced incidence of clonus compared with lac -Z only, unopeRated, and vehicle seizure groups. In contrast, infection of CNIC with GAD65 antisense virus resulted in 100% incidence of wild running and clonus behaviors in AGS animals. Unprimed animals not opeRated continued to show uniform absence of seizure activity. AdministRation of GAD65 antisense virus into CNIC produced novel wild running and clonus behaviors in some unprimed animals. Staining for β-galactosidase in all vector animals revealed no differences in pattern or numbers of immunoreactive cells at injection sites. Qualitatively, typical small and medium multipolar/stellate and medium fusiform neurons appeared in the CNIC of vector animals. These results demonstRate that HSV-1 vector constructs implanted into the CNIC can predictably influence incidence and severity of AGS and suggest that viral vectors can be useful in studying GABA mechanisms with potential for therapeutic application in epilepsy. This article is part of a Special Issue entitled “Genetic and Reflex Epilepsies, Audiogenic Seizures and Strains: From Experimental Models to the Clinic”.
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audiogenic seizures in the developmentally primed Long Evans Rat
Developmental Psychobiology, 1999Co-Authors: Karen C Ross, James R ColemanAbstract:The Long-Evans Rat is a hybrid rodent strain with little innate susceptibility to audiogenic seizures (AGS). The present study examines parameters of acoustic priming (induced susceptibility) and testing for AGS during postnatal development subsequent to auditory function, and identifies the effects of stimulus intensity, repeated testing, and gender upon AGS activity. Rats were exposed to 125-dB SPL 10-kHz tone bursts at 14-36 days of age and tested with white noise at 14 or 19 days following sound exposure. All priming/testing combinations yielded AGS susceptibility; animals primed at 18 days showed the highest incidence of clonic seizures when tested 14 days later. All subjects displayed clonus at testing intensities of 120 dB, although some seizure behaviors could be elicited at 100 dB. Repeated testing at 120 dB increased latency to clonus and clonus duRation, and total wild running activity. Gender differences for AGS expression were minimal. These results demonstRate the viability of the seizure-resistant Long-Evans Rat for study of AGS.
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latency alteRations of the auditory brainstem response in audiogenic seizure prone Long Evans Rats
Epilepsy Research, 1999Co-Authors: James R Coleman, Karen C Ross, Megan M Mullaney, William A CooperAbstract:Abstract Audiogenic seizure susceptibility in the normally seizure-resistant Long-Evans Rat may result from altered processing in the auditory pathway. Representative waveform latencies of the auditory brainstem responses (ABR) were recorded to examine geneRator alteRations at different levels of the auditory neuraxis. Male Long-Evans Rats primed for audiogenic seizures (AGS) on PND 14 with a 10 kHz pure tone at 120 dB SPL for 8 min were tested for AGS on PND 28 with 120 dB SPL continuous white noise. Primed subjects displayed wild running culminating in clonic convulsions. Following behavioral testing at 4–6 months, vertex recordings of ABR waves Ia–VI were made in anesthetized subjects using pure tone stimulus bursts. AGS subjects showed marginally elevated ABR thresholds. Shorter ABR wave latencies were elicited in AGS subjects for peripheral and central auditory components with stimulus intensities above 50 dB PeSPL at 8 and 40 kHz. Interpeak intervals were reduced for waves Ia–V and III–V in AGS subjects. These results reveal that intense sound stimulation during a sensitive period of development later reduces processing time at higher intensity levels.
Mary Beth Genter - One of the best experts on this subject based on the ideXlab platform.
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Evolution of alachlor-induced nasal neoplasms in the Long-Evans Rat.
Toxicologic Pathology, 2000Co-Authors: Mary Beth Genter, Dawn M. Burman, Michael W. Dingeldein, Ian Clough, Brad BolonAbstract:The chloracetanilide herbicide alachlor (2-chloro-2',6-diethyl-N-(methoxymethyl)-acetanilide) induces nasal neoplasms in Rats following chronic dietary exposure. The present study sought to identify the cellular origin and mechanisms of tumor induction and progression. Male Long-Evans Rats were fed alachlor (0 or 126 mg/kg/day) beginning at 6 weeks of age. Following 1 month of alachlor ingestion, neither histological abnormalities nor enhanced cell division (assessed by BrdU incorpoRation) occurred in any region of the nasal cavity. Six months of alachlor exposure resulted in prolifeRation of basal and nonbasal cells in the olfactory mucosa while inducing nasal masses in 7 of 15 animals. Tumors ranged from dysplastic plaques to polypoid adenomas and originated in the olfactory regions of the nasal cavity. Neoplasms were associated with regions of respiRatory metaplasia and were often covered with a low cuboidal, poorly ciliated epithelium. Tumor cells did not express characteristics of the olfactory mucosa, including olfactory marker protein (OMP, for neurons) and NMa (antibody recognizing cytochrome P450 [CYP] 2A3, found in Bowman's glands). Sites of plaque and tumor development coincided with regions of NMa immunoreactivity. These data suggest that local metabolism is important in alachlor-induced olfactory tumors and support the concept that metaplastic respiRatory epithelial cells give rise to the observed neoplasms.
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evidence for site specific bioactivation of alachlor in the olfactory mucosa of the Long Evans Rat
Toxicological Sciences, 1999Co-Authors: Barbara A Wetmore, Ann D Mitchell, Sharon A Meyer, Mary Beth GenterAbstract:Alachlor (2-chloro-2',6'-diethyl-N-[methoxymethyl]-acetanilide) is a restricted-use chloracetanilide herbicide which has been shown previously to produce a dose-dependent incidence of olfactory mucosal tumors in Rats following chronic dietary exposure. However, the mechanism of alachlor carcinogenicity is poorly understood. Alachlor was administered i.p. to male Long-Evans Rats for up to 28 days at doses that are carcinogenic in chronic studies in order to study olfactory lesion development and alteRations in cell prolifeRation. Neither treatment-related olfactory mucosal lesions nor regeneRative cell prolifeRation, as assessed with BrdU labeling, was detected. In vitro genotoxicity studies using Salmonella typhimurium strain TA100 showed that alachlor was non-mutagenic in the absence of metabolic activation. When pre-incubated with an olfactory mucosal S9 activation system, alachlor induced a weak, dose-dependent mutagenic response at 500-1250 micrograms/plate, with toxicity at higher doses. In contrast, an S9 activation system derived from nasal respiRatory mucosa, the tissue physically juxtaposed with the olfactory mucosa but reportedly not susceptible to alachlor-induced tumors, did not produce a mutagenic response for alachlor or the positive control. Thus, this result suggested site-specificity of alachlor activation consistent with the target site of carcinogenicity. The mutagenicity of alachlor to Salmonella, in the presence of an olfactory mucosal-activating system, was confirmed by a limited positive response in the mouse lymphoma assay. Here there were increases in small colony mutants (indicative of chromosomal effects) as well as large colony mutants (which reflect gene mutations). This study suggests that target tissue bioactivation of alachlor results in the formation of one or more mutagenic metabolite(s), which may be critical in alachlor-induced nasal tumorigenesis.
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evaluation of olfactory and auditory system effects of the antihyperthyroid drug carbimazole in the Long Evans Rat
Journal of Biochemical and Molecular Toxicology, 1998Co-Authors: Mary Beth GenterAbstract:Carbimazole (2-carbethoxythio-1-methylimidazole) is a thiocarbamide drug used in the treatment of hyperthyroidism in humans. Side effects associated with carbimazole treatment are reported to include impaired taste, impaired olfaction, and hearing loss. The structurally similar antihyperthyroid drug methimazole (1-methyl-2-mercaptoimidazole), also reportedly associated with impaired taste and olfaction in humans, has recently been demonstRated by this laboRatory to be an olfactory toxicant by both the oral and intraperitoneal routes of exposure in rodents. A systematic evaluation of sensory system effects of these compounds, either in rodents or humans, is not available in the liteRature. Male Long-Evans Rats were used to evaluate the auditory and olfactory toxicity of carbimazole by two routes of exposure. Histopathological evaluation of nasal cavities from Rats administered carbimazole via i.p. and oral routes revealed olfactory mucosal damage and early evidence of repair; a no-observed effect level (NOEL) of 100 mg/kg was observed for orally administered carbimazole. Further, these studies demonstRate evidence for the geneRation of the olfactory toxic metabolites of carbimazole by the olfactory mucosa itself, as incubation of carbimazole with an olfactory S9 prepaRation resulted in NADPH-dependent degradation of carbimazole. Evaluation of the auditory startle response in carbimazole-treated Rats revealed no deficits, demonstRating that carbimazole does not cause a global loss of hearing in Rats.
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olfactory toxicity of methimazole dose response and structure activity studies and characterization of flavin containing monooxygenase activity in the Long Evans Rat olfactory mucosa
Toxicologic Pathology, 1995Co-Authors: Mary Beth Genter, Nora J Deamer, Bonita L Blake, Deborah S Wesley, Patricia E LeviAbstract:Methimazole is a compound administered to humans for the treatment of hyperthyroidism and is used experimentally as a model substRate for the flavin-containing monooxygenase (FMO) system. Previous results from this laboRatory demonstRated that methimazole is an olfactory system toxicant, causing nearly complete destruction of the olfactory epithelium in the male Long-Evans Rat following a single ip dose of 300 mg/kg. The present studies were undertaken to determine the dose-response relationship for methimazole-induced olfactory mucosal damage and to determine whether or not similar damage occurs as a result of oral administRation, mimicking the relevant route of human exposure. We also investigated the mechanism of olfactory toxicity of methimazole by means of a structure-activity study and began the characterization of the form(s) of FMO present in the olfactory mucosa of the male Long-Evans Rat. Dose-response analysis demonstRated that methimazole causes olfactory mucosal damage at doses of 25 mg/kg ip and greater. The results of gavage studies showed that a single oral dose of 50 mg/kg also caused olfactory mucosal damage. Two structurally related compounds, methylimidazole and methylpyrrole, were not olfactory toxicants, suggesting that a reactive intermediate geneRated in the course of metabolizing methimazole to an S-oxide is the olfactory toxic species. Microsomal incubation studies revealed the presence of methimazole S-oxidation activity in olfactory mucosal microsomes at levels comparable to those in liver. An anti-mouse liver FMO antibody reacted on Western blots with olfactory mucosal microsomes. These findings demonstRate a dose-response for the olfactory toxicity of methimazole and suggest that characterization of human olfactory mucosal FMO activity may be necessary to assess the potential for human risk associated with therapeutic exposure to methimazole.
Shi-bin Cheng - One of the best experts on this subject based on the ideXlab platform.
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morphological study of orexin neurons in the hypothalamus of the Long Evans Rat with special reference to co expression of orexin and nadph diaphorase or nitric oxide synthase activities
Neuroscience Research, 2003Co-Authors: Shi-bin Cheng, Satoshi Kuchiiwa, Hong-zhi Gao, Toshiko Kuchiiwa, Shiro NakagawaAbstract:Abstract Orexins, novel neuropeptides, are exclusively localized in the hypothalamus and implicated in the regulation of a variety of activities, including food intake and energy balance. Nitric oxide (NO), an unconventional neurotransmitter, is widely present in numerous brain regions including the hypothalamus, and has similar physiological roles to those of the orexins. The present study was undertaken to examine the distribution of orexin neurons and the presence of neuronal nitric oxide synthase (nNOS) in the orexin neurons to clarify whether NO interacts with the orexins in the neuronal regulation activities in the Long–Evans Rat. We used two double-labeling methods: nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry in combination with orexin immunohistochemistry, and double-labeling fluorescent immunohistochemistry for orexin and nNOS. The majority of the orexin immunoreactive neurons were localized mainly in the areas of the dorsomedial hypothalamic nucleus (DMN), the dorsal part of the perifornical nucleus (PEF) and lateral hypothalamic area. The orexin immunoreactive cell bodies were medium in size, and triangular, round, elliptic, and fusiform in shape. The sizes and shapes of orexin neurons in the different parts were similar. Cell bodies coexpressing the orexin and nNOS or NADPH-d were present in the areas of the DMN and the PEF, and the nerve fibers containing orexin and nNOS were distributed in the DMN and PEF, arcuate nucleus (ARN) and ventromedial hypothalamic nucleus (VMH). These results provide morphological evidence that there exists a population of nNOS- or NADPH-d-/orexin-coexpressing neurons in the orexinergic cell group in the hypothalamus, and taken together with previous findings, suggest that NO may play a role in the mechanisms by which orexin neurons regulate food intake and energy balance.
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Up-regulation of methionine-enkephalin-like immunoreactivity by 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment in the forebrain of the Long-Evans Rat.
Journal of Chemical Neuroanatomy, 2003Co-Authors: Shi-bin Cheng, Satoshi Kuchiiwa, Akio Kawachi, Hong-zhi Gao, Atsushi Gohshi, Tomohiro Kozako, Toshiko Kuchiiwa, Shiro NakagawaAbstract:Abstract 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is considered to be one of the most toxic environmental contaminants, named dioxin. Exposure to TCDD induces a plethora of intoxication symptoms, including anorexia and hypothermia, in several mammals and human. Enkephalin, an endogenous pentapeptide, is an important neuroregulator of autonomic functions, such as food intake and body tempeRature. In this study, we investigated the effects of TCDD gastric administRation on methionine-enkephalin (MEK) immunoreactivity in the brain of the Long-Evans Rat, the species strain considered to be the most TCDD-susceptible, using immunohistochemical staining. A single dose of TCDD (dissolved in olive oil, 50 μg/kg) or olive oil alone was administRated to the Rats by gavage. Compared with the vehicle-treated Rat, a marked increase in the density of MEK immunoreactive cell bodies, fibers and terminals was found 2 weeks after TCDD treatment in the forebrain of the TCDD-treated Rat, i.e. the central amygdaloid nucleus, field CA3 of the hippocampus, paraventricular hypothalamic nucleus, medial preoptic nucleus, interstitial nucleus of the posterior limb of the anterior commissure, lateral globus pallidus, ventral pallidum and lateral division of the bed nucleus of the stria terminalis. These results demonstRated for the first time a site-specific increased enkephalinergic activity in certain brain regions of the Long-Evans Rat. It is suggested that the increased MEK immunoreactivity may act as a compensatory adaptation for the pathophysiological alteRations caused by TCDD exposure.
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2,3,7,8-Tetrachlorodibenzo-p-dioxin treatment induces c-Fos expression in the forebrain of the Long-Evans Rat.
Brain research, 2002Co-Authors: Shi-bin Cheng, Satoshi Kuchiiwa, Toshiko Kuchiiwa, Itsugi Nagatomo, Yasuaki Akasaki, Masahiro Uchida, Masataka Tominaga, Wataru Hashiguchi, Shiro NakagawaAbstract:2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is one of the most toxic environmental pollutants. In the present study, we examined c-Fos expression in the central nervous system (CNS) after administRation of a lethal dose of TCDD to the adult Long-Evans Rat to clarify if the CNS participates in TCDD-induced intoxication. A single dose of TCDD (dissolved in olive oil, 50 microg/kg) or olive oil alone was administered to the Rats by gavage. Animals were allowed to survive for 1 day to 5 weeks. Three days after the administRation, a significantly large number of Fos-immunopositive cells were found in the hypothalamus (i.e. dorsomedial hypothalamic nucleus, paraventricular hypothalamic nucleus, medial preoptic nucleus), central amygdaloid nucleus and bed nucleus of the stria terminalis. These results suggest that some TCDD toxicity may be induced by its direct action on the CNS.
Anna Y Klintsova - One of the best experts on this subject based on the ideXlab platform.
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single day postnatal alcohol exposure induces apoptotic cell death and causes Long term neuron loss in rodent thalamic nucleus reuniens
Neuroscience, 2020Co-Authors: Zachary H Gursky, Emma C Spillman, Anna Y KlintsovaAbstract:Abstract Fetal alcohol spectrum disorders (FASD) constitute a prevalent, yet preventable, developmental disorder worldwide. While a wealth of research demonstRates that altered function of hippocampus (HPC) and prefrontal cortex may underlie behavioral impairments in FASD, only one published paper to date has examined the impact of developmental alcohol exposure (AE) on the region responsible for coordinated prefrontal–hippocampal activity: thalamic nucleus reuniens (Re). In the current study, we used a rodent model of human third trimester AE to examine both the acute and lasting impact of a single-day AE on Re. We administered 5.25 g/kg of ethanol to male and female Long Evans Rat pups on postnatal day (PD) 7. We used unbiased stereological estimation to evaluate cell death or cell loss at three time points: 12 h after alcohol administRation; 4 days after alcohol administRation (i.e., PD11); in adulthood (i.e.,PD 72). AE on PD7 increased apoptotic cell death in Re on PD7, and caused short-term cell loss on PD11. This relationship between short-term cell death versus cell number suggests that alcohol-related cell loss is driven by induction of apoptosis. In adulthood, alcohol-exposed animals displayed permanent cell loss (mediating volume loss in the Re), which included a reduction in neuron number (relative to procedural controls). Both procedural controls and alcohol exposed animals displayed a deficit in non-neuronal cell number relative to typically-developing controls, suggesting that Re cell populations may be vulnerable to early life stress as well as AE in an insult- and cell type-dependent manner.
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nucleus reuniens of the midline thalamus of a Rat is specifically damaged after early postnatal alcohol exposure
Neuroreport, 2019Co-Authors: Zachary H Gursky, Lisa M Savage, Anna Y KlintsovaAbstract:Individuals diagnosed with fetal alcohol spectrum disorders often show behavioral impairments in executive functioning. Mechanistic studies have implicated coordination between the prefrontal cortex and the hippocampus (through thalamic nucleus reuniens) as essential for such executive functions. This study is the first to report the Long-term neuroanatomical alteRations to the ventral midline thalamus after alcohol exposure on postnatal days 4-9 (a rodent model of binge drinking during the third-trimester of human pregnancy). Alcohol added to a milk formula was administered to female Long-Evans Rat pups on postnatal days 4-9 (5.25 g/kg/day of ethanol, intragastric intubation). Control animals were intubated without the administRation of liquid. In adulthood, brains were immunohistochemically labeled for a neuronal marker (NeuN) conjugated with Cy3 fluorophore and stained with Hoechst33342 to visualize nuclei. Total non-neuronal cell number (NeuN/Hoechst) and neuron number (NeuN/Hoechst), and total volume were estimated using unbiased stereology in two neighboring midline thalamic nuclei: reuniens and rhomboid. Estimates were analyzed using linear mixed modeling to account for animal and litter as clustering variables. A 21% reduction in the total neuron number (resulting in altered neuron-to-non-neuron Ratio) and an 18% reduction in total volume were found exclusively in thalamic nucleus reuniens in Rats exposed to ethanol. Non-neuronal cell number was not changed in reuniens. No ethanol-induced changes on any measures were observed in rhomboid nucleus. These specific neuroanatomical alteRations provide a necessary foundation for further examination of circuit-level alteRations that occur in fetal alcohol spectrum disorder.
