Neonatal ethanol exposure results in dose-dependent impairments in the acquisition and timing of the conditioned eyeblink response and altered cerebellar interpositus nucleus and hippocampal CA1 unit activity in adult rats

Lindquist, Derick H.; Sokoloff, Greta; Steinmetz, Joseph E.

doi:10.1016/j.alcohol.2013.05.007

Cited by 20 publications

(13 citation statements)

References 88 publications

(128 reference statements)

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“…Interestingly, other in vitro electrophysiology experiments showed that alcohol exposure led to relatively greater inhibitory inputs to the Purkinje cells in the vermis ( 40 ). In the cerebellar deep nuclei, activity in the interpositus nucleus of the cerebellum was diminished and did not develop as rapidly in neonatal alcohol-exposed rats relative to controls during EBC ( 41 , 42 ).…”

Section: Laboratory Animal Workmentioning

confidence: 87%

Eyeblink Classical Conditioning in Alcoholism and Fetal Alcohol Spectrum Disorders

et al. 2015

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Alcoholism is a debilitating disorder that can take a significant toll on health and professional and personal relationships. Excessive alcohol consumption can have a serious impact on both drinkers and developing fetuses, leading to long-term learning impairments. Decades of research in laboratory animals and humans have demonstrated the value of eyeblink classical conditioning (EBC) as a well-characterized model system to study the neural mechanisms underlying associative learning. Behavioral EBC studies in adults with alcohol use disorders and in children with fetal alcohol spectrum disorders report a clear learning deficit in these two patient populations, suggesting alcohol-related damage to the cerebellum and associated structures. Insight into the neural mechanisms underlying these learning impairments has largely stemmed from laboratory animal studies. In this mini-review, we present and discuss exemplary animal findings and data from patient and neuroimaging studies. An improved understanding of the neural mechanisms underlying learning deficits in EBC related to alcoholism and prenatal alcohol exposure has the potential to advance the diagnoses, treatment, and prevention of these and other pediatric and adult disorders.

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Section: Laboratory Animal Workmentioning

confidence: 87%

Eyeblink Classical Conditioning in Alcoholism and Fetal Alcohol Spectrum Disorders

et al. 2015

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“…Data indicates that disruption of memory by ethanol is due to its effect on attention, sensory-motor function, emotion or motivation that impairs the efficiency of learning and encoding [ 231 ]. Ethanol might induce destructions of hippocampus-dependent learning and memory [ 232 , 233 ] and impair of the cholinergic neuronal system [ 234 ] by oxidative stress via the generation of ROS and lipid peroxidation [ 235 ]. Ethanol-induces presynaptic dysfunction in dorsal hippocampal glutamatergic neurons and thereby causes deficits in spatial memory [ 19 ].…”

Section: Toxin-induced Experimental Models Of Memory Impairmentmentioning

confidence: 99%

Toxin-Induced Experimental Models of Learning and Memory Impairment

Kumar

Cho

et al. 2016

IJMS

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Animal models for learning and memory have significantly contributed to novel strategies for drug development and hence are an imperative part in the assessment of therapeutics. Learning and memory involve different stages including acquisition, consolidation, and retrieval and each stage can be characterized using specific toxin. Recent studies have postulated the molecular basis of these processes and have also demonstrated many signaling molecules that are involved in several stages of memory. Most insights into learning and memory impairment and to develop a novel compound stems from the investigations performed in experimental models, especially those produced by neurotoxins models. Several toxins have been utilized based on their mechanism of action for learning and memory impairment such as scopolamine, streptozotocin, quinolinic acid, and domoic acid. Further, some toxins like 6-hydroxy dopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and amyloid-β are known to cause specific learning and memory impairment which imitate the disease pathology of Parkinson’s disease dementia and Alzheimer’s disease dementia. Apart from these toxins, several other toxins come under a miscellaneous category like an environmental pollutant, snake venoms, botulinum, and lipopolysaccharide. This review will focus on the various classes of neurotoxin models for learning and memory impairment with their specific mechanism of action that could assist the process of drug discovery and development for dementia and cognitive disorders.

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“…This includes significant loss of pyramidal neurons in CA1 and CA3 and granule neurons in the dentate gyrus (Ieraci & Herrera, 2007; Ikonomidou et al, 2000; Klintsova et al, 2007; Livy, Miller, Maier, & West, 2003; Tran & Kelly, 2003; Uban et al, 2010). Developmental ethanol exposure also produces neuroanatomical and electrophysiological defects in hippocampal circuitry (Diaz et al, 2014; Everett, Licon-Munoz, & Valenzuela, 2012; Lindquist, Sokoloff, Milner, & Steinmetz, 2013; Sakata-Haga et al, 2003). Defects in the hippocampus correlate with behavioral deficits, particularly with learning and memory (Banuelos et al, 2012; El Shawa et al, 2013; Hamilton et al, 2010; Idrus, McGough, Riley, & Thomas, 2014; Kelly, Pierce, & West, 1987; Thomas, Idrus, Monk, & Dominguez, 2010; Wagner, Zhou, & Goodlett, 2014; West, Kelly, & Pierce, 1987; Zink et al, 2011).…”

Section: Fasd Neuropathology In Animal Modelsmentioning

confidence: 99%

Fetal Alcohol Spectrum Disorders and Neuroimmune Changes

Drew

Kane

2014

International Review of Neurobiology

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The behavioral consequences of fetal alcohol spectrum disorders (FASD) are serious and persist throughout life. The causative mechanisms underlying FASD are poorly understood. However, much has been learned about FASD from human structural and functional studies as well as from animal models, which have provided a greater understanding of the mechanisms underlying FASD. Using animal models of FASD, it has been recently discovered that ethanol induces neuroimmune activation in the developing brain. The resulting microglial activation, production of proinflammatory molecules, and alteration in expression of developmental genes are postulated to alter neuron survival and function and lead to long-term neuropathological and cognitive defects. It has also been discovered that microglial loss occurs, reducing microglia’s ability to protect neurons and contribute to neuronal development. This is important, because emerging evidence demonstrates that microglial depletion during brain development leads to long-term neuropathological and cognitive defects. Interestingly, the behavioral consequences of microglial depletion and neuroimmune activation in the fetal brain are particularly relevant to FASD. This chapter reviews the neuropathological and behavioral abnormalities of FASD and delineates correlates in animal models. This serves as a foundation to discuss the role of the neuroimmune system in normal brain development, the consequences of microglial depletion and neuroinflammation, the evidence of ethanol induction of neuroinflammatory processes in animal models of FASD, and the development of anti-inflammatory therapies as a new strategy for prevention or treatment of FASD. Together, this knowledge provides a framework for discussion and further investigation of the role of neuroimmune processes in FASD.

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Neonatal ethanol exposure results in dose-dependent impairments in the acquisition and timing of the conditioned eyeblink response and altered cerebellar interpositus nucleus and hippocampal CA1 unit activity in adult rats

Cited by 20 publications

References 88 publications

Eyeblink Classical Conditioning in Alcoholism and Fetal Alcohol Spectrum Disorders

Eyeblink Classical Conditioning in Alcoholism and Fetal Alcohol Spectrum Disorders

Toxin-Induced Experimental Models of Learning and Memory Impairment

Fetal Alcohol Spectrum Disorders and Neuroimmune Changes

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