Literature DB >> 28809846

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders.

Tuan D Tran1, Aenia Amin2, Keith G Jones3, Ellen M Sheffer4, Lidia Ortega4, Keith Dolman3.   

Abstract

Neonatal rats were administered a relatively high concentration of ethyl alcohol (11.9% v/v) during postnatal days 4-9, a time when the fetal brain undergoes rapid organizational change and is similar to accelerated brain changes that occur during the third trimester in humans. This model of fetal alcohol spectrum disorders (FASDs) produces severe brain damage, mimicking the amount and pattern of binge-drinking that occurs in some pregnant alcoholic mothers. We describe the use of trace eyeblink classical conditioning (ECC), a higher-order variant of associative learning, to assess long-term hippocampal dysfunction that is typically seen in alcohol-exposed adult offspring. At 90 days of age, rodents were surgically prepared with recording and stimulating electrodes, which measured electromyographic (EMG) blink activity from the left eyelid muscle and delivered mild shock posterior to the left eye, respectively. After a 5 day recovery period, they underwent 6 sessions of trace ECC to determine associative learning differences between alcohol-exposed and control rats. Trace ECC is one of many possible ECC procedures that can be easily modified using the same equipment and software, so that different neural systems can be assessed. ECC procedures in general, can be used as diagnostic tools for detecting neural pathology in different brain systems and different conditions that insult the brain.

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Year:  2017        PMID: 28809846      PMCID: PMC5614106          DOI: 10.3791/55350

Source DB:  PubMed          Journal:  J Vis Exp        ISSN: 1940-087X            Impact factor:   1.355


  67 in total

1.  Cortical involvement in acquisition and extinction of trace eyeblink conditioning.

Authors:  A P Weible; M D McEchron; J F Disterhoft
Journal:  Behav Neurosci       Date:  2000-12       Impact factor: 1.912

Review 2.  Neural substrates of eyeblink conditioning: acquisition and retention.

Authors:  Kimberly M Christian; Richard F Thompson
Journal:  Learn Mem       Date:  2003 Nov-Dec       Impact factor: 2.460

Review 3.  Conditioning, awareness, and the hippocampus.

Authors:  K S LaBar; J F Disterhoft
Journal:  Hippocampus       Date:  1998       Impact factor: 3.899

Review 4.  Fetal alcohol-induced brain damage and the problem of determining temporal vulnerability: a review.

Authors:  J R West
Journal:  Alcohol Drug Res       Date:  1987

5.  Lesions of the inferior olivary complex cause extinction of the classically conditioned eyeblink response.

Authors:  D A McCormick; J E Steinmetz; R F Thompson
Journal:  Brain Res       Date:  1985-12-16       Impact factor: 3.252

6.  Eyeblink conditioning discriminates Alzheimer's patients from non-demented aged.

Authors:  D S Woodruff-Pak; R G Finkbiner; D K Sasse
Journal:  Neuroreport       Date:  1990-09       Impact factor: 1.837

7.  Temporal determinants of neonatal alcohol-induced cerebellar damage and motor performance deficits.

Authors:  C R Goodlett; K R Lundahl
Journal:  Pharmacol Biochem Behav       Date:  1996-12       Impact factor: 3.533

Review 8.  The Anatomy and Physiology of Eyeblink Classical Conditioning.

Authors:  Kaori Takehara-Nishiuchi
Journal:  Curr Top Behav Neurosci       Date:  2018

9.  Differentiation of Purkinje cells and their relationship to other components of developing cerebellar cortex in man.

Authors:  N Zecevic; P Rakic
Journal:  J Comp Neurol       Date:  1976-05-01       Impact factor: 3.215

10.  Hippocampectomy disrupts trace eye-blink conditioning in rabbits.

Authors:  J R Moyer; R A Deyo; J F Disterhoft
Journal:  Behav Neurosci       Date:  1990-04       Impact factor: 1.912

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