Widespread neuroanatomical damage and learning deficits following chronic alcohol consumption or vitamin-B1 (thiamine) deficiency in rats

Irle, Eva; Markowitsch, Hans J.

doi:10.1016/0166-4328(83)90133-x

Cited by 73 publications

(23 citation statements)

References 37 publications

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“…The notion that excitotoxicity may be a factor in the pathogenesis of WKS is based on data from experiments with a rat model of pyrithiamine-indueed thiamine deficiency (PTD); a model characterized by a pattern of subcortical brain lesions similar to that found postmortem in WKS patients (Troncosco et al 1981 ;Butterworth 1986;Mair et al 1988) and by chronic impairments of memory function (Irle and Markowitsch 1983;Mair et al 1988).…”

Section: Glutamate In Disorders Of Learning and Memorymentioning

confidence: 99%

Glutamate: its role in learning, memory, and the aging brain

1993

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L-Glutamate is the most abundant of a group of endogenous amino acids in the mammalian central nervous system which presumably function as excitatory neurotransmitters and under abnormal conditions may behave as neurotoxins. As neurotransmitters, these compounds are thought to play an important role in functions of learning and memory. As neurotoxins, they are believed to be involved in the pathogenesis of a variety of neurodegenerative disorders in which cognition is impaired. Moreover, brain structures which are considered anatomical substrata for learning and memory may be particularly vulnerable to the neurotoxic actions of these excitatory amino acids, especially in the elderly who are also the segment of the population most susceptible to impairments of mnemonic function. This paper is a review of data concerning the role of excitatory amino acids in the processes of learning and memory and in the pathogenesis and treatment of disorders thereof.

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Section: Glutamate In Disorders Of Learning and Memorymentioning

confidence: 99%

Glutamate: its role in learning, memory, and the aging brain

1993

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“…Large amounts of dietary alcohol can also affect the integrity of the myelin of white matter fibers (eg, Harper and Kril, 1988;Wiggins et al, 1988). A histological study (Irle and Markowitsch, 1983) examined three groups of Sprague-Dawley rats: an alcohol-only group, which for 20 months had available 30% alcohol in water as the only liquid; a thiamine-deficient group, which for 3-4 weeks had no thiamine in the diet; and a control group. The clearest damage in the alcohol group occurred in the dentate gyrus of the dorsal hippocampus, neurons of the mammillary nuclei, and shrinkage of the granular layer and of pyramidal cells in the dorsal vermis.…”

Section: Interaction Of Thiamine Deficiency and Alcohol Exposurementioning

confidence: 99%

Development and Resolution of Brain Lesions Caused by Pyrithiamine- and Dietary-Induced Thiamine Deficiency and Alcohol Exposure in the Alcohol-Preferring Rat: A Longitudinal Magnetic Resonance Imaging and Spectroscopy Study

Pfefferbaum

Adalsteinsson

Bell

et al. 2006

Neuropsychopharmacol

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Wernicke's encephalopathy (WE) is characterized by lesions in thalamus, hypothalamus (including mammillary nuclei), and inferior colliculi, results in serious disabilities, has an etiology of thiamine deficiency, is treatable with thiamine, and occurs most commonly with alcoholism. Despite decades of study, whether alcohol exposure exacerbates the neuropathology or retards its resolution remains controversial. To examine patterns of brain damage and recovery resulting from thiamine deprivation with and without alcohol exposure, we conducted in vivo magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) at 3 T in alcohol-preferring (P) rats, which had voluntarily consumed large amounts of alcohol before thiamine manipulation. A total of 18 adult male P rats (nine alcohol-exposed) received a thiamine-deficient diet for 2 weeks: 10 (five alcohol-exposed) received intraperitoneal (i.p.) pyrithiamine (PT) and eight (four alcohol-exposed) received i.p. thiamine supplementation. Neurological signs developed by day 14. Rats were scanned before thiamine depletion and 18 and 35 days after thiamine repletion. Two-dimensional J-resolved MRS single-voxel spectra with water reference were collected in a voxel subtending the thalamus; metabolite quantification was corrected for voxel tissue content. MRI identified significant enlargement of dorsal ventricles and increase in signal intensities in thalamus, inferior colliculi, and mammillary nuclei of PT compared with thiamine-treated (TT) groups from MRI 1-2, followed by significant normalization from MRI 2-3 in thalamus and colliculi, but not mammillary nuclei and lateral ventricles. Voxel-by-voxel analysis revealed additional hyperintense signal clusters in the dorsal and ventral hippocampus and enlargement of the fourth ventricle. MRS showed a significant decline and then partial recovery in thalamic N-acetylaspartate, a marker of neuronal integrity, in PT compared with TT rats, with no change detected in creatine, choline, or glutamate. PT rats with prior alcohol exposure exhibited attenuated recovery in the thalamus and arrested growth of the corpus callosum; further, two of the five alcohol-exposed PT rats died prematurely. Parenchymal and ventricular changes with thiamine manipulation concur with human radiological signs of WE. The enduring macrostructural and neurochemical abnormalities involving critical nodes of Papez circuit carry liabilities for development of amnesia and incomplete recovery from other cognitive and motor functions subserved by the affected neural systems.

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“…That the mamiUary body is related to processes involving memory has been shown in both man (18,19) and animals (20). When the mamillary body is damaged, there is a diminished ability to memorize or acquire learning.…”

Section: Discussionmentioning

confidence: 97%

Asymmetric incorporation of [14C]cyanate and of fluorescein isothiocyanate in mamillary body of conditioned rats

1988

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A marked decrease in overall learning capacity has been observed in rats injected with cyanate. Therefore it was of interest to test whether learning influenced carbamylation of brain proteins. Incorporation of [14C]cyanate into proteins of the mamillary body was selectively modified following operant conditioning of the rat, so that trained rats showed an asymmetric image with higher levels of incorporation in the right side than in the left side, as compared to control rats. These results were confirmed using fluorescein isothiocyanate. The asymmetry persisted once the learning had been well established.

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Widespread neuroanatomical damage and learning deficits following chronic alcohol consumption or vitamin-B1 (thiamine) deficiency in rats

Cited by 73 publications

References 37 publications

Glutamate: its role in learning, memory, and the aging brain

Glutamate: its role in learning, memory, and the aging brain

Development and Resolution of Brain Lesions Caused by Pyrithiamine- and Dietary-Induced Thiamine Deficiency and Alcohol Exposure in the Alcohol-Preferring Rat: A Longitudinal Magnetic Resonance Imaging and Spectroscopy Study

Asymmetric incorporation of [14C]cyanate and of fluorescein isothiocyanate in mamillary body of conditioned rats

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