Hippocampal AgNOR activity after chronic alcohol consumption and alcohol deprivation in rats

García‐Moreno, Luis Miguel; Conejo, Nélida M.; Pardo, Héctor González; Gómez, Manuel; Martín, Francisco Ricardo Alvira; Alonso, Mariana; Árias, Jorge L.

doi:10.1016/s0031-9384(00)00408-x

Cited by 27 publications

(10 citation statements)

References 38 publications

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“…A prominent feature of chronic ethanol intake in rodents is impairment of hippocampal-dependent learning and memory (e.g., Cagetti, Pinna, Guidotti, Baicy, & Olsen, 2004; Lukoyanov, Pereira, Paula-Barbosa, & Cadete-Leite, 2003), which occurs as a consequence of the vulnerability of the hippocampus to ethanol-induced neurodegeneration (Garcia-Moreno et al, 2001; Paula-Barbosa, Brandao, Madeira, & Cadete-Leite, 1993). However, the degree of cognitive impairment is dependent upon the duration of ethanol exposure, the degree of resultant malnutrition, the animal strain, and number of withdrawal episodes.…”

Section: Introductionmentioning

confidence: 99%

Alcohol-related amnesia and dementia: Animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment

Vetreno

Hall

Savage

2011

Neurobiology of Learning and Memory

126

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Chronic alcoholism is associated with impaired cognitive functioning. Over 75% of autopsied chronic alcoholics have significant brain damage and over 50% of detoxified alcoholics display some degree of learning and memory impairment. However, the relative contributions of different etiological factors to the development of alcohol-related neuropathology and cognitive impairment are questioned. One reason for this quandary is that both alcohol toxicity and thiamine deficiency result in brain damage and cognitive problems. Two alcohol-related neurological disorders, alcohol-associated dementia and Wernicke-Korsakoff syndrome have been modeled in rodents. These pre-clinical models have elucidated the relative contributions of ethanol toxicity and thiamine deficiency to the development of dementia and amnesia. What is observed in these models-from repeated and chronic ethanol exposure to thiamine deficiency-is a progression of both neural and cognitive dysregulation. Repeated binge exposure to ethanol leads to changes in neural plasticity by reducing GABAergic inhibition and facilitating glutamatergic excitation, longterm chronic ethanol exposure results in hippocampal and cortical cell loss as well as reduced hippocampal neurotrophin protein content critical for neural survival, and thiamine deficiency results in gross pathological lesions in the diencephalon, reduced neurotrophic protein levels, and neurotransmitters levels in the hippocampus and cortex. Behaviorally, after recovery from repeated or chronic ethanol exposure there is impairment in working or episodic memory that can recover with prolonged abstinence. In contrast, after thiamine deficiency there is severe and persistent spatial memory impairments and increased perseverative behavior. The interaction between ethanol and thiamine deficiency does not produce more behavioral or neural pathology, with the exception of reduction of white matter, than long-term thiamine deficiency alone.

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Section: Introductionmentioning

confidence: 99%

Alcohol-related amnesia and dementia: Animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment

Vetreno

Hall

Savage

2011

Neurobiology of Learning and Memory

126

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“…The silver-stained NOR (AgNOR) represents the site of ribosomal RNA synthesis and transcriptionally active NOR and is synonymous with the nucleolar area. Therefore, cellular activity, in terms of the transcriptional activity of rDNA, can be approximated by measuring AgNOR (Ploton et al 1986(Ploton et al , 1992Ploton 1994;Rü schoff et al 1995;Derenzini 2000;Garcia-Moreno et al 2001). Many studies revealed the positive correlation between the karyometric parameters, especially the nuclear area and the neuronal activity (Reinhardt et al 1969;Bandaranayake 1974;Gonzalez-Pardo et al 1994;Qü et al 1994;Mennel and Mü ller 1994;GonzalezGonzalez et al 1996;Rubio et al 1997;Garcia Moreno et al 1997Vargas et al 2000).…”

Section: Introductionmentioning

confidence: 99%

The changes of AgNOR parameters of anterior cingulate pyramidal neurons are region-specific in suicidal and non-suicidal depressive patients

Gos

Krell

Brisch

et al. 2007

The World Journal of Biological Psychiatry

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The anterior cingulate cortex (AC) is consistently implicated in the pathophysiology of depression. While suicide has been shown in previous reports to be closely related to depression, it is still a distinct phenomenon. The aim to differentiate between depression and suicide was approached by the karyometric analysis of AC pyramidal neurons. The study was performed on paraffin-embedded brains from 20 depressive patients (10 of whom had committed suicide) and 24 matched controls. The karyometric parameters of the layer III and V pyramidal neurons of the dorsal and ventral AC were evaluated bilaterally by Argyrophilic Nucleolar Organiser (AgNOR) silver staining method. Control-specific was the increased nuclear area in ontogenetically younger pyramidal neurons layer III in the left dorsal compared with ventral AC (Wilcoxon test, P<0.01). The decreased AgNOR number per nucleus in these cells in the right ventral AC was depression-specific compared with controls (t-test, P=0.047). On the other hand, the diffuse decrease in AgNOR ratio throughout pyramidal neurons on the left side was specific for suicidal depressive patients compared with non-suicidal patients and controls (ANOVA, P=0.028). The results suggest that regionally differentiated depression- and suicide-specific disturbed function of the most important AC output cells exists in depressive patients.

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“…This appears to be especially true for the pyramidal neurons of the CA3 region, an observation that has recently been replicated in primates (McMillan et al, 2004). Early animal data suggest that injury to this specific region may play a role in the memory disorders related to the heavy, chronic drinking characteristic of alcohol dependence (AD; Garcia-Moreno et al, 2001;Lukoyanov et al, 1999;Nelson et al, 1999). Additionally, recent research suggests a link between apparent cortisol-mediated hippocampal volume reductions and problems in memory and other cognitive processes (Eriksson et al, 2001;MacLullich et al, 2005;O'Brien et al, 2004;Vythilingam et al, 2004).…”

mentioning

confidence: 96%

Hypercortisolism in Alcohol Dependence and Its Relation to Hippocampal Volume Loss

Beresford¹,

Arciniegas²,

Alfers³

et al. 2006

J. Stud. Alcohol

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E ARLY STUDIES OF ALCOHOL USE and the hypothalamic-pituitary-adrenal (HPA) axis noted an increase in cortisol production among chronic heavy drinkers. This was manifested clinically by apparent adrenal insufficiency or a pseudo-Cushing's syndrome (Farmer and Fabre, 1975). In experimental conditions, chronic heavy drinkers demonstrated increased cortisol levels with ingestion of ethanol acutely and with greater increases in the early stages of

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Hippocampal AgNOR activity after chronic alcohol consumption and alcohol deprivation in rats

Cited by 27 publications

References 38 publications

Alcohol-related amnesia and dementia: Animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment

Alcohol-related amnesia and dementia: Animal models have revealed the contributions of different etiological factors on neuropathology, neurochemical dysfunction and cognitive impairment

The changes of AgNOR parameters of anterior cingulate pyramidal neurons are region-specific in suicidal and non-suicidal depressive patients

Hypercortisolism in Alcohol Dependence and Its Relation to Hippocampal Volume Loss

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