Correlation between phosphorylation level of a hippocampal 86kDa protein and extinction of a behaviour in a model of Wernicke–Korsakoff syndrome

Pires, Rita Gomes Wanderley; Pereira, Simone Cardoso Lisboa; Carvalho, Fabiana M.; Oliveira-Silva, Ieda F.; Ferraz, Vany; Ribeiro, Ângela Maria

doi:10.1016/j.bbr.2007.02.017

Cited by 6 publications

(4 citation statements)

References 46 publications

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“…Perhaps the first to study this systematically in laboratory animals was Schneider-Rivas and his group. The decline of extinction seen in old rats correlates with changes in brain serotonin and 5-hydroxy-indole acetic acid in neocortex, hippocampus, thalamus, and dorsal raphe nucleus compatible with predictions from the serotonin hypothesis of depression, as well as with other brain neurochemical correlates ([82], see also [84, 85]). Others have reported an abnormality of forced extinction in aged rats submitted to removal of the escape platform in a water maze ([83, 86–88], see also [89]).…”

Section: Aging and Extinctionsupporting

confidence: 75%

The Role of the Entorhinal Cortex in Extinction: Influences of Aging

et al. 2008

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The entorhinal cortex is perhaps the area of the brain in which neurofibrillary tangles and amyloid plaques are first detectable in old age with or without mild cognitive impairment, and very particularly in Alzheimer's disease. It plays a key role in memory formation, retrieval, and extinction, as part of circuits that include the hippocampus, the amygdaloid nucleus, and several regions of the neocortex, in particular of the prefrontal cortex. Lesions or biochemical impairments of the entorhinal cortex hinder extinction. Microinfusion experiments have shown that glutamate NMDA receptors, calcium and calmodulin-dependent protein kinase II, and protein synthesis in the entorhinal cortex are involved in and required for extinction. Aging also hinders extinction; it is possible that its effect may be in part mediated by the entorhinal cortex.

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Section: Aging and Extinctionsupporting

confidence: 75%

The Role of the Entorhinal Cortex in Extinction: Influences of Aging

et al. 2008

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“…For instance, studies have shown that hippocampal dependent learning stimulated the ERK dependent phosphorylation of synapsin I [23,24] and that deficits in spatial learning could, in part, be attributed to depressed levels of synapsin I [25]. These results are in agreement with our previous study indicating changes in the phosphorylation levels of some proteins in the hippocampus of rats after the PTD treatment, particularly the p86 protein [14]. Moreover, performance on the water maze correlated with the amount of phosphorylation of the p86 protein, of which synapsin I is a possible candidate.…”

supporting

confidence: 92%

“…Synapsin I tethers small synaptic vesicles to the actin cytoskeleton in a phosphorylation-dependent manner thereby regulating vesicular availability in the nerve terminals and subsequent neurotransmitter release [13]. Pires et al [14] found alterations in a number of hippocampal phosphorylated proteins in rats following chronic ethanol exposure and thiamine deficiency. Importantly, these studies found changes in a hippocampal 86 kDa protein and was suggested to be synapsin I.…”

mentioning

confidence: 99%

Thiamine deficiency degrades the link between spatial behavior and hippocampal synapsin I and phosphorylated synapsin I protein levels

Resende

Ribeiro

Werner

et al. 2012

Behavioural Brain Research

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The links between spatial behavior and hippocampal levels of synapsin I and phosphosynapsin I were assessed in normal rats and in the pyrithiamine-induced thiamine deficiency (PTD) rat model of Wernicke–Korsakoff’s syndrome. Synapsin I tethers small synaptic vesicles to the actin cytoskeleton in a phosphorylation-dependent manner, is involved in neurotransmitter release and has been implicated in hippocampal-dependent learning. Positive correlations between spontaneous alternation behavior and hippocampal levels of both synapsin I and phosphorylated synapsin I were found in control rats. However, spontaneous alternation performance was impaired in PTD rats and was accompanied by a significant reduction (30%) in phosphorylated synapsin I. Furthermore, no correlations were observed between either form of synapsin I and behavior in PTD rats. These data suggest that successful spontaneous alternation performance is related to high levels of hippocampal synapsin I and phosphorylated synapsin I. These results not only support the previous findings that implicate impaired hippocampal neurotransmission in the spatial learning and memory deficits associated with thiamine deficiency, but also suggest a presynaptic mechanism.

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“…These data suggest that mice treated with amprolium PO developed neurological disorders, similar to that observed in other TD models. Studies have reported quite wide alterations in TD rodents, such as cognitive, learning, and memory dysfunctions (NAKAGAWASAI et al, 2004;PIRES et al, 2007;PITKIN;SAVAGE, 2004), and motor activity impairments (FERREIRA-VIEIRA et al, 2016). Additionally, these behavioural dysfunctions were correlated with changes in cholinergic, GABAergic, and glutamatergic neurotransmission (FERREIRA-VIEIRA et al, 2016;FREITAS-SILVA et al, 2010;PITKIN;SAVAGE, 2004).…”

Section: Discussionmentioning

confidence: 99%

Amprolium-induced thiamine deficiency in mice: evaluation of a practical model by oral administration

Córdova

Cordova

Medeiros

et al. 2017

AVB

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Thiamine is an essential cofactor for several cellular functions. Your deficiency results in important neurological disorders, with mechanisms and lesions not fully understood. The purpose of this work was to evaluate a thiamine deficiency through the model of oral administration of amprolium in mice. The animals, treated for 20 or 80 days, received amprolium in drinking water at doses of 10, 20, and 30 mg/mL (deficient groups A, B, and C, respectively). Deficient groups A and B showed reduction in body weight gain and performance changes in the open field (decreased distance and rearing, and increased grooming) and rotarod (reduced latency to fall) behavioural tests, when treated for 80 days. However, no histological changes were observed in the central nervous system. Moreover, group B animals exposed to amprolium developed proteinuria, with moderate tubular nephrosis, at 80 days. At the highest dose (group C) there was no interest to drink water. The data suggest that the use of oral amprolium in mice may be an interesting and viable model, when using adequate exposure times and doses. The amprolium induces thiamine deficiency progressively and moderately, which may be potentially useful for disturbed pathogenesis studies.

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Correlation between phosphorylation level of a hippocampal 86kDa protein and extinction of a behaviour in a model of Wernicke–Korsakoff syndrome

Cited by 6 publications

References 46 publications

The Role of the Entorhinal Cortex in Extinction: Influences of Aging

The Role of the Entorhinal Cortex in Extinction: Influences of Aging

Thiamine deficiency degrades the link between spatial behavior and hippocampal synapsin I and phosphorylated synapsin I protein levels

Amprolium-induced thiamine deficiency in mice: evaluation of a practical model by oral administration

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