Morphologic and neurochemical alterations in the superior colliculus of the genetically epilepsy-prone hamster (GPG/Vall)

Fuentes–Santamaría, Verónica; Alvarado, Juan Carlos; Herranz, Arantxa; García-Atarés, Natividad; López, Dolores E.

doi:10.1016/j.eplepsyres.2007.06.005

Cited by 16 publications

(15 citation statements)

References 79 publications

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“…Since various studies have reported that taurine could have a neuroprotective role in epilepsy (Lehmann et al, 1985; French et al, 1986; Schurr et al, 1987; Trenkner, 1990; Wu et al, 1994, 2005; Birdsall, 1998; Gupta et al, 2005; Junyent et al, 2009), we decided to use this experimental model for its relation with taurine neuroprotection. Moreover alterations in taurine levels in the brain due to epilepsy have also been reported using the KA model (Baran, 2006; Fuentes‐Santamaria et al, 2007). Moreover, it has been demonstrated that taurine deficits prolong seizure activities and cause persistent hyperexcitability states in the brain (Barbeau and Donaldson, 1974; Mutani et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

Content and traffic of taurine in hippocampal reactive astrocytes

et al. 2011

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Taurine is one of the most abundant free amino acids in the mammalian central nervous system, where it is crucial to proper development. Moreover, taurine acts as a neuroprotectant in various diseases; in epilepsy, for example, it has the capacity to reduce or abolish seizures. In the present study, taurine levels has been determine in mice treated with Kainic Acid (KA) and results showed an increase of this amino acid in hippocampus but not in whole brain after 3 and 7 days of KA treatment. This increase occurs when gliosis was observed. Moreover, taurine transporter (TAUT) was found in astrocytes 3 and 7 days after KA treatment, together with an increase in cysteine sulfinic acid decarboxylase (csd) mRNA, that codifies for the rate-limiting enzyme of taurine synthesis, in the hippocampus at the same times after KA treatment. Glial cultures enriched in astrocytes were developed to demonstrate that these cells are responsible for changes in taurine levels after an injury to the brain. The cultures were treated with proinflammatory cytokines to reproduce gliosis. In this experimental model, an increase in the immunoreactivity of GFAP was observed, together with an increase in CSD and taurine levels. Moreover, an alteration in the taurine uptake-release kinetics was detected in glial cells treated with cytokine. All data obtained indicate that astrocytes could play a key role in taurine level changes induced by neuronal damage. More studies are, therefore, needed to clarify the role taurine has in relation to neuronal death and repair.

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Section: Discussionmentioning

confidence: 99%

Content and traffic of taurine in hippocampal reactive astrocytes

et al. 2011

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“…The densitometry procedure to evaluate immunostaining was performed as described elsewhere (Fuentes-Santamaría et al, 2003, 2005a,b, 2007a,b, 2008; Alvarado et al, 2004, 2005, 2007, 2009) using the public domain image analysis software Scion Image for Windows (version beta 4.0.2; developed by Scion Corp). The CN subdivisions were defined based on previous studies (for review, see Cant and Benson, 2003).…”

Section: Analysis Of Immunostainingmentioning

confidence: 99%

Wistar rats: a forgotten model of age-related hearing loss

Alvarado

Fuentes–Santamaría²,

Gabaldón-Ull³

et al. 2014

Front. Aging Neurosci.

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Age-related hearing loss (ARHL) is one of the most frequent sensory impairments in senescence and is a source of important socio-economic consequences. Understanding the pathological responses that occur in the central auditory pathway of patients who suffer from this disability is vital to improve its diagnosis and treatment. Therefore, the goal of this study was to characterize age-related modifications in auditory brainstem responses (ABR) and to determine whether these functional responses might be accompanied by an imbalance between excitation and inhibition in the cochlear nucleus of Wistar rats. To do so, ABR recordings at different frequencies and immunohistochemistry for the vesicular glutamate transporter 1 (VGLUT1) and the vesicular GABA transporter (VGAT) in the ventral cochlear nucleus (VCN) were performed in young, middle-aged and old male Wistar rats. The results demonstrate that there was a significant increase in the auditory thresholds, a significant decrease in the amplitudes and an increase in the latencies of the ABR waves as the age of the rat increased. Additionally, there were decreases in VGLUT1 and VGAT immunostaining in the VCN of older rats compared to younger rats. Therefore, the observed age-related decline in the magnitude of auditory evoked responses might be due in part to a reduction in markers of excitatory function; meanwhile, the concomitant reduction in both excitatory and inhibitory markers might reflect a common central alteration in animal models of ARLH. Together, these findings highlight the suitability of the Wistar rat as an excellent model to study ARHL.

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“…Further evidence that SC is involved in the propagation of seizure activity was provided in GEPR‐9s by in situ hybridization for c‐fos mRNA (Ribak et al., 1994). More recently, Fuentes‐Santamaría et al. (2007) showed morphologic and neurochemical abnormalities in SC deep layers in genetically epilepsy‐prone hamsters (GPG/Vall).…”

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confidence: 99%

Role of the superior colliculus in the expression of acute and kindled audiogenic seizures in Wistar audiogenic rats

et al. 2009

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SUMMARYPurpose: The role of the superior colliculus (SC) in seizure expression is controversial and appears to be dependent upon the epilepsy model. This study shows the effect of disconnection between SC deep layers and adjacent tissues in the expression of acute and kindling seizures. Methods: Subcollicular transections, ablation of SC superficial and deep layers, and ablation of only the cerebral cortex were evaluated in the Wistar audiogenic rat (WAR) strain during acute and kindled audiogenic seizures. The audiogenic seizure kindling protocol started 4 days after surgeries, with two acoustic stimuli per day for 10 days. Acute audiogenic seizures were evaluated by a categorized seizure severity midbrain index (cSI) and kindled seizures by a severity limbic index (LI). Results: All subcollicular transections reaching the deep layers of the SC abolished audiogenic seizures or significantly decreased cSI. In the unlesioned kindled group, a reciprocal relationship between limbic and brainstem pattern of seizures was seen. The increased number of stimuli provoked an audiogenic kindling phenomenon. Ablation of the entire SC (ablation group) or of the cerebral cortex only (ctx-operated group) hampered the acquisition of limbic behaviors. There was no difference in cSI and LI between the ctx-operated and ablation groups, but there was a difference between ctx-operated and the unlesioned kindled group. There was also no difference in cSI between SC deep layer transection and ablation groups. Results of histologic analyses were similar for acute and kindled audiogenic seizure groups. Conclusions: SC deep layers are involved in the expression of acute and kindled audiogenic seizure, and the cerebral cortex is essential for audiogenic kindling development.

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Morphologic and neurochemical alterations in the superior colliculus of the genetically epilepsy-prone hamster (GPG/Vall)

Cited by 16 publications

References 79 publications

Content and traffic of taurine in hippocampal reactive astrocytes

Content and traffic of taurine in hippocampal reactive astrocytes

Wistar rats: a forgotten model of age-related hearing loss

Role of the superior colliculus in the expression of acute and kindled audiogenic seizures in Wistar audiogenic rats

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