A Comparison of Cochlear Microphonics and N<sub>1</sub>in Audiogenic-Seizure-Susceptible and Control Rats<sup>1</sup>

Glenn, D W; Jobe, Phillip C.; Penny, J. E.; Bourn, W.M.

doi:10.1080/01616412.1980.11739573

Cited by 18 publications

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“…The genetically epilepsy‐prone rat (GEPR) is an animal model that exhibits generalized tonic–clonic seizures when exposed to sound stimulation (94). Several abnormalities in the organ of Corti of these animals have been observed, including missing inner and outer hair cells and abnormally long stereocilia that might contribute to susceptibility and intensity of audiogenic seizures (82,83,95). Similar to the GEPR, in the GPG/Vall hamster, a loss of outer hair cells in the organ of Corti was also observed.…”

Section: Discussionmentioning

confidence: 99%

Morphologic and Neurochemical Abnormalities in the Auditory Brainstem of the Genetically Epilepsy‐prone Hamster (GPG/Vall)

et al. 2005

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Summary:Purpose: This study was performed to evaluate whether audiogenic seizures, in a strain of genetically epilepsyprone hamsters (GPG/Vall), might be associated with morphologic alterations in the cochlea and auditory brainstem. In addition, we used parvalbumin as a marker of neurons with high levels of activity to examine changes within neurons.Methods: Cochlear histology as well as parvalbumin immunohistochemistry were performed to assess possible abnormalities in the GPG/Vall hamster. Densitometry also was used to quantify levels of parvalbumin immunostaining within neurons and fibers in auditory nuclei.Results: In the present study, missing outer hair cells and spiral ganglion cells were observed in the GPG/Vall hamster. In addition, an increase was noted in the size of spiral ganglion cells as well as a decrease in the volume and cell size of the cochlear nucleus (CN), the superior olivary complex nuclei (SOC), and the nuclei of the lateral lemniscus (LL) and the inferior colliculus (IC). These alterations were accompanied by an increase in levels of parvalbumin immunostaining within CN, SOC, and LL neurons, as well as within parvalbumin-immunostained fibers in the CN and IC.Conclusions: These data are consistent with a cascade of atrophic changes starting in the cochlea and extending along the auditory brainstem in an animal model of inherited epilepsy. Our data also show an upregulation in parvalbumin immunostaining in the neuropil of the IC that may reflect a protective mechanism to prevent cell death in the afferent sources to this nucleus. Key Words: Calcium-binding protein-AGS-Animal model-Hamster.Animal models of inherited epilepsy are essential to understand the origin of epileptic seizures because they represent an abnormal nervous system and reproduce the mechanisms of hyperexcitability than occur in nature (1). In numerous species, including rat (2,3), mouse (4,5), gerbil (6), and baboon (7), genetic models of epilepsy are available. In these models, several steps have been identified in the cascade leading from seizure-activity episodes to long-lasting and quasi-permanent modifications of the neuronal circuitry organization. These include neuron atrophy (8), cell death (9), neuronal degeneration (10), synaptic rearrangement (11), abnormalities in the expression of neurotransmitters and/or their receptors (12)(13)(14), and changes in intracellular signaling pathways in which calcium-related mechanisms are involved (15-17).

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Section: Discussionmentioning

confidence: 99%

Morphologic and Neurochemical Abnormalities in the Auditory Brainstem of the Genetically Epilepsy‐prone Hamster (GPG/Vall)

et al. 2005

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“…Since AS are evoked by a high-intensity acoustic stimulus, the primary auditory pathway has been the first cluster of structures to be evaluated in audiogenic susceptible rodent strains. In this context, several research groups have detected peripheral alterations associated with AS susceptibility, such as hearing loss (Saunders et al, 1972;Glenn et al, 1980;Faingold et al, 1990), unbalance between GABAergic and Glutamatergic neurotransmissions between the inner hair cells and the cochlear nerve (Altschuler et al, 1989;Bobbin et al, 1990;Lefebvre et al, 1991), and tinnitus followed by intensity sound exposure (Heffner and Harrington, 2002;Chen et al, 2013). Similarly, anatomical and morphological alterations in the organ of Corti and in the inner and outer hair cells of the GEPRs have already been observed (Penny et al, 1983(Penny et al, , 1986.…”

Section: Neuronal Network Involved In Audiogenic Seizuresmentioning

confidence: 97%

Cannabinoids in Audiogenic Seizures: From Neuronal Networks to Future Perspectives for Epilepsy Treatment

Lazarini-Lopes

Silva

Silva-Júnior

et al. 2021

Front. Behav. Neurosci.

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Cannabinoids and Cannabis-derived compounds have been receiving especial attention in the epilepsy research scenario. Pharmacological modulation of endocannabinoid system's components, like cannabinoid type 1 receptors (CB1R) and their bindings, are associated with seizures in preclinical models. CB1R expression and functionality were altered in humans and preclinical models of seizures. Additionally, Cannabis-derived compounds, like cannabidiol (CBD), present anticonvulsant activity in humans and in a great variety of animal models. Audiogenic seizures (AS) are induced in genetically susceptible animals by high-intensity sound stimulation. Audiogenic strains, like the Genetically Epilepsy Prone Rats, Wistar Audiogenic Rats, and Krushinsky-Molodkina, are useful tools to study epilepsy. In audiogenic susceptible animals, acute acoustic stimulation induces brainstem-dependent wild running and tonic-clonic seizures. However, during the chronic protocol of AS, the audiogenic kindling (AuK), limbic and cortical structures are recruited, and the initially brainstem-dependent seizures give rise to limbic seizures. The present study reviewed the effects of pharmacological modulation of the endocannabinoid system in audiogenic seizure susceptibility and expression. The effects of Cannabis-derived compounds in audiogenic seizures were also reviewed, with especial attention to CBD. CB1R activation, as well Cannabis-derived compounds, induced anticonvulsant effects against audiogenic seizures, but the effects of cannabinoids modulation and Cannabis-derived compounds still need to be verified in chronic audiogenic seizures. The effects of cannabinoids and Cannabis-derived compounds should be further investigated not only in audiogenic seizures, but also in epilepsy related comorbidities present in audiogenic strains, like anxiety, and depression.

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“…The underlying biochemical mechanisms responsible for AGS-susceptibility have not been conclusively established but there is some evidence for a defect in noradrenergic and possibly serotoninergic transmission in the central nervous system of these animals (Jobe et al 1973;Shaywitz et al 1978;Jobe et al 1982). Changes in central neurotransmitters may be the consequence of a genetically determined cochlear impairment (Glenn et al 1980) leading to a reduced auditory input during the ontogenetic development of the central nervous system (Jobe 1981).…”

mentioning

confidence: 99%

A Study on Benzodiazepine Receptor Binding in Audiogenic Seizure‐susceptible Rats

Tacke

Bræstrup

1984

Acta Pharmacologica et Toxicologica

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Benzodiazepine receptors were investigated in the cerebral cortex, the hippocampus, the brainstem, and the cerebellum of audiogenic seizure (AGS)‐susceptible and seizure‐resistant (ER) control rats. In AGS‐susceptible rats of Sprague‐Dawley descent, muscimol (10‐6 M and 3 × 10‐5 M) activated the binding of 3H‐diazepam (0.4 nM) significantly less than in ER‐rats. This finding may be strain selective, since it was not observed in AGS‐susceptible rats of Wistar descent. Specific binding of the convulsant benzodiazepine receptor ligand methyl 6,7‐dimethoxy‐4‐ethyl carboline‐3‐carboxylate (3H‐DMCM), the benzodiazepine receptor ligand 3H‐diazepam and the chloride channel directed cage convulsant t‐butylbicyclophosphorothion‐ate 35S‐TBPS were not significantly changed in AGS‐susceptible as compared to control rats. Our findings indicate that a disturbance at the level of the benzodiazepine receptor/GABA receptor/chloride channel complex is not a likely general aetiological factor for audigenic seizures in rats.

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A Comparison of Cochlear Microphonics and N₁in Audiogenic-Seizure-Susceptible and Control Rats¹

Cited by 18 publications

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Morphologic and Neurochemical Abnormalities in the Auditory Brainstem of the Genetically Epilepsy‐prone Hamster (GPG/Vall)

Morphologic and Neurochemical Abnormalities in the Auditory Brainstem of the Genetically Epilepsy‐prone Hamster (GPG/Vall)

Cannabinoids in Audiogenic Seizures: From Neuronal Networks to Future Perspectives for Epilepsy Treatment

A Study on Benzodiazepine Receptor Binding in Audiogenic Seizure‐susceptible Rats

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A Comparison of Cochlear Microphonics and N1in Audiogenic-Seizure-Susceptible and Control Rats1

Cited by 18 publications

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Morphologic and Neurochemical Abnormalities in the Auditory Brainstem of the Genetically Epilepsy‐prone Hamster (GPG/Vall)

Morphologic and Neurochemical Abnormalities in the Auditory Brainstem of the Genetically Epilepsy‐prone Hamster (GPG/Vall)

Cannabinoids in Audiogenic Seizures: From Neuronal Networks to Future Perspectives for Epilepsy Treatment

A Study on Benzodiazepine Receptor Binding in Audiogenic Seizure‐susceptible Rats

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A Comparison of Cochlear Microphonics and N₁in Audiogenic-Seizure-Susceptible and Control Rats¹