GABAergic neurotransmission in the C57BL10, spssps mouse mutant: A model of absence seizures

Ortíz, José G.; Negrón, Arnaldo E.; Thomas, Aleyamma P.; Heimer, Hakon; Moreira, Jaime; Cordero, Mayra L.; Aranda, J. V.; Bruno, Maria S.

doi:10.1016/0014-4886(91)90024-7

Cited by 10 publications

(1 citation statement)

References 24 publications

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“…The results of BZD-GABAA receptor binding in animal models of absence seizures are very dependent on the model studied. In the tottering mouse, [3H]flunitrazepam binding to the BZD-GABAA receptor was normal (Psarropoulou et al, 1987), but in a mouse mutant with audiogenic "absences" [3H]flunitrazepam binding was reduced in all areas except hippocampus (Ortiz et al, 1991). In inbred rats with spontaneous absence seizures, which are believed to be more representative of the condition in humans, [3H]flunitrazepam binding was normal (Knight and Bowery, 1992;Snead et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Benzodiazepine‐GABA_A Receptors in Idiopathic Generalized Epilepsy Measured with [¹¹C]Flumazenil and Positron Emission Tomography

et al. 1995

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The neurochemical basis of absence seizures and the mechanism of their suppression by valproate (VPA) are uncertain. We used positron emission tomography (PET) to determine whether an abnormality of [11C]flumazenil binding to benzodiazepine (BZD)-GABAA receptors exists in patients with childhood and juvenile absence epilepsy and to examine the effects of VPA on [11C]flumazenil binding. The regional cerebral volume of distribution (Vd) of [11C]flumazenil in patients not treated with VPA was not different from that in normal controls; Vd was lower in patients treated with VPA, and the number of receptors available for binding was significantly reduced in such patients as compared with normal controls. There was no evidence of a primary abnormality of the BZD-GABAA receptor in childhood and juvenile absence epilepsy (CAE/JAE), but the data suggest that treatment with VPA is associated with a reduction in [11C]flumazenil binding that may be relevant to its mode of action in CAE/JAE.

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Section: Discussionmentioning

confidence: 99%

Benzodiazepine‐GABA_A Receptors in Idiopathic Generalized Epilepsy Measured with [¹¹C]Flumazenil and Positron Emission Tomography

et al. 1995

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GABA-gated chloride ion influx in brains of tremor rats

et al. 1993

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We measured the GABA-gated chloride ion influx and GABA concentrations in the cerebral cortex and the hippocampus of young (5 weeks old) and older (15 weeks old) tremor rats. GABA-gated chloride ion influx in these tremor rats was significantly greater than in the controls of both the 5 week- and 15 week-old groups. GABA concentrations in the cerebral cortex and hippocampus of the tremor rats increased compared with controls of 5 weeks and decreased compared with controls of 15 weeks. These findings suggest that the GABAergic presynaptic neurons in the cortex and hippocampus of the tremor rat are disturbed with aging. This change may be related to the appearance of absence-like seizures in the rats. The increased GABA-gated chloride ion influx in tremor rats may be a compensatory mechanism against the genetically-determined seizure susceptibility of these rats. Furthermore, the increased GABA levels and GABA-gated chloride ion influx found in 5 week-old tremor rats may be related to the tremor movements.

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Altered GABAergic and glutamatergic transmission in audiogenic seizure-susceptible mice

et al. 1994

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The C57BL/10 SPS/sps mouse mutant are audiogenic seizure-susceptible. The enzymatic activities of glutamate decarboxylase (GAD), GABA aminotransferase (GABA-T), alanine aminotransferase (ALA-T), aspartate aminotransferase (ASP-T), and glutamate dehydrogenase (GDH) of whole brain supernatant are significantly reduced in these epileptic mice. GABA uptake is decreased in cortex, midbrain, and pons medulla. Previous studies showed the presence of two sodium-dependent GLU uptake systems in normal (SPS/SP) mice. Glutamate Umax by System 1 is significantly decreased in these mice, whereas the Umax value for System 2 is significantly increased in the epileptic mice.

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GABAergic neurotransmission in the C57BL10, spssps mouse mutant: A model of absence seizures

Cited by 10 publications

References 24 publications

Benzodiazepine‐GABA_A Receptors in Idiopathic Generalized Epilepsy Measured with [¹¹C]Flumazenil and Positron Emission Tomography

Benzodiazepine‐GABA_A Receptors in Idiopathic Generalized Epilepsy Measured with [¹¹C]Flumazenil and Positron Emission Tomography

GABA-gated chloride ion influx in brains of tremor rats

Altered GABAergic and glutamatergic transmission in audiogenic seizure-susceptible mice

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GABAergic neurotransmission in the C57BL10, spssps mouse mutant: A model of absence seizures

Cited by 10 publications

References 24 publications

Benzodiazepine‐GABAA Receptors in Idiopathic Generalized Epilepsy Measured with [11C]Flumazenil and Positron Emission Tomography

Benzodiazepine‐GABAA Receptors in Idiopathic Generalized Epilepsy Measured with [11C]Flumazenil and Positron Emission Tomography

GABA-gated chloride ion influx in brains of tremor rats

Altered GABAergic and glutamatergic transmission in audiogenic seizure-susceptible mice

Contact Info

Product

Resources

About

Benzodiazepine‐GABA_A Receptors in Idiopathic Generalized Epilepsy Measured with [¹¹C]Flumazenil and Positron Emission Tomography

Benzodiazepine‐GABA_A Receptors in Idiopathic Generalized Epilepsy Measured with [¹¹C]Flumazenil and Positron Emission Tomography