Effects of GABAB receptor antagonists on learning and memory retention in a rat model of absence epilepsy

Getova, D.; Bowery, Norman G.; Spassov, V.

doi:10.1016/s0014-2999(96)00877-1

Cited by 66 publications

(31 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4 Clinically, atypical absence seizures are more complex than typical absence seizures and have a different natural history. The frequency of spike-and-wave is slower than 3Hz.…”

Section: 2mentioning

confidence: 99%

Hormonal regulation of atypical absence seizures

Persad

Wong

Cortez

et al. 2004

Annals of Neurology

View full text Add to dashboard Cite

A time course study that examined the effects of the female estrous cycle on the chronic slow spike-and-wave discharges (SSWDs), gamma-aminobutyric B receptor (GABA(B)R) binding, and GABA(B)R protein expression was conducted in Long Evans hooded rats treated during development with a cholesterol synthesis inhibitor AY9944 (AY). In addition, a pharmacological study using the hormones progesterone, 17 beta-estradiol, mifepristone (intracellular progesterone receptor antagonist), tamoxifen (intracellular estrogen receptor antagonist), and allopregnanolone (progesterone metabolite) was performed to determine their effects on AY-induced seizures. The data indicate that there is a significant increase in both the duration of SSWD and GABA(B)R binding in the AY model, during the proestrus stage of the estrous cycle, the stage during which the levels of progesterone are at their highest. No changes in GABA(B)R1a or R2 protein levels were observed. In addition, the administration of both progesterone and allopregnanolone exacerbated seizures in the AY model, whereas 17 beta-estradiol attenuated the SSWD duration. Neither mifepristone nor tamoxifen blocked the effects of progesterone and 17 beta-estradiol, respectively, on SSWD duration in the AY model, suggesting that these two sex hormones are working in a manner independent of their intracellular receptors. These data suggest an important role for steroid hormones in the regulation and maintenance of AY-induced atypical absence seizures.

show abstract

“…4 Clinically, atypical absence seizures are more complex than typical absence seizures and have a different natural history. The frequency of spike-and-wave is slower than 3Hz.…”

Section: 2mentioning

confidence: 99%

Hormonal regulation of atypical absence seizures

Persad

Wong

Cortez

et al. 2004

Annals of Neurology

View full text Add to dashboard Cite

show abstract

“…Moreover, possible clinical application of GABA B agonists/antagonists include spasticity [Bowery, 1993], epilepsy [Caddick and Hosford, 1996], drug withdrawal [Shoaib et al, 1998;Capasso, 1999], anxiety, depression, and cognitive dysfunction [Kerr and Ong, 1995;Getova et al, 1997].…”

Section: Introductionmentioning

confidence: 99%

Evidence for the gamma‐amino‐butyric acid type B receptor 1 (GABBR1) gene as a susceptibility factor in obsessive‐compulsive disorder

Zai

Arnold

Burroughs

et al. 2005

American J of Med Genetics Pt B

View full text Add to dashboard Cite

Obsessive-compulsive disorder (OCD) is a well-recognized severe neuropsychiatric illness. Genetic factors are believed to be important etiologically. Although historically genetic testing has focused on the serotonergic and dopaminergic systems, there is increasing evidence that the major inhibitory neurotransmitter, gamma-aminobutyric acid (GABA), may also be functionally involved. Furthermore the GABA type B receptor 1 (GABBR1) gene has been localized to chromosome 6p21.3 region, which has shown linkage to OCD. We investigated five polymorphisms (A-7265G substitution; C10497G substitution; A33795G substitution in the 3'-UTR; Ser-491-Ser-T1473C transition; Phe-659-Phe-T1977C transition) in the GABBR1 gene in a sample of 159 DSM-IV OCD probands and their families, using the transmission disequilibrium test (TDT). A trend was observed with an over-transmission of -7265A allele at the A-7265G polymorphism and OCD (chi2 = 3.270, P = 0.071). Moreover, the TDT haplotype analysis using TRANSMIT showed a trend toward association with the haplotype of the five polymorphisms together [2.1.1.2.1 (A-7265G.C10497G.Ser-491-Ser.Phe-659-Phe.A33795G)] with a Chi-square value of 3.418, which corresponds to a P-value of 0.065 (overall chi2 = 6.353, 5 df, P = 0.273). Moreover, a trend was observed for the total Yale-Brown obsessive-compulsive scale score in the A-7265G polymorphism (-7265A: z = 1.934, P = 0.053) using the Family-Based Association Test, considering the diagnosis of OCD and then the clinically relevant quantitative phenotypes. The observed trends suggest that further investigations of the role of the GABBR1 gene in OCD are warranted.

show abstract

“…In addition, potential candidates, for which susceptibility loci have been mapped in vicinity to the GABA B R1 gene, i.e., close to the HLA-F gene, include schizophrenia (SCZD3), reading disability (DYX2), and epilepsy [Greenberg et al, 1988;Cardon et al, 1994;Schwab et al, 1995;Straub et al, 1995;Wang et al, 1995;Sander et al, 1997]. Possible clinical applications of GABA B agonists/antagonists include spasticity [Bowery, 1993], epilepsy [Bowery, 1989;Caddick and Hosford, 1996], drug withdrawal [Shoaib et al, 1998;Capasso, 1999], anxiety, depression, and cognitive dysfunction [Kerr and Ong, 1995;Getova et al, 1997].…”

mentioning

confidence: 99%

Association of EEG coherence and an exonic GABA_BR1 gene polymorphism

Winterer

Smolka

Samochowiec

et al. 2002

American J of Med Genetics Pt B

View full text Add to dashboard Cite

The GABA(B) receptor 1 gene is mapped to chromosome 6p21.3 within the HLA class I region close to the HLA-F gene. Susceptibility loci for epilepsy and schizophrenia have been mapped in this region. Based on pharmacological evidence, it has been suggested that GABA(B) receptors may play a crucial role in the synchronization of EEG oscillations, which in turn can be abnormal in neuropsychiatric disorders. In the present study, the hypothesis was tested, whether three exonic variants of the gene encoding the human GABA(B) receptor (GABA(B)R1) modify cortical synchronization measured as scalp-recorded EEG-coherence. Two principal components of EEG coherence (frontal coherence, parietotemporal coherence) were investigated in 104 healthy subjects during three conditions: resting EEG, activated EEG, and event-related EEG. No significant associations were found between the frontal coherence component and any polymorphism or between the parietotemporal coherence component and the exon 1a1 polymorphism. However, parietotemporal coherence showed statistically highly significant associations across all three experimental conditions with exon 7 and trend associations with exon 11. The results provide evidence that the translated polymorphism of exon 7 may be functionally meaningful and impact cortical EEG oscillations. Since variations of EEG coherence have been described for several neuropsychiatric disorders, the present association should be tested in clinical samples using EEG coherence as an intermediate phenotype.

show abstract

Effects of GABAB receptor antagonists on learning and memory retention in a rat model of absence epilepsy

Cited by 66 publications

References 15 publications

Hormonal regulation of atypical absence seizures

Hormonal regulation of atypical absence seizures

Evidence for the gamma‐amino‐butyric acid type B receptor 1 (GABBR1) gene as a susceptibility factor in obsessive‐compulsive disorder

Association of EEG coherence and an exonic GABA_BR1 gene polymorphism

Contact Info

Product

Resources

About

Effects of GABAB receptor antagonists on learning and memory retention in a rat model of absence epilepsy

Cited by 66 publications

References 15 publications

Hormonal regulation of atypical absence seizures

Hormonal regulation of atypical absence seizures

Evidence for the gamma‐amino‐butyric acid type B receptor 1 (GABBR1) gene as a susceptibility factor in obsessive‐compulsive disorder

Association of EEG coherence and an exonic GABABR1 gene polymorphism

Contact Info

Product

Resources

About

Association of EEG coherence and an exonic GABA_BR1 gene polymorphism