Thyroid hormonal modulation of the binding and activity of the GABAA receptor complex of brain

Martin, Joseph V.; Williams, Daniel B.; Fitzgerald, Raina; Im, H. K.; VonVoigtlander, Philip F.

doi:10.1016/0306-4522(96)00052-8

Cited by 69 publications

(46 citation statements)

References 54 publications

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“…The inhibition of [ 35 S]-TBPS binding observed at higher concentrations of somatostatin, may represent a direct activation of the GABA-dependent Cl⁻ channels, as suggested for some neuromodulators acting at the GABA A receptor complex (Sieghart, 2012;Samochocki and Stroszndjer, 1993;Concas et al, 1994;Quinn and Harris, 1995;Martin et al, 1996;Sanna et al, 1996). This suggestion is consistent with the evidence that somatostatin-induced inhibition of [ 35 S]-TBPS binding, is blocked by bicuculline (Concas et al, 1994).…”

Section: Discussionsupporting

confidence: 79%

MODULATION OF THE GABA<sub>A</sub> RECEPTOR BY SRIF IN RAT THALAMUS

Chigr¹

2012

American Journal of Neuroscience

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Somatostatin has been reported to modulate GABA A receptor complex in many brain structures. This study was conducted to investigate somatostatin modulation of the GABA A receptor binding in several rat diencephalic structures, focusing primarily on the thalamus, as this structure plays important roles. Animals were assigned to control conditions. Changes in specific binding of GABA A receptor as labelled with [35 S]tButylbicyclophosphorothionate (TBPS) were assessed by in vitro quantitative autoradiography with the aid of a computer assisted image analysis system. Our results reveal the presence of higher densities in several thalamic structures located principally in the part of thalamus. We demonstrate for the first time the presence of a modulatory effect of somatostatin on the GABA A receptor complex in this brain region in rats. Indeed, the peptide affected in a concentration-dependent manner; the binding of

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Section: Discussionsupporting

confidence: 79%

MODULATION OF THE GABA<sub>A</sub> RECEPTOR BY SRIF IN RAT THALAMUS

Chigr¹

2012

American Journal of Neuroscience

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“…In this context, Martin et al (1996) have demonstrated that TH could modulate GABA A receptors. Moreover, the shortterm effects of the TH mediated by the activity of GABA receptors that we are evidencing in the present report are in line with Chapell et al (1998), who described that micromolar concentrations of T 3 can directly activate GABA A receptor chloride channels, and these responses were inhibited by picrotoxin but not bicuculline.…”

Section: Discussionmentioning

confidence: 98%

Short-Term Effects of Thyroid Hormones on Cytoskeletal Proteins Are Mediated by GABAergic Mechanisms in Slices of Cerebral Cortex from Young Rats

et al. 2006

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: Thyroid hormones play important roles in brain function. However, few information is available about the effect of 3,5,3'-triiodo-L-thyronine (T(3)) or thyroxine (T(4)) on the in vitro phosphorylation of intermediate filament (IF) proteins from cerebral cortex of rats. In this study we investigated the involvement of GABAergic mechanisms mediating the effects of T(3) and T(4) on the in vitro incorporation of (32)P into IF proteins from cerebral cortex of 10-day-old male rats. Tissue slices were incubated with or without T(3), T(4), gamma-aminobutiric acid (GABA), kinase inhibitors or specific GABA antagonists and (32)P-orthophosphate for 30 min. The IF-enriched cytoskeletal fraction was extracted in a high salt Triton-containing buffer and the in vitro (32)P incorporation into IF proteins was measured. We first observed that 1 microM T(3) and 0.1 microM T(4) significantly increased the in vitro incorporation of (32)P into the IF proteins studied through the PKA and PKCaMII activities. A similar effect on IF phosphorylation was achieved by incubating cortical slices with GABA. Furthermore, by using specific GABA antagonists, we verified that T(3) induced a stimulatory effect on IF phosphorylation through noncompetitive mechanisms involving GABA(A), beyond GABA(B) receptors. In contrast, T(4) effects were mediated mainly by GABA(B) mechanisms. In conclusion, our results demonstrate a rapid nongenomic action of T(3) and T(4) on the phosphorylating system associated to the IF proteins in slices of cerebral cortex of 10 day-old male rats and point to GABAergic mechanisms mediating such effects.

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“…Research in rodent models suggests a complex interaction between thyroid hormone and GABA, with each regulating secretion or uptake of the other. Thyroid hormones appear to inhibit uptake of GABA in central nervous system neurons [16,17], while GABA inhibits thyrotropin (TSH)-induced release of thyroid hormone from thyroid follicular cells [18].…”

Section: Introductionmentioning

confidence: 99%

GABA Receptor Expression in Benign and Malignant Thyroid Tumors

Roberts

Mendonca-Torres

Jensen

et al. 2009

Pathol. Oncol. Res.

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Neurotransmitter systems have recently been shown to be involved in multiple malignancies including breast, colon and prostate cancers. The role of neurotransmitters and neurotrophic factors has not yet been examined in thyroid cancer. To determine the possible involvement of neurotransmitter systems in thyroid carcinogenesis we characterized the patterns of gamma-aminobutyric acid (GABA) receptor expression in normal thyroid and thyroid tumors. We examined the expression patterns of the GABAergic system in 70 human thyroid tumor samples (13 follicular adenomas, 14 follicular carcinomas, 43 papillary carcinomas) and adjacent normal thyroid by immunohistochemistry. GABAergic system mRNA expression in thyroid cancer cell lines derived from primary (FTC133) and metastatic tumors (FTC236 and FTC238) was examined by real time PCR. Overall, GABA receptor expression is increased in tumors compared to normal thyroid tissue. Expression of GABAA receptor beta2 was detected in the vasculature of normal thyroid and thyroid tumors but not in thyroid cancer cells. GABAA alpha2 was detected in metastatic-derived but not in primary-tumor derived cell lines. Expression levels of GABAB R2 and GABA receptor associated protein (GABARAP) are increased in adenomas and thyroid cancer suggesting their role in early stages of thyroid tumorigenesis. This study represents the first demonstration of GABA receptor expression in human thyroid tissue and suggests that the GABAergic system is involved in thyroid carcinogenesis.

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Thyroid hormonal modulation of the binding and activity of the GABAA receptor complex of brain

Cited by 69 publications

References 54 publications

MODULATION OF THE GABA<sub>A</sub> RECEPTOR BY SRIF IN RAT THALAMUS

MODULATION OF THE GABA<sub>A</sub> RECEPTOR BY SRIF IN RAT THALAMUS

Short-Term Effects of Thyroid Hormones on Cytoskeletal Proteins Are Mediated by GABAergic Mechanisms in Slices of Cerebral Cortex from Young Rats

GABA Receptor Expression in Benign and Malignant Thyroid Tumors

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