Relating MEG measured motor cortical oscillations to resting γ-Aminobutyric acid (GABA) concentration

Putrescine is the major source of gamma-aminobutyric acid (GABA) in the rat adrenal gland. Diamine oxidase, and not monoamine oxidase, is essential for GABA formation from putrescine in the adrenal gland. Aminoguanidine, a diamine oxidase inhibitor, decreases the GABA concentration in the adrenal gland by more than 70% after 4 h, and almost to zero in 24 h. Studies using [14C]putrescine confirm that [14C]GABA is the major metabolite of putrescine in the adrenal gland. Inhibition of GABA transaminase by amino-oxyacetic acid does not change the GABA concentration in the adrenal gland, as compared with the brain, where the GABA concentration rises. With aminoguanidine, the turnover time of GABA originating from putrescine in the adrenal gland is 5.6 h, reflecting a slower rate of GABA metabolism compared with the brain. Since GABA in the adrenal gland is almost exclusively derived from putrescine, the role of GABA may relate to the role of putrescine as a growth factor and regulator of cell metabolism.

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Zinc downmodulates thf GABAc receptor current in cone horizontal cells acutely isolated from the catfish retina

Journal of Neurophysiology ◽

10.1152/jn.1995.73.2.916 ◽

1995 ◽

Vol 73 (2) ◽

pp. 916-919 ◽

Cited By ~ 36

Author(s):

C. J. Dong ◽

F. S. Werblin

Keyword(s):

Horizontal Cells ◽

Aminobutyric Acid ◽

Hill Coefficient ◽

Gamma Aminobutyric Acid ◽

Gaba Concentration ◽

Patch Clamp Technique ◽

Whole Cell Patch Clamp ◽

Inhibition Concentration ◽

Gabac Receptor ◽

The Hill

1. We studied the effect of zinc on the gamma-aminobutyric acid-C (GABAC) receptor in acutely isolated catfish cone horizontal cells using the whole cell patch-clamp technique. 2. GABA activates the GABAC receptor with a half-activation concentration (EC50) of 2.99 microM. The Hill coefficient is 1.32. Desensitization of the receptor is evident when GABA concentration is > 3 microM. 3. Zinc downmodulates the GABAc receptor current, elicited by 30 microM GABA, with a half-inhibition concentration (IC50) of 8.20 microM. 4. The inhibition of zinc is both competitive and noncompetitive. In the presence of 10 microM zinc, the maximum GABA response was reduced to approximately 60 percent of control and the EC50 increased to 17.32 microM, whereas the Hill coefficient (1.39) was not significantly altered. 5. The steady-state block by zinc is virtually voltage independent. 6. These results suggest that the GABAC receptor of horizontal cells can be modulated by endogenous zinc found in photoreceptors.

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Long-term vigabatrin treatment modifies pentylenetetrazole-induced seizures in mice: focused on GABA brain concentration

Pharmacological Reports ◽

10.1007/s43440-019-00037-6 ◽

2019 ◽

Vol 72 (2) ◽

pp. 322-330

Author(s):

Mariusz J. Świąder ◽

Katarzyna Świąder ◽

Izabela Zakrocka ◽

Maciej Krzyżanowski ◽

Andrzej Wróbel ◽

...

Keyword(s):

Aminobutyric Acid ◽

Seizure Threshold ◽

Long Term Memory ◽

Anticonvulsive Activity ◽

Gaba Concentration ◽

Term Memory ◽

Long Term Effect ◽

Brain Gaba ◽

Gad Activity

Abstract Background The goal of our study was to examine the long-term effect of vigabatrin (VGB), a γ-aminobutyric acid aminotransferase (GABA-AT) inhibitor on clonazepam (CLO), ethosuximide (ETX) and valproate (VPA) anticonvulsive activity against pentylenetetrazole (PTZ)-induced seizures in mice. Methods VGB was administered for 3 and 7 days. Convulsions were evoked by PTZ at its CD97 (99 mg/kg). The influence of CLO, ETX and VPA alone or in combination with VGB on motor performance and long-term memory was analyzed. γ-aminobutyric acid (GABA) concentration in mice brain and plasma as well as glutamate decarboxylase (GAD) activity was measured. Results After 3 days of treatment, VGB in doses up to 500 mg/kg increased PTZ-induced seizure threshold, whereas after 7 days VGB (at the dose of 125 mg/kg) inhibited clonic seizures in experimental mice. 7 days of VGB administration did not change the protective effect of CLO, ETX and VPA against PTZ-induced seizures. 7 days of VGB treatment at a subthreshold dose of 75 mg/kg decreased TD50 of ETX and CLO in the chimney test, but did not affect TD50 value for VPA. 7 days of VGB administration in combination with AEDs did not affect long-term memory in mice. VGB after 3 days or 7 days of administration increased brain GABA concentration. GAD activity was decreased after 3 and 7 days of VGB administration. Conclusions The presented results confirm anticonvulsive activity of VGB through GABA metabolism alteration and suggest care when combining VGB with ETX or CLO in the therapy.

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