Binary and ternary Cu(II) complexes of pregabalin with excitatory and inhibitory neurotransmitters and their antiepileptic effect

2020 ◽  
Vol 110 ◽  
pp. 110650 ◽  
Author(s):  
M.A. Mahmoud ◽  
S.A. Zaitone ◽  
A.M. Ammar
2020 ◽  
Vol 8 (9) ◽  
pp. 4569-4572
Author(s):  
Usha K S ◽  
Gurdip Singh

Epileptic seizures are caused due to imbalance in the excitatory and inhibitory neurotransmitters. Serum electrolytes like sodium, potassium and calcium play a key role in maintaining the epileptic threshold. In the quest of effective treatment in epilepsy ketogenic diet has been promising. It is found to increase the inhibitory Gamma amino butyric acid and thus increase the epileptic threshold. In this context Maha Panvhagavya Ghrita recommended in the treatment of Apasmara seems to be the drug of choice.


Author(s):  
A.L. Sherwin ◽  
O. Vernet ◽  
F. Dubeau ◽  
A. Olivier

ABSTRACT:We measured biochemical markers of excitability in brain excised for neurosurgical therapy of epilepsy. Intraoperative electrocorticography was used to identify and compare samples from regions of persistent interictal spike discharges and areas of the cerebral convexity which were free of interictal piking. We found that interictal spiking was associated with elevated tissue levels of the excitatory amino acids glutamic acid (26%, p < 0.001) and aspartic acid (25%, p < 0.05). There was also a significant increase in the activity of the enzymes glutamic acid dehydrogenase (20%, p < 0.01) and aspartate acid aminotransferase (18%, p < 0.01) which are involved in their formation. There was no change in the levels of the inhibitory neurotransmitters GABA or taurine. We also found a significant increase in the activity of tyrosine hydroxylase (52%, p < 0.001), the rate controlling enzyme in catecholamine biosynthesis. There was a reduction in the density (Bmax) of cortical alpha-1 adrenoceptors (26%, p < 0.01) and a concommitant diminution of receptor coupled phosphatidylinositide metabolism (21%, p < 0.01). This blunting of inhibitory noradrenergic transmembrane signaling may contribute to a relative imbalance between excitatory and inhibitory mechanisms in epileptogenic neocortex.


Physiology ◽  
1998 ◽  
Vol 13 (4) ◽  
pp. 164-170 ◽  
Author(s):  
Esa R. Korpi ◽  
Riikka Mäkelä ◽  
Mikko Uusi-Oukari

Molecular biological tools have revealed receptor proteins for excitatory and inhibitory neurotransmitters on cell membranes as targets of ethanol action. Behavioral and pharmacogenetic assays using rodent lines have supported this neurotransmitter theory of ethanol action and given a firm basis for future identification of the relevant genes and the central physiological processes vulnerable to ethanol.


1994 ◽  
Vol 14 (6) ◽  
pp. 3736-3750 ◽  
Author(s):  
CT Drake ◽  
GW Terman ◽  
ML Simmons ◽  
TA Milner ◽  
DD Kunkel ◽  
...  

2015 ◽  
Vol 309 (1) ◽  
pp. H174-H184 ◽  
Author(s):  
Vineet C. Chitravanshi ◽  
Kazumi Kawabe ◽  
Hreday N. Sapru

We have previously reported that stimulation of the hypothalamic arcuate nucleus (ARCN) by microinjections of N-methyl-d-aspartic acid (NMDA) elicits tachycardia, which is partially mediated via inhibition of vagal inputs to the heart. The neuronal pools and neurotransmitters in them mediating tachycardia elicited from the ARCN have not been identified. We tested the hypothesis that the tachycardia elicited from the ARCN may be mediated by inhibitory neurotransmitters in the nucleus ambiguus (nAmb). Experiments were done in urethane-anesthetized, artificially ventilated, male Wistar rats. In separate groups of rats, unilateral and bilateral microinjections of muscimol (1 mM), gabazine (0.01 mM), and strychnine (0.5 mM) into the nAmb significantly attenuated tachycardia elicited by unilateral microinjections of NMDA (10 mM) into the ARCN. Histological examination of the brains showed that the microinjections sites were within the targeted nuclei. Retrograde anatomic tracing from the nAmb revealed direct bilateral projections from the ARCN and hypothalamic paraventricular nucleus to the nAmb. The results of the present study suggest that tachycardia elicited by stimulation of the ARCN by microinjections of NMDA is mediated via GABAA and glycine receptors located in the nAmb.


Author(s):  
Antônio José Rocha ◽  
Renan Rhonalty Rocha ◽  
Francisco Leandro Laurindo de Moraes ◽  
Maria Vitória Laurindo ◽  
Soraya Lília da Rocha

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