Most of the natural products isolated at present are heterocyclic compounds, so heterocyclic compounds occupy an important position in the research of organic chemistry. A compound: 148-51-6, is researched, SMILESS is OC1=C(C)C(CO)=CN=C1C.[H]Cl, Molecular C8H12ClNO2Journal, Article, Brain Research called Convulsive effects of 4-deoxypyridoxine and of bicuculline in photosensitive baboons (Papio papio) and in rhesus monkeys (Macaca mulatta), Author is Meldrum, B. S.; Horton, R. W., the main research direction is pyridoxine antagonist convulsant; bicuculline convulsant; aminobutyrate neurotransmitter epilepsy.Reference of 5-(hydroxymethyl)-2,4-dimethylpyridin-3-ol hydrochloride.
4-Deoxypyridoxine HCl (I) [148-51-6] administered i.v. at 40-100 mg/kg enhanced the natural syndrome of photosynthetic epilepsy in baboons and increased the severity of photically-induced myoclonus so that it progressed to a tonic-clonic seizure. In subconvulsive doses I provoked epileptic afterdischarges in the occipital cortex of monkeys exposed to photic stimulation. In both species I at 100-150 mg/kg induced spontaneous seizures which originated unilaterally in the occipital cortex and began with a horizontal nystagmus. When the occipital discharges no longer generalized, the animals had a normal electroencephalogram. A 4:1 excess of pyridoxine [65-23-6] in baboons blocked the increase in photically-induced responses and drug-induced seizures. Bicuculline (II) [485-49-4] administered i.v. at 0.1-0.4 mg/kg induced generalized seizures in both species, and at 0.3-0.6 mg/kg induced prolonged (150-300 min) seizures characterized by sustained myoclonic activity and relative absence of episodes of postictal silence in baboons. At 0.1-0.3 mg/kg II sometimes caused a brief myoclonic jerk associated with frontorolandic spikes and waves. There seem to be 2 inhibitory systems which differ in their pharmacol. responsiveness but both probably involve γ-aminobutyric acid [56-12-2] as the neurotransmitter. One system seems to be intracortical and its functional failure causes occipital discharges and spontaneous seizures after administration of the pyridoxine antagonists. The other is probably a collateral inhibitory system within the pathways afferent to the somatomotor cortex.
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Reference:
Pyrimidine | C4H4N2 – PubChem,
Pyrimidine – Wikipedia