Activation of Phosphoinositide Metabolism by Cholinergic Agents.

摘要: Abstract : The primary acute, toxic effect of cholinergic agonists in the central nervous system is seizures. One activated by hydrolysis phosphoinositides (PI), a major site action lithium which potentiates convulsions associated with agonists. Our goal was to determine how PI affected seizures and modulated, especially excitatory amino acids (EAA) mediate brain damage. Modulation due specific EAA receptor quisqualate. Two effects quisqualate were identified, activation itself inhibition other neurotransmitters, norepinephrine. Several agents these responses, notably calcium sodium. An inhibitory acid had generally opposite Seizures caused changes similar those EAA; selective impairment norepinephrine-induced hydrolysis. also increased mediated receptors. Thus, stimulatory systems (cholinergic, EAA) reduced norepinephrine system. activity protein kinase C unaltered but tyrosine increased. agonist- induced cause alterations important second messenger- generating hydrolysis, part turn are influenced number factors, most calcium.