The mechanisms of photodynamic (PD) damage to neurons and gliocytes are discussed. The spike reactions of neurons are described, with stimulation at high concentrations of photosensitizer and inhibition at low concentrations, accompanying necrosis. Glial cells developed both necrosis and apoptosis. Local laser inactivation of neurons increased light-induced apoptosis of gliocytes, i.e., neurons maintained gliocyte survival. Inter-and intracellular signaling plays an important role in the photolesioning of these cells. Studies using inhibitors and activators of signal proteins demonstrated the involvement of the Ca(2+)-dependent, adenylate cyclase, and tyrosine kinase pathways in the responses of neurons and gliocytes to PD treatment. Pharmacological modulation may alter the selectivity of PD neuron and gliocyte damage and the efficacy of PD treatment.

The effect of new agent Vp (9-butylamine-3,3-dimethyl-3,4-dihydroacridine-1(2H) hydrochloride) on lifetime of isolated mechanoreceptive crayfish neurons was evaluated by the duration of its impulse activity. Vp significantly and dose-dependently prolonged the lifetime of both spontaneously degrading neurons and neurons degrading under conditions of inhibition of various stages of the energy metabolism: glycolysis and oxidative phosphorylation. The effect of Vp in a concentration of 10(-7) M surpassed that of amiridine. Piracetam also prolonged the lifetime of spontaneously degrading neurons, but only in very high concentration (10(-2) M). It is concluded that Vp possesses a neuroprotective activity.

Amiridine and tacrine are found to have a concentration-dependent effect on the spontaneous activity of an isolated neuron from crawfish. Amiridine in a concentration of 1 pM reliably prolongs the lifetime of the neuron, whereas lower concentrations are inactive and a high concentration (10 p.M) reduces spontaneous activity. Tacrine is unable to prolong the lifetime of the neuron. It is suggested that, unlike tacrine, the therapeutic effect of amiridine stems from its ability to prolong neuronal functioning.

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