Changes in intracellular potentials of snail neurons induced by ß-phenylglutamic acid hydrochloride.

ß-Phenylglutamic acid hydrochloride (RGPU-135, neuroglutamine, or glutarone) in concentrations of 1, 10, 100, and 1000 µM reversibly and dose-dependently modulated the intracellular action potentials in Plantorbarius corneus snail neurons and hyperpolarized the membrane by 9.1±2.5% with maximum shift of resting potential at 100 µM. Hyperpolarization was accompanied by up-regulation of synaptic activity and changes in the pattern of impulse activity manifested by a decrease in the discharge rate, shortening of the interburst time, increase in the mean number of spikes in the bursts, and shortening of the interspike time within the bursts. Both hyperpolarization and impulse activity rearrangement persisted for 10-20 min after washing of RGPU-135.

Effect of metabotropic receptor agonists on ionic current of snail neurons.

The dose-dependent and reversible changes of sodium (I(Na)), calcium (I(ca)), slow potassium (I(Ks)), and fast potassium (I(Kf)) currents were recorded in isolated snail neurons under the action of κ-opioid agonist butorphanol and chemical agent RU-1203 applied in a concentration range of 1-1000 µM.

Elucidation of the mechanisms of membranotropic effects of RU-1203 on ionic channels of Lymnaea stagnalis neurons.

RU-1203-induced norBNI-irreversible inhibition of sodium (INa), calcium (ICa), and slow and fast potassium currents (IKs and IKf) was demonstrated in isolated neurons of Lymnaea stagnalis.

Effects of helium-neon laser irradiation and local anesthetics on potassium channels in pond snail neurons.

Intracellular dialysis and membrane voltage clamping were used to show that He-Ne laser irradiation of a pond snail neuron at a dose of 0.7 x 10(-4) J (power density 1.5 x 10(2) W/m2) increases the amplitude of the potential-dependent slow potassium current, while a dose of 0.7 x 10(-3) J decreases this current. Bupivacaine suppresses the potassium current. Combined application of laser irradiation at a dose of 0.7 x 10(-3) J increased the blocking effect of 10 microM bupivacaine on the slow potassium current, while an irradiation dose of 0.7 x 10(-4) J weakened the effect of bupivacaine.

Responses of neurons in the spinal nucleus of the trigeminal nerve to electrical stimulation of the dura mater of the rat brain.

The pathogenesis of migraine is based on the aseptic inflammation of dura mater tissues surrounding the large cranial vessels, such as the superior sagittal sinus. This inflammation develops in conditions of antidromic activation of sensory terminals of the trigeminal nerve and is accompanied by changes in the responses of neurons in the spinal nucleus of the trigeminal nerve to electrical stimulation of the superior sagittal sinus. However, the characteristics of the responses of these neurons to this stimulation have received virtually no study. Experiments on anesthetized rats were performed with recording of the responses of 387 neurons in the spinal nucleus of the trigeminal nerve to electrical stimulation of the superior sagittal sinus. The results showed that the responses of neurons to this stimulation was biphasic, consisting of a short initial phase with a latent period of 7-19 (11.4 +/- 0.17) msec, followed by a longer-lived discharge with a latent period of 20-50 (34.2 +/- 0.8) msec. It is suggested that the first phase reflects orthodromic activation of perivascular A(delta) and C fibers of the trigeminal nerve, while the second phase is associated with activation of meningeal C fibers with low conduction velocities and/or secondary activation of the perivascular sensory endings of the trigeminal nerve by algogenic and vasoactive substances released from them during antidromic activation. These changes seen in animal experiments may serve as an indicator of the efficacy of antimigraine agents.

Local neurotoxicity of epidural clofelin.

Morphological and quantitative histoenzymological changes in neurons of dog spinal cord and spinal ganglion were studied in acute and chronic experiments with epidural administration of 0.01% clofelin. No morphofunctional changes were revealed after bolus injection of clofelin in a single dose of 6.5 mg/kg. After administration of clofelin in a daily dose of 15 microg/kg for 14 days permeability of capillaries in the nervous tissue decreased at the site of injection, but increased in intact areas. Compensatory changes in energy supply to neurons manifested in activation of aerobic and anaerobic oxidation. Sufficient level of nucleic acids synthesis confirms qualitative validity of nervous cells. Epidural clofelin did not cause dystrophy and necrosis in neurons of the spinal and spinal ganglion.