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In voltage clamp experiments on the frog Ranvier node, the specific protein reagent, N-bromacetamide, significantly decelerates the sodium inactivation kinetics and makes it incomplete. After treatment with N-bromacetamide, both fast and slow inactivation time constants are increased and the proportion of inactivation components is changed favouring the slowly inactivating one in the wide range of membrane potentials. The results are consistent with a single channel population following the 3-state model of inactivation.

Ionic currents of normal and aconitine modified sodium channels of the Ranvier node membrane were measured under voltage clamp conditions. The experiments with local anesthetics in the external Ringer solution have showed that dissociation constant (Kdis) of normal channel-anesthetic complex for procaine is 0.27 + 0.03 mM, and for benzocaine is 0.68 +/- 0.04 mM. With aconitine modified channels, Kdis increases and becomes 1.32 +/- 0.5 mM and 1.52 +/- 0.3 mM for procaine and benzocaine, respectively. It is ascertained that the development of aconitine effect is inhibited by neutral benzocaine to a lesser extent than by procaine. It is shown that the aconitine effect cannot be reversed by a high concentration of anesthetic. Hence, it appears that aconitine and anesthetic receptors do not coincide.

Ultrastructural changes of the terminal plates of the bushy receptors in the frog urinary bladder have been studied after two hours' exposition in 0.05% novocaine solution and one hour's exposition in 0.05% dicaine and trimecaine solution. During these periods a steady block of the receptor impulse activity develops. The local anesthetics essentially change ultramicroscopic structure of the terminals. The reaction to the anesthetics investigated has both some features in common and certain peculiarities. At each effect three types of changes can be determined, characterized with various degree of rearrangement in neurilemma, neuroplasm and organelles. Each type of the changes is supposed to reflect a certain phase of the plate reactive response. Specificities of the reaction to novocaine are minimal changes of mitochondria, accumulation of glycogen granules, deformity and decreasing amount of vesicles. Under dicaine effect mitochondria do not change, amount of vesicles increases, their form does not change; under trimecaine effect mitochondria undergo most noticeable alterations. The changes of the terminal plates observed are interpreted as adaptive. The effect of the local anesthetics on the receptors is not limited with the blockade of the sodium canals of the afferent fibers, in parallel, biochemical processes, occurring in cytosol of the terminals also change; their morphological manifestations are the ultrastructural changes observed.

Studies have been made on the effect of trypsin, chymotrypsin, pronase, lipases, hyaluronidase and digitonin on electrophysiological properties of the neurons of the snail H. pomatia under external application. Proteases and lipases gradually depolarize the neuronal membrane, decrease the amplitude and prevent the onset of action potentials, initially increase and then decrease the membrane resistance. The decrease in the membrane resistance coincides with the period of maximum inhibition of resting and action potentials in the neurons. The enzymes studied do not affect the membrane capacitance. Changes in electrophysiological characteristics induced by the enzymes are partially reversible provided the preparation is soaked in Ringer's solution for a sufficient time. Digitonin rapidly and irreversibly depolarizes the membrane, decreases its resistance and blocks action potentials. Hyaluronidase does not significantly affect neuronal electrophysiological properties when applied solely, but facilitates the development of changes during subsequent effect of proteases.

The depressing action of epinephrine on the giant neurons is due to a progressively increasing passive potassium conductivity of the membrane, hyperpolarization and derangement of its generating properties. The triggering factor in the mechanism of the developing epinephrine hyperpolarization is an epinephrine induced increment of passive potassium conduction of the neuronal membrane.

Asymmetrical displacement currents in the Ranvier node membrane were recorded in the normal Ringer and under the action of a neurotoxin from the scorpion Buthus eupeus venom and of the alcaloid aconitine. In the total displacement current (DC) at the beginning of the pulse (Ion), two-exponentially decaying components were extracted: a rapid component with the maximum time constant of decay about 70 microns, and a slower one with the time constant of decay--300 microns. At high negative levels of conditioning prepulse (Vc) (-130 divided by -145 mV), the maximum value of the charge transferred by the fast and slow components was estimated to be 2.6 x 10(-14) and 4.8 x 10(-14) C, respectively. The slow component of Ion decreased with lowering Vc and was inhibited by the scorpion neurotoxin and aconitine. The fast phase of Ion remained unchanged with decreasing Vc from -145 to -100 mV and toxin-treated axons. Aconitine evoked a shift in the curve relating the change displaced by the fast component to the membrane potential in the direction of hyperpolarization by 40--50 mV. The results obtained suggest that the fast and the slow components of DC are associated with the initial potential-dependent stages of the processes of channel activation and inactivation, respectively.

The ionic currents of the nodal membrane were measured under voltage clamp conditions. The membrane being +40 mv. The replacing of the external Na+-ions to K+- and NH4+-ions have showed that the relative pearmeabilities of the veratrine-modified channels calculated from the constant field theory are arranged in the following row: PNa:PK:PNH4 = 1:0.29:0.61, which differs from the same row for the normal channels. The decreasing of the slope of current-voltage relations of the modified channels with the replacing of Na+-ions to K+- and NH4+-ions is the evidence of a more strong binding of these ions to external mouth of the modified channel compared to the binding of Na+-ions.

Acetylcholine (10(-6)--10(-3) M) added to the rat brain homogenate increased that activity of microsomal Na, K-ATPase and (14C)-amino acid incorporation in microsomal proteins. Actinomicin D (5.10(-5) M) eliminated the effect of acetylcholine. It is concluded that acetylcholine induced the synthesis of either Na, K-ATPase itself or some other proteins involved in the enzyme activity regulation.