The effects of varying concentrations of deltamethrin on a number of the parameters of electrophysiological activity in the cockroach ventral nerve cord have been studied. Deltamethrin, at concentrations greater than 100 nM, caused repetitive firing in the central nervous system (CNS), prior to conduction block, the effect getting faster as the concentration was increased. Whilst 10-nM deltamethrin eventually caused conduction block with no apparent increase in the level of CNS activity, it induced a gradual decrease in the amplitudes of all spike activity. Deltamethrin at 1 O p~ induced a significant increase in the latency of electrically evoked responses, and this was attributed to a synaptic mechanism. It was shown for the first time that 1 0 -p~ deltamethrin causes a significant elevation of the extra-axonal K+ activity; the possible consequences of this are discussed.
After intravaginal application of SCE-A vaginal cream, absorption of estrogens was lower compared with absorption after oral administration. At steady state, the systemic exposure of equilin, estradiol, and estrone was significantly lower after twice-weekly administration of 1 g SCE-A vaginal cream compared with that achieved with an oral daily dose of a 0.3 mg SCE-A tablet.
The activity of K+ and the control of influx of + into the extracellular space (micro-environment) of the central nervous system of the cockroach, Periplaneta americana, were measured directly with K+-sensitive microelectrodes. Using an in vivo preparation, it was possible to follow the effects of changes in K+ concentration in the medium bathing the nervous system on extracellular K+ and spontaneous and evoked neuronal activity. For bath K+ levels less than 31 mmoll−1, roughly corresponding to maximal haemolymph level in natural physiological conditions, the blood-brain barrier was found to be suitably efficient in restricting the influx of K+ and thereby allowing normal neural activity. At an external K+ concentration of 100 mmoll−1, however, the system was unable to maintain a sufficiently low extracellular K+ concentration and neuronal activity was suppressed. Influx of K+ from the external medium into the micro-environment occurred mainly in two phases. The early phase had a fast time course and probably reflects the physical aspects of the blood-brain barrier. The later, second phase was a slower process possibly corresponding to activation of metabolic ion pumps. The time courses of the functioning of these two systems and their control of the extraaxonal K+ activity are also discussed.
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