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No abstract

The brainstem of anesthetized cats was electrically stimulated to examine the changes in the Intracranial pressure (ICP). There were pressor and depressor sites, which preferentially produced an immediate increase and decrease in ICP in association with the arterial pressor and depressor responses, respectively. A preferential increase in ICP was also observed by stimulation of some depressor sites. The stimulus-induced ICP responses were usually different from the secondary ICP changes due to nonneurogenic alteration of arterial blood pressure (BP) as evoked by arterial bleeding and infusion of saline solution; the stimulus-induced increase in ICP was greatly enhanced when the stimulation to the pressor sites was applied at lowered BP levels and at moderately elevated ICP levels. In addition, when a gradual elevation in ICP was spontaneously observed with the lowering of the BP level, the pressor site-induced increase in ICP exceeded 70-100 mmHg at the peak plateau-like waves, regardless of the magnitude of accompanying arterial pressor response. We propose that the stimulus-induced ICP responses cannot be explained merely by the metabolic changes, the decreased intracranial compliance, and the secondary transmural action on the intracranial space of the arterial pressor and depressor responses. A neurogenic mechanism that directly affects Intracranial blood diameter may be involved in the ICP responses, especially those observed ,at a lower BP level, in addition to extracranic action of sympathetic and parasympathetic nerve activities.

1. The depressant actions of taurine applications on lumbar motoneurons in the isolated frog spinal cord were studied using conventional intracellular recordings and the two-electrode voltage-clamp technique. 2. With microelectrodes containing K+-acetate, 0.75-2 mM taurine mostly induced a hyperpolarization that often faded or turned into depolarization during the continuous application. A higher concentration (5-7.5 mM) depolarized a majority of cells. The effects on the membrane potential were associated with an increase in input conductance (approximately 285%). 3. The reversal potential of the taurine-induced currents was approximately -70 mV, with microelectrodes containing K+-acetate. In recordings using KCl-filled electrodes, taurine (less than or equal to 2 mM) produced a large depolarization (greater than or equal to 20 mV) at resting potentials near -50 mV, thereby indicating that the reversal potential was positively shifted by loading the cell with Cl-. These results suggest that the taurine potentials were mediated predominantly by an increased Cl- permeability. 4. Voltage-dependent relaxations of taurine currents were observed in 10 of 14 neurons. 5. A linear relation was found between the input conductance and the amount of current required to generate a 1-mV increment in EPSP at resting potential. 6. Polysynaptic excitatory postsynaptic potentials (EPSPs) and currents (EPSCs) were more susceptible to taurine than the monosynaptic responses. Taurine (less than 1 mM) seemed to suppress the interneurons mediating polysynaptic pathways. 7. Monosynaptic EPSPs and EPSCs were decreased with higher concentrations of taurine (greater than 1 mM). The percent reduction of EPSPs and that of the corresponding EPSCs had a positive correlation (r = 0.95), whereas, there was no significant correlation between changes in EPSPs and in input conductance, and between changes in EPSCs and in input conductance. The amount of current required to produce a 1-mV increment of EPSP was increased in the presence of taurine, in association with the increased input conductance. 8. Taurine suppressed synaptic potentiation of EPSPs evoked by paired stimuli, at an interval of 60-180 ms. Gamma-D-glutamylglycine, an antagonist of receptors for excitatory amino acids, greatly reduced the amplitude of EPSPs, but had little effect on synaptic potentiation. 9. Taurine suppressed glutamate currents evoked at membrane potentials, clamped near rest in low Ca2+, high Mg2+ solution. 10. These findings suggest that the taurine-induced reduction of EPSPs is due mainly to suppression of EPSCs, through both presynaptic and postsynaptic mechanisms.(ABSTRACT TRUNCATED AT 400 WORDS)

An increase in intracranial pressure (ICP) was produced by stimulating brainstem pressor sites in cats anesthetized with alpha-chloralose. The ICP responses were augmented by lowering prestimulus BP and reduced by elevating prestimulus BP. In contrast, stimulus-induced pressor response of BP showed no consistent correlation to prestimulus BP. When the mean amplitude of stimulus-induced ICP responses at the control prestimulus ICP (within 18 mmHg) was plotted against the mean of the prestimulus BP levels for each site examined, the sites were classified into 2 groups by the regression line; sites generating a marked ICP response above the line and those generating a small ICP response on and under the line. The former sites were located in the paramedian region of the reticular formation including nuclei parvocellularis and gigantocellularis. The latter sites scattered throughout the brainstem pressor area. The ICP response at the former sites was markedly increased at an elevated prestimulus ICP. The peak ICP response at 30-50 mmHg of prestimulus ICP was 70-100 mmHg, similar to plateau waves. The ratio of ICP response size to BP response size was negatively correlated to prestimulus BP and the regression line was 2-5 times steeper at an elevated prestimulus ICP (18-60 mmHg) than at the control ICP. On the other hand, the negative relation between the response ratio and the BP for the latter sites produced no such change at the increased prestimulus ICP. These findings suggest that the ICP response is produced primarily by neurogenic intracranial vasodilation, which works most effectively at moderately decreased cerebral perfusion pressure. This mechanism may be involved in a series of events that results in plateau waves.