PubMed · 7284895
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G M Wyant. 1981. Electroconvulsive therapy.. https://doi.org/10.1007/bf03010365
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The mammalian thalamus is the gateway to the cortex for most sensory modalities. Nearly all thalamic nuclei also receive massive feedback projections from the cortical region to which they project. In this study, the spatiotemporal properties of synchronized thalamic spindle oscillations (7 to 14 hertz) were investigated in barbiturate-anesthetized cats, before and after removal of the cortex. After complete ipsilateral decortication, the long-range synchronization of thalamic spindles in the intact cortex hemisphere changed into disorganized patterns with low spatiotemporal coherence. Local thalamic synchrony was still present, as demonstrated by dual intracellular recordings from nearby neurons. In the cortex, synchrony was insensitive to the disruption of horizontal intracortical connections. These results indicate that the global coherence of thalamic oscillations is determined by corticothalamic projections.
We have stimulated the rostral ventrolateral medulla of the central nervous system to increase renal sympathetic nerve activity (RSNA), and measured the effect on renal blood flow, glomerular filtration rate, and urinary excretion. Increases in RSNA were produced by infusion of 0.02 M glutamate at a rate of 30-50 nl/min into the subretrofacial nucleus for 40 min, in 10 urethane anaesthetized rabbits. Changes in RSNA were quantified as the mean nerve activity per 1 s period and as the frequency and amplitude of individual discharges (reflecting the number of activated nerve fibres). Glutamate infusion increased RSNA 59 +/- 11% over control levels. This was predominantly due to a 65 +/- 15% increase in the frequency of discharges (3.0 +/- 0.35 to 4.6 +/- 0.4 Hz), rather than the amplitude of the discharges (+9 +/- 3% over control). The effects of these changes on the kidney were made against data collected in the last 20 min of the infusion and the 40 min pre-and post-stimulation periods, when arterial pressure and heart rate were unchanged from control levels. Renal blood flow fell significantly from 31.3 +/- 4.5 to 17.7 +/- 5.1 ml/min (47% decrease) and filtration fraction significantly increased from 12.7 +/- 1.1 to 15.7 +/- 2.1% (24% increase) during glutamate infusion. Each of these variables returned to their pre-stimulus levels after ceasing the central stimulation. Fluid, sodium and potassium excretion were not changed by this stimulus. In conclusion, the results in this study suggest that a selective increase in sympathetic nerve activity to the kidney without change in renal perfusion pressure can cause constriction of the renal vasculature without alteration in sodium and water excretion.
The rostral ventrolateral medulla (RVLM) is part of the vasomotor centre which controls the cardiovascular system and may therefore be critical to the genesis of postoperative hypertension. This area is probably a common site of termination of different inputs involved in the baroreflex. It contains at least two classes of neurons exhibiting spontaneous activities and projecting to sympathetic preganglionic neurons located in the intermediolateral cell-column (IML) of the spinal cord. The first class of neurons corresponds to cells with slow axonal conduction velocities (< 0.8 m s-1) and which contain immunoreactive phenylethanolamine-N-methyltransferase (CI cells); the second class, characterized by faster conduction velocities (2.5-8 m s-1), is considered as glutamatergic, although the C1 cells may also release glutamate alongside catecholamine. The purpose of the present study was to investigate the involvement of the "fast-conducting' RVLM barosensitive bulbospinal (RVLM-BB) neurons in the hypertension occurring upon emergence from halothane anaesthesia. Rats were anaesthetized with halothane, paralysed, and their lungs mechanically ventilated. Avoidable pain, distress or discomfort was consistently avoided as required by the fundamental principles of ethical animal research. Hence, all pressure points and surgical wounds, as well as tracheal tube were carefully covered or infiltrated with adequate local anaesthetic. Control experiments have been performed, allowing us to assert that hypertension accompanying halothane withdrawal was not due to suffering (see Discussion). Under halothane anaethesia, fast conducting (2.7 +/- 1.0 m s-1) RVLM-BB neurons (n = 10) exhibited a continuous discharge (8.4 +/- 7.5 Hz). Five minutes after discontinuing halothane, in increase in arterial blood pressure was recorded (AP 19 +/- 6 mmHg), which was accompanied by an increase in the unitary activities (n = 8.43 +/- 23%). Afterwards, both AP and unitary activity frequencies further increased to reach a maximum value at the end of the sequence (34 +/- 9 mmHg and 161 +/- 120% respectively, n = 10). After resumption of halothane administration, both AP and unitary activities fall down to the baseline level within 5 min (n = 10). This study shows that emergence from halothane anaesthesia reversibly induces RVLM-BB units activation, suggesting that a putative glutamatergic bulbospinal pathway may be involved in the genesis of hypertension occurring upon emergence from anaesthesia. These data may therefore contribute to better understanding of postoperative hypertension and to improve its pharmacological treatment in man.