1. In cats under Althesin (alphaxalone-alphadalone) anaesthesia, sites in the amygdala and brain-stem defence areas have been electrically stimulated by means of monopolar, semi-microelectrodes. 2. Such stimulation evoked a consistent pattern of visceral changes characteristic of the alerting stage of the defence reaction as it has been described by previous workers. This "visceral alerting reaction" included increases in arterial blood pressure, heart-rate and cardiac output with vasoconstriction in kidney, intestines and skin but vasodilatation in the hind limbs. 3. These results differ strikingly from those reported previously n that, under conventional anaesthetics, such as chloralose or barbiturate, the full visceral alerting reaction cannot be evoked by amygdala stimulation, or any other manoeuvre which involves transmission through the brain stem defence areas. 4. The area of the amygdala from which such responses can be elicited under althesin closely resembles that which has been reported to evoke defence reactions in conscious animals. 5. It is concluded that Althesin, used in the manner described, does not distort synaptic transmission in the forebrain in the way that conventional anaesthetics do. It is suggested that this steroid anaesthetic may be invaluable in any studies of fore-brain physiology in the cat.
SUMMARY1. In cats anaesthetized with Althesin, the efferent descending pathway from the brain-stem defence areas has been traced through the medulla by identifying sites at which electrical stimulation evoked the characteristic pattern of the visceral alerting (defence) response. This response includes an increase in arterial blood pressure resulting from increased heart rate and cardiac output and vasoconstriction in renal and splanchnic beds, accompanied by active vasodilatation in skeletal muscle.2. The efferent pathway runs as a narrow strip, about 3 mm from the mid line, ventral to the superior olive and the nucleus of the trapezoid body, extending caudally to the rostral portion of the inferior olive where it lies ventral to the facial nucleus. It was found to lie very close to the ventral medullary surface just rostral to and within the area at which bilateral topical application of glycine results in a profound fall in arterial blood pressure and cessation of respiration.3. On bilaterial application of glycine to the sensitive area of the ventral medulla, the visceral alerting response evoked by stimulation in the defence areas of the amygdalo-hypothalamic complex, or the mid-brain central grey or tegmentum, was attenuated in parallel with the fall in arterial pressure, the vasoconstrictor responses being most strongly reduced. As soon as arterial blood pressure had fallen to its lowest level the visceral alerting response was virtually abolished.4. A small radio-frequency lesion made in the ventral medullary efferent pathway, in the rostral part of the 'glycine-sensitive area', had the same effect as that produced by unilateral application of glycine: it resulted in little respiratory or cardiovascular effect itself, but application of glycine to the contralateral area then produced the full effect otherwise seen only on bilateral application of glycine.5. It is suggested (1) that the effects of glycine result from blockade of a synaptic relay, close to the ventral surface of the medulla, in the efferent pathway from the defence areas to the preganglionic sympathetic neurones, and (2) that the neurones which receive an input from the alerting (defence) areas normally provide an essential, tonic excitatory drive to the sympathetic output and probably to respiration also. After sudden withdrawal of this drive, vasomotor tone and the normal level of arterial blood pressure are not maintained.
SUMMARY1. In cats under Althesin anaesthesia, the hind limb area of the motor cortex has been stimulated by means of monopolar, semi-micro-electrodes with careful experimental control so as to avoid reflex effects evoked through stimulation of meningeal afferent fibres or stimulus spread to non-cortical structures.2. Localized cortical stimulation which elicited muscle contractions in the contralateral hind limb also elicited vasodilatation in the same limb: the stimulus threshold was the same for both effects, and the magnitude of the dilatation was related to the strength of contraction.3. Reduction of the somatic motor response, caused by lesions in the medullary pyramidal tract, was accompanied by a parallel reduction of the vascular response.4. Prevention of the motor response by gallamine or by spinal cord section at L4-L5 (which leaves the sympathetic outflow to the hind limbs intact) led to abolition of the vascular response. During recovery from gallamine, contraction and vasodilatation returned in parallel.5. The muscle vasodilatation was insensitive to atropine or guanethidine. 6. It is concluded that the hind limb vasodilatation observed on stimulation of the motor cortex is simply a post-contraction hyperaemia, and that it is independent of the sympathetic nervous system. Previous conclusions of a sympathetically mediated vasodilatation probably resulted from inadequate control of the stimulus or a failure to recognize weak muscle contractions.
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