Biomedical subjects
Publications and source records attributed to S L Handley.
Pressures of up to 100 mm Hg applied to the mouse tail caused marked enhancement of the cataleptogenic potency of morphine, haloperidol and arecoline. Visual and auditory stimuli of moderate intensity also enhanced morphine catalepsy. Thus potentiation of cataleptogens by alteration of sensory input appears to be a fairly general phenomenon. The significance of these findings is discussed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
1. At an ambient temperature of 20 degrees C, intraventricular injection of noradrenaline in the mouse resulted in hypothermia accompanied by a fall in metabolic rate and by cutaneous vasodilatation. Subcutaneous injection of noradrenaline resulted in hyperthermia with raised metabolic rate and cutaneous vasodilatation.2. The hypothermia and fall in oxygen consumption rate following intraventricular noradrenaline were prevented by pre-treatment with subcutaneous propranolol, while the cutaneous vasodilatation was un-affected. However, the effects of subcutaneously injected noradrenaline were completely abolished by subcutaneous propranolol. Intraventricular propranolol did not modify the hypothermic effect of intraventricular noradrenaline.3. The direction of the effect on body temperature of intraventricular noradrenaline was dependent upon ambient temperature; hypothermia occurring at low (15 degrees C) and hyperthermia at high (36 degrees C) ambient temperatures. However, when the possibility of any peripheral action of noradrenaline escaping into the systemic circulation was prevented by prior subcutaneous injection of propranolol, significant hypothermia could be detected at temperatures as high as 32 degrees C.4. The possibility that the effects of intraventricular noradrenaline could be due to complete abolition of central temperature regulation was further excluded by the occurrence of thermal salivation in all animals during experiments performed at 36 degrees C.5. It is suggested that, in the mouse, the hypothermic actions of intraventricular noradrenaline are due to a central effect, while its hyperthermic effects at high ambient temperature are due to escape of noradrenaline into the peripheral circulation. The hypothermia could be the result of selective activation of central heat loss mechanisms.6. Intraventricular noradrenaline was without effect on brain plasma-space although exposure to 100% oxygen caused a detectable fall.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
1. Changes in temperature were determined following injection of noradrenaline, adrenaline, isoprenaline, dopamine and 5-hydroxytryptamine (5-HT) into the cerebral ventricles of the conscious mouse.2. Noradrenaline (1-20 mug) and dopamine (10-160 mug) caused falls in body temperature. Adrenaline (1-20 mug) caused a slight and transient rise in body temperature followed by a fall. Isoprenaline (5-20 mug) caused a rise in body temperature, hypothermia only occurring after very high doses (200 mug) of this catecholamine.3. alpha- and beta-adrenergic blocking agents, phentolamine (> 2 mug) and propranolol (> 5 mug) respectively, caused falls in body temperature when injected into the cerebral ventricles of the mouse.4. Specific drug antagonism studies were limited owing to the intrinsic effects of the alpha- and beta-adrenergic blocking agents. However, some evidence was obtained to indicate that noradrenaline mediated its effects through a central alpha-type adrenergic receptor.5. 5-HT (10-160 mug) caused a fall in body temperature. The action of this indoleamine and the catecholamines in regard to thermoregulatory function is discussed.
Although much evidence supports the proposal that 5-HT neurones promote anxiety, there is also substantial evidence that the actual situation is more complex. The recent idea that 5-HT neurones, alerted by the forebrain, also function to restrain more primitive brainstem mechanisms has additional explanatory power but neither proposal accounts for the lack of responsiveness of 5-HT neurones to aversive stimulation from the environment. Evidence from the elevated X-maze anxiety model indicates that it is sensitive to multiple anxiety mechanisms which are not fully accounted for by either hypothesis. In addition, findings presented here indicate that open arm preference, risk assessment and overall motility load on separate factors in a factor analysis and that the anxiogenic action of 8-OH-DPAT under control conditions is a selective effect on open arm preference. This anxiogenic effect can be switched to anxiolytic at will by simple changes in experimental conditions. The outcome of 5-HT system manipulations on experimental anxiety may be the result of unstable balance between effects on different brain areas. It is suggested that 5-HT neurones do not carry information about threats in the environment, instead, this information is input locally where it modulates 5-HT release; this released 5-HT can have different consequences in different brain areas.