1 Schizophrenia is considered to be a neurodevelopmental disorder with origins in the prenatal or neonatal period. Brains from subjects with schizophrenia have enlarged ventricles, reduced cortical thickness (CT) and increased neuronal density in the prefrontal cortex compared with those from normal subjects. Subjects with schizophrenia have reduced pain sensitivity and niacin skin flare responses, suggesting that capsaicin-sensitive primary afferent neurons might be abnormal in schizophrenia. 2 This study tested the hypothesis that intrinsic somatosensory deprivation, induced by neonatal capsaicin treatment, causes changes in the brains of rats similar to those found in schizophrenia. Wistar rats were treated with capsaicin, 50 mg kg À1 subcutaneously, or vehicle (control) at 24-36 h of life. At 5-7 weeks behavioural observations were made, and brains removed, fixed and sectioned. 3 The mean body weight of capsaicin-treated rats was not significantly different from control, but the mean brain weight of male, but not female, rats, was significantly lower than control. 4 Capsaicin-treated rats were hyperactive compared with controls. The hyperactivity was abolished by haloperidol. 5 Coronal brain sections of capsaicin-treated rats had smaller cross-sectional areas, reduced CT, larger ventricles and aqueduct, smaller hippocampal area and reduced corpus callosum thickness, than brain sections from control rats. Neuronal density was increased in several cortical areas and the caudate putamen, but not in the visual cortex. 6 It is concluded that neonatal capsaicin treatment of rats produces brain changes that are similar to those found in brains of subjects with schizophrenia.

PET/CT improves the clinical prediction of SPN, but its greatest use is in proving benignity. High PET scores had high false positive rates and did not add to clinical prediction. PET should be incorporated early in decision-making to allow for more effective biopsy strategies.

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During hypoxia specific deficits in neural control caused by propofol (2,6‐diisopropylphenol) anesthesia (Prop) are unknown. Dose‐related effects were analysed in rabbits with and without carotid body denervation (CBD) to partition arterial chemo‐baroreflex control. Minute ventilation (VE), tidal volume (VT), respiratory frequency (f), heart rate (HR), mean arterial pressure (MAP) were measured in 12 awake rabbits mask‐breathing room air, then 15 minutes of low oxygen air (PaO2 < 35 mm Hg), during Prop alone (0.2 and 0.5 mg kg−1min−1i.v.), and during matched Prop plus hypoxia. Prop alone caused dose‐related depression in f and rise in HR. Prop plus hypoxia abolished bradycardia, while MAP, VE and VT effects remained intact. CBD eliminated all chemoreflex responses to hypoxia and MAP fell while HR rose, effects enhanced by Prop in a dose‐related way. It is concluded that during Prop, carotid body function for respiratory and MAP defense is functionally intact. Central activation of the vagus is inhibited selectively, because electrical stimulation of peripheral vagus during Prop evokes normal bradycardia blocked by atropine. By contrast, Prop inhibits arterial baroreflex‐vagosympathetic defense against widespread hypoxic vasodilatation. We speculate that the data reflect dominant central GABAA receptor agonist effects on the arterial chemo‐baroreflex arc. Funding: ANZCA and HMRI.