Abstract
It has been shown previously that rats treated as neonates with capsaicin exhibited hyperactivity in a novel environment and had brain changes, including reduced brain weight, reduced hippocampal area, reduced cortical thickness and increased neuronal density in several cortical areas
Highlights
More than 40 years ago Jancsó et al[1,2] showed that treatment of neonatal rats with the vanilloid, capsaicin, the hot principle in chillies, produced life-long elimination of chemo sensitive primary afferent neurons and loss of chemogenic pain and neurogenic inflammation
Over the few years substance P was demonstrated to be responsible for antidromic vasodilatation and neurogenic inflammation[9] and to be released from the central synapses of small diameter primary afferent neurons on noxious stimulation[10]
The observations that subjects with schizophrenia have deficits in pain sensation and flare responses to niacin prompted a study by Newson et al[21] of the effect of neonatal capsaicin treatment on rat brain and behaviour
Summary
More than 40 years ago Jancsó et al[1,2] showed that treatment of neonatal rats with the vanilloid, capsaicin, the hot principle in chillies, produced life-long elimination of chemo sensitive primary afferent neurons and loss of chemogenic pain and neurogenic inflammation. The predominately primary afferent location of the site of action of capsaicin at first seemed to be confirmed when several studies showed little or very restricted localization of TRPV1 channels in the CNS12,18,19. Further studies using methods with increased sensitivity, showed that TRPV1 channels were not restricted to primary afferent neurons but were widely distributed in the CNS, albeit at levels 20-30 times lower than those in the peripheral nervous system[20]. Investigation of the role of TRPV1 channels and of the effects of capsaicin in the brain lagged behind studies of the peripheral actions
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