The induction of Fos protein was used to localise hypothalamic neurones activated by ramps of noxious skin heating delivered at a rate of 2.5°C s _1 to preferentially activate C-nociceptors. This was combined with retrograde transport of cholera toxin subunit B from identified 'pressor' and 'depressor' sites in the dorsolateral/lateral or the ventrolateral columns of the periaqueductal grey. Fos-positive neurones were found throughout the rostral hypothalamus. Despite this wide distribution, those neurones double labelled retrogradely from the periaqueductal grey were focused in the lateral area of the anterior hypothalamus. More than 20 % of Fos-positive neurones in this region projected to depressor sites in the ventrolateral periaqueductal grey, and 10 % projected to its dorsolateral/lateral sector. These results are discussed in relation to the peripheral inputs to hypothalamic-midbrain pathways and their role in the cardiovascular responses to different components of the pain signal.
Modulation of spinal nociception from the anterior hypothalamus/preoptic area (AH/POA), and consequent alterations in the pain experience may contribute to integrated responses brought into play during fear or stress and as part of the sickness response. This study was designed to compare the effects of descending control from AH/POA on A- versus C-fibre-evoked spinal nociception, since any differential control is of behavioural and clinical importance given that A-fibre and C-fibre nociceptors convey different qualities of the pain signal (first and second pain, respectively), and play different roles in the development and maintenance of chronic pain states. In anaesthetised rats, electromyographic responses were recorded to monitor thresholds of withdrawal to slow (2.5 degrees Cs(-1)) or fast (7.5 degrees Cs(-1)) rates of skin heating of the hindpaw, to preferentially activate C- or A-nociceptors, respectively. Neuronal activation by microinjection of dl-homocysteic acid at sites within a specific region of AH/POA, lateral area of the anterior hypothalamus (LAAH), significantly increased response thresholds to slow heating rates (p<0.02, n=11), but not those to fast rates of heating (p=0.48, n=10). Injection of DLH adjacent to LAAH (n=9) had no significant effect on responses to slow (n=8) or fast (n=9) rates of skin heating. The functional significance of differential descending control of spinal processing of C- and A-nociceptive inputs is discussed with respect to roles both of the LAAH in pain processing, and of C- and A-nociceptive inputs in acute and chronic pain.
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