Brainstem mechanisms which

Afferent input from cutaneous and visceral nociceptors is known to converge on spinal neurons, which accounts for the referral of pain between visceral and cutaneous structures (e.g. cardiac pain gets referred to the chest and left upper arm in patients suffering from angina pectoris). Projection neurons in the spinal dorsal horn project to cell nuclei in supraspinal areas such as the thalamus, brainstem and midbrain. Of these, the synaptic junctions in the thalamus play a very important role in the integration and modulation of spinal nociceptive and non-nociceptive inputs. Nociceptive inputs are finally conducted to the cortex where the sensation of pain is perceived (Fig. 1). The mechanisms via which the cortex processes nociceptive inputs are only poorly understood. 

Not much is known about the mechanisms subserving the increase of W and reduction of REMS after activation of 5-HT3 receptor. This receptor is well known for stimulating the release of DA, ACh, NA, 5-HT, and GABA in the brainstem, the limbic system, the basal forebrain, and the cortex, which can tentatively explain its disruption of sleep variables. However, further studies are needed to resolve this issue. 

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