Medullary pain facilitating neurons mediate allodynia in headache-related pain.

Objective: To develop and validate a model of cutaneous allodynia triggered by dural inflammation for pain associated with headaches. To explore neural mechanisms underlying cephalic and extracephalic allodynia.

Methods: Inflammatory mediators (IM) were applied to the dura of unanesthetized rats via previously implanted cannulas, and sensory thresholds of the face and hind-paws were characterized.

Nerve injury-induced tactile allodynia is present in the absence of FOS labeling in retrogradely labeled post-synaptic dorsal column neurons.

The dorsal column pathway consists of direct projections from primary afferents and of ascending fibers of the post-synaptic dorsal column (PSDC) cells. This pathway mediates touch but may also mediate allodynia after nerve injury. The role of PSDC neurons in nerve injury-induced mechanical allodynia is unknown.

Spinal NK-1 receptor expressing neurons mediate opioid-induced hyperalgesia and antinociceptive tolerance via activation of descending pathways.

Opioids can induce hyperalgesia in humans and in animals. Mechanisms of opiate-induced hyperalgesia and possibly of spinal antinociceptive tolerance may be linked to pronociceptive adaptations occurring at multiple levels of the nervous system including activation of descending facilitatory influences from the brainstem, spinal neuroplasticity, and changes in primary afferent fibers. Here, the role of NK-1 receptor expressing cells in the spinal dorsal horn in morphine-induced hyperalgesia and spinal antinociceptive tolerance was assessed by ablating these cells with intrathecal injection of SP-saporin (SP-SAP).

Retrograde analyses of spinothalamic projections in the macaque monkey: input to posterolateral thalamus.

The distribution of retrogradely labeled spinothalamic tract (STT) neurons was analyzed in macaque monkeys following variously sized, physiologically guided pressure or iontophoretic injections of cholera toxin subunit B (CTb) in order to determine whether different STT termination sites receive input selectively from different sets of STT cells. This report focuses on posterolateral thalamus, where prior anterograde tracing observations identified the posterior part of the ventromedial nucleus (VMpo) as the major projection target of lamina I STT neurons. Large injections in posterolateral thalamus labeled predominantly STT cells in lamina I throughout the spinal cord.

Selective mediation of nerve injury-induced tactile hypersensitivity by neuropeptide Y.

Prevention of nerve injury-induced tactile, but not thermal, hypersensitivity is achieved by ipsilateral lesions of the dorsal columns or lidocaine microinjection into the nucleus gracilis (n. gracilis). These and other data support the possibility that tactile hyperresponsiveness after nerve injury may be selectively mediated by a low-threshold myelinated fiber pathway to the n.