Spinal sources of noxious visceral and noxious deep somatic afferent drive onto the ventrolateral periaqueductal gray of the rat

Abstract

Studies utilizing the expression of Fos protein as a marker of neuronal activation have revealed that pain of deep somatic or visceral origin selectively activates the ventrolateral periaqueductal gray (vlPAG). Previous anatomical tracing studies revealed that spinal afferents to the vlPAG arose from the superficial and deep dorsal horn and nucleus of the dorsolateral funiculus at all spinal segmental levels, with approximately 50% of vlPAG-projecting spinal neurons found within the upper cervical spinal cord. This study utilized detection of Fos protein to determine the specific populations of vlPAG-projecting spinal neurons activated by noxious deep somatic or noxious visceral stimulation. Pain of cardiac or peritoneal (i.e., visceral) origin activated neurons in the superficial and deep dorsal horn and nucleus of the dorsolateral funiculus of the thoracic cord, whereas pain of hindlimb (i.e., deep somatic) origin activated neurons in the same laminar regions but in the lumbosacral cord. Each of these deep noxious manipulations also activated neurons in the superficial and deep dorsal horn and nucleus of the dorsolateral funiculus of the upper cervical spinal cord. In a second set of experiments, the combination of retrograde tracing and Fos immunohistochemistry revealed that vlPAG-projecting spinal neurons activated by deep somatic pain were located in both the upper cervical and lumbosacral cord, whereas those activated by visceral pain were restricted to the thoracic spinal cord. Thus pain arising from visceral versus deep somatic body regions influences neural activity within the vlPAG via distinct spinal pathways. The findings also highlight the potential significance of the upper cervical cord in integrating pain arising from deep structures throughout the body.

A Novel Pressor Area at the Medullo-Cervical Junction That Is Not Dependent on the RVLM: Efferent Pathways and Chemical Mediators

“…In this respect, effects of MCPA excitation on sympathetic outflows, other than the cervical sympathetic and splanchnic tested here, will be of interest. Furthermore, cell groups in a similar region to the MCPA are activated after pain to deep somatic regions of the body (Clement et al, 2000), indicating that the MCPA may be important in signaling autonomic effects in response to pain.…”

Nociception after intraperitoneal injection of a sodium pentobarbitone formulation with and without lidocaine in rats quantified by expression of neuronal c-fos in the spinal cord – a preliminary study

“…The presence of the FLI neurones in laminae I, II, V and X of the spinal dorsal horn is in agreement with the fact that these laminae mainly receive input from visceral nociceptive fibres (Mené trey et al 1989, Hammond et al 1992, Clement et al 2000. The FLI neurones were found in the entire length of the spinal cord examined which is in accordance with findings described in the above-referred papers and in accordance with a global intraperitoneal distribution of the injected fluid.…”

“…Mené trey et al (1989), Hammond et al (1992) and Clement et al (2000) applied in their studies a dose volume of 0.5 mL/rat. In the behavioural study of Ambrose et al (2000), a dose volume of 1.5 mL/kg was applied in order to obtain a lethal effect.…”

Estimulação do córtex motor e antinocicepção: envolvimento da via de analgesia serotonérgica descendente.

“…Neurônios das subdivisões da coluna lateral estão mais envolvidos com a informação aferente relacionada a insultos cutâneos, enquanto a coluna ventrolateral está relacionada com dor visceral e somática profunda (CLEMENT et al, 2000;BANDLER, 1993;KEAY et al, 1994;). A PAG recebe aferências de diferentes origens, tais como hipotálamo, córtex frontal e insular, amígdala, núcleo parafascicular do tálamo, LC, formação reticular e CPME (AGGLETON, 1992;BEITZ, 1982;HERBERT;SAPER, 1992).…”

“…Neurônios da NMR projetam-se diretamente para a medula espinhal, onde inibem a transmissão nociceptiva FIELDS, 1984;MASON, 1991). As lâminas I, II e III da CPME possuem massiva expressão do receptor inibitório do subtipo 5HT 1A (CROUL et al, 1998). Da mesma forma, a conexão PAG -LC coopera para a inibição nociceptiva, onde a ativação de neurônios noradrenérgicos do LC via SP, dopamina e/ou glutamato resulta na liberação de noradrenalina na CPME (MILLAN, 2002).…”