Neurochemical changes in the RVM associated with peripheral inflammatory pain stimuli

  title={Neurochemical changes in the RVM associated with peripheral inflammatory pain stimuli},
  author={Valerie A. Smith and Chad E. Beyer and Michael R. Brandt},
  journal={Brain Research},

Lateral Hypothalamic-Induced Alpha-Adrenoceptor Modulation Occurs in a Model of Inflammatory Pain in Rats

The hypothesis that the LH-induced nociceptive modulation is mediated through an α-adrenoceptor opposing response in a model of inflammatory pain is supported.

Microdialysis in central nervous system disorders and their treatment

Serotonin—pain modulation

Supraspinal Shaping of Adaptive Transitions in the State of Functional Connectivity Between Segmentally Distributed Dorsal Horn Neuronal Populations in Response to Nociception and Antinociception

The present observations provide additional information on the state of self-organized criticality that leads to the adaptive behavior of the dorsal horn neuronal networks during nociception and antinociceptive both shaped by supraspinal descending influences.

Effect of Treadmill Exercise on Serotonin Immunoreactivity in Medullary Raphe Nuclei and Spinal Cord Following Sciatic Nerve Transection in Rats

Both the aerobic treadmill exercise training and the nervous lesion appear to contribute to changes in serotonin immunoreactivity in trained and sedentary rats.

Expression of TRPV4 in the stimulated rat oral mucous membrane--nociceptive mechanisms of lingual conical papillae.

The results suggest that TRPV4 in the oral mucosa is nociceptor of peripheral hyperalgesia, and pERK expression in the Sp5C is closely related with central hyperAlgesia of the nocICEption.



Plasticity in excitatory amino acid receptor-mediated descending pain modulation after inflammation.

There is a time-dependent increase in EAA neurotransmission in the RVM after inflammation and NMDA receptors play an important role in AMPA-produced inhibition.

The Analgesic Effects of Supraspinal μ and δ Opioid Receptor Agonists Are Potentiated during Persistent Inflammation

Results indicate that peripheral inflammatory injury alters the pharmacology of excitatory and inhibitory inputs that modulate the activity of RVM neurons in such a manner as to enhance the effects of opioid agonists in this region.

Neurogenic hyperalgesia: psychophysical studies of underlying mechanisms.

It was postulated that there exist special chemosensitive primary afferent nerve fibers that are more effective in producing mechanical hyperalgesia than are the known thermo- and mechanosensitive nociceptive nerve fibers.

Changes in gene expression and neuronal phenotype in brain stem pain modulatory circuitry after inflammation.

The results suggest that enhanced NMDA receptor activation mediates time-dependent changes in excitability of RVM pain modulatory circuitry and provides a novel mechanism underlying activity-dependent plasticity and enhanced net descending inhibition after inflammation.

Supraspinal contributions to hyperalgesia.

  • M. UrbanG. Gebhart
  • Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1999
Data suggest a prominent role for the RVM in mediating the sensitization of spinal neurons and development of secondary hyperalgesia, and results to date suggest that peripheral injury and persistent input engage spinobulbospinal mechanisms that may be the prepotent contributors to central sensitization and development.

Descending control of pain