Formalin-induced central sensitization in the rat: somatosensory evoked potential data

Molecular and electrophysiological changes in the prefrontal cortex–amygdala–dorsal periaqueductal grey pathway during persistent pain state and fear-conditioned analgesia

“…Furthermore, this increase in dPAG field potential is attenuated in rats expressing FCA. Our data suggest that there is a direct correlation between the magnitude of evoked field potentials in the dPAG and the expression of pain-related behaviour, similar to the cortical somatosensory evoked potential data described by Lebrun and colleagues [32]. To our knowledge, the present study is that the first to determine electrophysiological correlates in any brain region of animals expressing FCA (or any form of stress-induced analgesia).…”

The major histocompatibility complex genes impact pain response in DA and DA.1U rats

“…The consequent increase of spontaneous firing then initiates a second phase [43][44][45]. In addition, this intense activation of nociceptive afferents by formalin leads to increase excitability of neurons in the central nervous system [46]. In the present study, the sensitization of C and Aδ units from primary sensory nerve was consistent with the increase of lifting and licking, indicating that the activation of primary sensory nerve might contribute to these two behaviors induce by formalin.…”

Functional magnetic resonance imaging studies of opioid receptor-mediated modulation of noxious-evoked BOLD contrast in rats

“…The lack of effect of morphine on formalin-evoked increases in BOLD signal intensity in the thalamus is of particular interest and requires further investigation. Previously, systemic morphine was shown to attenuate formalin-evoked behavioural responses (Dubuisson and Dennis 1977) and cortical somatosensory evoked potentials (Lebrun et al 2000). A number of studies have demonstrated the importance of various brain sites, including the PAG (Lewis and Gebhart 1977;Manning and Franklin 1998), thalamus (Cohen and Melzack 1985;Yang et al 2002), hypothalamus (Manning and Franklin 1998) and amygdala (Manning and Mayer 1995), in mediating the analgesic effects of morphine.…”

“…The actions of morphine are mediated by sites of action at the level of the spinal cord and numerous supraspinal sites, including the PAG (Yeung et al 1977;Lewis and Gebhart 1977), thalamus (Cohen and Melzack 1985;Yang et al 2002) and amygdala (Manning and Mayer 1995). The systemic administration of μ-opioid receptor agonists inhibits acute and persistent noxious-evoked responses, for example formalin-evoked behavioural response (Dubuisson and Dennis 1977), neuronal response (Haley et al 1990), cortical somatosensory evoked potential (Lebrun et al 2000) and the expression of c-Fos (Presley et al 1990). Recent studies demonstrated that fMRI can be used to determine the effect of pharmacological treatments, such as the analgesic morphine Tuor et al 2000Tuor et al , 2002Chang and Shyu 2001) and a cannabinoid receptor agonist (Shah et al 2004) in rats.…”