Pain-like behaviours in animals ? how human are they?

Pharmacological characterisation of place escape/avoidance behaviour in the rat chronic constriction injury model of neuropathic pain

“…Peripheral nerve injury procedures where the nerve is lesioned, cut or ligated are probably the most commonly used chronic models that create reproducible symptoms of neuropathic pain, including allodynia and hyperalgesia (Bennett and Xie 1988;Seltzer et al 1990; Kim and Chung 1992;Decosterd and Woolf 2000). Given the relative paucity of effective drugs currently available for treating neuropathic pain in human patients, a number of questions have been raised in relation to the face and construct properties of these models (Blackburn-Munro 2004). For example, the occurrence of spontaneous nociceptive behaviours in peripheral nerve models is all too infrequently reported despite being the most prevalent sign of neuropathic pain in clinic (Mogil and Crager 2004).…”

“…For example, the occurrence of spontaneous nociceptive behaviours in peripheral nerve models is all too infrequently reported despite being the most prevalent sign of neuropathic pain in clinic (Mogil and Crager 2004). Crucially, the negative impact mediated by the unremitting nature of such pain on cognitive performance in these models may be largely ignored (Blackburn-Munro 2004).…”

“…Pain affect in turn is also closely related to the complex behaviours of escape and avoidance (Price and Dubner 1977;Price et al 1980). Although a complex interplay exists between these two related dimensions of pain processing, the ability to selectively assess drug effects on either component in animal models might conceivably translate to an improved treatment of neuropathic pain in humans (Blackburn-Munro 2004).…”

Venlafaxine compromises the antinociceptive actions of gabapentin in rat models of neuropathic and persistent pain

“…It is now well-established that nerve damage induces plasticity changes within the dorsal horn, which underlie central sensitization and manifest behaviourally as allodynia and hyperalgesia (Woolf and Salter 2000;Blackburn-Munro 2004). Crucially, abnormal functioning of serotonin (5-HT)-containing and noradrenaline (NA)-containing inputs originating from supraspinal structures, also appears to contribute to the maintenance of central sensitization (Millan 2002).…”

Anti-nociception is selectively enhanced by parallel inhibition of multiple subtypes of monoamine transporters in rat models of persistent and neuropathic pain

“…Reciprocal connections are made via the PAG with the rostral ventromedial medulla (RVM) and the dorsolateral pontine tegmentum (DLPT), two structures which send serotonin (5-HT)-containing and noradrenaline (NA)-containing projections, respectively, to the spinal dorsal horn (Millan 2002). It is now well established that damage to nerves arising as a consequence of viral infection, metabolic disturbance or direct physical insult induces plasticity changes within the dorsal horn, which underlie central sensitisation and manifest behaviourally as allodynia and hyperalgesia (Woolf and Salter 2000;Blackburn-Munro 2004). Crucially, a shift in the balance between descending inhibitory and facilitatory inputs also appears to contribute to the mechanistic processes involved in the maintenance of central sensitisation (Ren and Dubner 2002;Burgess et al 2002;Gardell et al 2003).…”