Spontaneous activity of rat dorsal horn cells in spinal segments of sciatic projection following transection of sciatic nerve or of corresponding dorsal roots

Effects of Sciatic Nerve Axotomy on Excitatory Synaptic Transmission in Rat Substantia Gelatinosa

“…This contrasts with the effects of CCI, reported to increase the expression of N-type Ca 2ϩ channels in the dorsal horn (Cizkova et al 2002). Despite these differences, it is well established that axotomy, like CCI, increases spontaneous activity in both primary afferent fibers (Govrin-Lippmann and Devor 1978; Wall and Devor 1983;Zhang et al 1997) and in dorsal horn neurons (Dalal et al 1999).…”

“…decreases that to inhibitory neurons. Both types of change, which are also seen with CCI (Balasubramanyan et al 2006), could contribute to the overall increase in dorsal horn excitability that follows peripheral nerve injury (Dalal et al 1999;Woolf 1983). …”

Etiology and Pharmacology of Neuropathic Pain

“…These laminae contain wide dynamic range (projection) neurons that receive direct Ab fiber input from primary afferents as well as polysynaptic inputs that convey nociceptive information from superficial laminae (Peirs and Seal, 2016). Their rate of discharge is thus correlated to the type of input, with painful sensation eliciting high frequency discharge and innocuous stimuli generating more modest discharge (Dalal et al, 1999). These laminae are involved in the complex processing of tactile information such as object size, shape, texture as well as vibration, and direction of stimulus movement.…”

Investigation of the central and peripheral analgesic and anti-inflammatory activity of Draksharishta an Indian Ayurvedic formulation

“…[18] The inflammatory pain (second phase) is caused by the release of inflammatory mediators like histamine, prostaglandins, bradykinin, serotonin in the peripheral tissues, [19] and from functional changes in the spinal dorsal horn. [20] Our results showed that DRK had no effect on neurogenic pain suppression (first phase) but had effective antinociceptive effect in the peripheral inflammatory (second phase) pain. Cotreatment with naloxone partially blocked the activity of Tramadol in both the phases while that of DRK and Diclofenac Sodium remained unaffected.…”