Expansion of receptive fields of spinal lamina I projection neurons in rats with unilateral adjuvant-induced inflammation: the contribution of dorsal horn mechanisms

Hylden, Janice L.K.; Nahin, Richard L.; Traub, Richard J.; Dubner, Ronald

doi:10.1016/0304-3959(89)90135-8

Cited by 378 publications

(132 citation statements)

References 43 publications

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“…Neurons in the dorsal horn of the spinal cord with receptive fields adjacent to a cutaneous heat injury expand their receptive fields to incorporate the site of injury (McMahon and Wall 1984). Similar recept~ve field expansions have been observed in spinal cord following mechanical (Cervero et al 1988), chemical (Hoheisel and Mense 1989;Woolf and King 1990), inflammatory (Hylden et a!. 1989) and nerve (Devor and Wall 1978) injuries, as well as following the induction of polyarthritis (Menetry and Besson 1982;Calvino et al 1987) and in response to electrical nerve stimulation (Cook et al 1987).…”

Section: Central Sensitizationmentioning

confidence: 71%

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Coderre

Katz

Vaccarino

et al. 1993

Pain

1,829

703

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SummaryPeripheral tissue damage or nerve injury often leads to pathological pain processes, such as spontaneous pain, hyperalgesia and allodynia, that persist for years or decades after all possible tissue healing has occurred. Although peripheral neural mechanisms, such as nociceptor sensitization and neuroma formation, contribute to these pathological pain processes, recent evidence indicates that changes in central neural function may also playa significant role. In this review, we examine the clinical and experimental evidence which points to a contribution of central neural plasticity to the development of pathological pain. We also assess the physiological, biochemical, cellular and molecular mechanisms that underlie plasticity induced in the central nervous system (eNS) in response to noxious peripheral stimulation. Finally, we examine theories which have been proposed to explain how injury or noxious stimulation lead to alterations in eNS function which influence subsequent pain experience.

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Section: Central Sensitizationmentioning

confidence: 71%

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Coderre

Katz

Vaccarino

et al. 1993

Pain

1,829

703

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“…It is well established that peripheral nerve damage causes major alterations in physiology of the somatosensory system at the spinal, thalamic, and cortical levels (Devor and Wall, 1981a,b;Hylden et al, 1989;Hu and Sessle, 1989;Calford and Tweedale, 1988;Mao et al, 1993;Guilbaud et al, 1991Guilbaud et al, , 1992Halligan et al, 1993;Rasmusson et al, 1993;Elbert et al, 1994;Salimi et al, 1994). We recently reported increased resting (no overt stimulation) forebrain activity in somatosensory and limbic structures in CCI animals exhibiting spontaneous pain and hyperalgesia 2 weeks after surgery (Paulson et al, 2000).…”

Section: Discussionmentioning

confidence: 90%

Long-term changes in behavior and regional cerebral blood flow associated with painful peripheral mononeuropathy in the rat

Paulson

Casey

Morrow

2002

Pain

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We identified long-term (up to 12 weeks), bilateral changes in spontaneous and evoked pain behavior and baseline forebrain activity following a chronic constriction injury (CCI) of the sciatic nerve. The long-term changes in basal forebrain activation following CCI were region-specific and can be divided into forebrain structures that showed either: (1) no change, (2) an increase, or (3) a decrease in activity with regard to the short-term (2 weeks) changes we previously reported. All the rats showed spontaneous pain behaviors that persisted throughout the 12-week observation period, resembling the pattern of change found in four limbic system structures: the anterior dorsal thalamus, habenular complex, and the cingulate and retrosplenial cortices. In contrast, heat hyperalgesia was delayed in onset until 4 weeks following CCI, but then persisted, showing a nearly constant level of increased responsiveness. The forebrain activation that resembles this behavioral pattern of change is found in somatosensory cortex, and in the hypothalamic paraventricular nucleus and the basolateral amygdala. Finally, mechanical allodynia, which was maximal during the first 2 weeks following nerve injury and gradually recovered by the seventh post-operative week uniquely matches the time course of changes in ventrolateral and ventroposterolateral thalamic activity. Our results indicate that peripheral nerve damage results in persistent changes in behavior and resting forebrain systems that modulate pain perception. The persistent abnormalities in the somatosensory cortex and thalamus suggest that the sensory thalamocortical axis is functionally deranged in certain chronic pain states.

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“…The case for a central mechanism was supported by two main findings: the selective enhancement of ATP-evoked responses by NS, but not WDR, units in superficial laminae, despite the fact that P2X3 receptor expression was found in superficial and deep laminae (data not shown) and, second, enlarged pinch RF areas of WDR units in superficial and deep laminae compared with LE2 females. Enlargement of high-threshold cutaneous RF areas of dorsal horn neurons after peripheral tissue injury has traditionally been explained by central mechanisms such as disinhibition (Cook et al 1987;Hylden et al 1989;Laird and Cervero 1989). However, in hippocampus and other forebrain areas E2 significantly altered dendritic spine density (see Cooke and Woolley 2005;McEwen et al 2001), suggesting that structural effects of E2 also could have contributed to the changes in TMJ-evoked activity and cutaneous RF areas of Vc/C1-2 neurons.…”

Section: Mechanisms Of E2 Modulation Of Atp-evoked Activation Of Tmj mentioning

confidence: 99%

Differential Effects of Estradiol on Encoding Properties of TMJ Units in Laminae I and V at the Spinomedullary Junction in Female Rats

Tashiro¹,

Okamoto²,

Milam³

et al. 2007

Journal of Neurophysiology

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Tashiro A, Okamoto K, Milam SB, Bereiter DA. Differential effects of estradiol on encoding properties of TMJ units in laminae I and V at the spinomedullary junction in female rats. J Neurophysiol 98: 3242-3253, 2007. First published October 10, 2007 doi:10.1152/jn.00677.2007. To determine whether estrogen status modulated dorsal horn neural activity relevant to temporomandibular joint (TMJ) processing single units were recorded in superficial and deep laminae at the trigeminal subnucleus caudalis/upper cervical cord (Vc/C1-2) junction of ovariectomized (OvX) female rats under barbiturate anesthesia after 17␤-estradiol (E2) treatment for 2 days. E2 dose-dependently enhanced the response to intra-TMJ stimulation by adenosine triphosphate (ATP) of neurons classified as nociceptive specific (NS), but not wide dynamic range (WDR), in superficial laminae. ATP caused similar responses among NS and WDR neurons from deep laminae in all groups. By contrast, the cutaneous receptive field areas of WDR, but not NS, units in superficial and deep laminae were enlarged in high E2-treated (HE2) compared with low E2-treated (LE2) females. Units from untreated or vehicle-treated male rats displayed responses similar to those of LE2 females. TMJ units in superficial laminae from females were more likely to receive convergent cutaneous input and respond to jaw movement than males, independent of E2 treatment. Western blot analysis revealed similar levels of P2X2 and P2X3 receptor protein in Vc/C1-2 or trigeminal ganglion samples in all groups. Immunohistochemistry revealed dense terminal labeling for P2X3 receptors in superficial laminae and moderate labeling in deep laminae at the Vc/C1-2 junction. These data indicated a significant linkage between estrogen status and the magnitude of articular input evoked by ATP from TMJ neurons in the superficial laminae at the Vc/C1-2 junction, whereas estrogenic modulation of TMJ neurons in deep laminae affected only the convergent input from overlying facial skin.

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Expansion of receptive fields of spinal lamina I projection neurons in rats with unilateral adjuvant-induced inflammation: the contribution of dorsal horn mechanisms

Cited by 378 publications

References 43 publications

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

Long-term changes in behavior and regional cerebral blood flow associated with painful peripheral mononeuropathy in the rat

Differential Effects of Estradiol on Encoding Properties of TMJ Units in Laminae I and V at the Spinomedullary Junction in Female Rats

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