Allodynia-like effects in rat after ischaemic spinal cord injury photochemically induced by laser irradiation

Abstract

We report behaviours suggesting the presence of allodynia elicited by non-noxious brushing and mechanical pressure following photochemically induced ischaemic spinal cord injury in the rat. Female rats were intravenously injected with Erythrosin B and the T10 vertebra was irradiated with a laser beam for 1, 5 or 10 min. These procedures initiated an intravascular photochemical reaction, resulting in ischaemic spinal cord injury. After irradiation a clear allodynia was observed in most rats. The animals vocalized intensely to light touch during gentle handling and were clearly agitated to light brushing of the flanks. The vocalization threshold in response to the mechanical pressure measured with von Frey hairs was markedly decreased during this period. In some animals the existence of spontaneous pain was suggested by spontaneous vocalization. The duration of the allodynia varied among animals from several hours to several days. The severity and duration of allodynia seemed not to be related to the duration of irradiation. In sham-operated rats a slight, transient allodynia was also noted around the wound within a few hours after surgery, which was effectively relieved by systemic morphine (2 mg/kg, i.p.). Morphine (2 mg/kg, i.p.) also partially relieved the allodynia in spinally injured rats 4 h after irradiation. However, morphine, even at a higher dose (5 mg/kg, i.p.), failed to alleviate the allodynia in spinally injured rats 24-48 h after the injury. Systemic injection of the GABAB agonist baclofen (0.01-0.1 mg/kg, i.p.), but not the GABAA agonist muscimol (1 mg/kg, i.p.), effectively relieved allodynia during this period. Pretreatment with guanethidine 24 h and just prior to the irradiation (20 mg/kg, s.c.) did not prevent the occurrence of allodynia in spinal cord injured rats. The present observation is the first to show that ischaemic spinal cord injury could result in cutaneous mechanical allodynia. This phenomenon is resistant to morphine and may not involve the sympathetic system. Histological examination of allodynic animals 3 days after spinal cord injury revealed considerable morphological damage in the dorsal spinal cord of a rat irradiated for 5 min. The related dorsal roots were also slightly affected in this animal, while the dorsal root ganglia were normal. However, in rats irradiated for 1 min, despite the existence of strong allodynia, no damage could be found at this time in the spinal cord, dorsal roots or dorsal root ganglia. It is suggested that functional deficits in the GABAB system in the spinal cord may be related to this allodynia-like phenomenon.(ABSTRACT TRUNCATED AT 400 WORDS)

Pain following spinal cord injury

“…Valid models would appear to be those that mimic the histological eects of human SCI. Four are currently utilized: an ischaemic model, 45,46 an excitotoxic model, 47 a spinal cord contusion model, 48 and a hemisection model. 49 ± 51 The ischaemic model developed by WiesenfeldHallin and her colleagues 46 uses a photochemical method to produce graduated ischemia in the spinal cord.…”

Mechanisms of Spinal Cord Stimulation in Neuropathic Pain

“…This model differs from the previously mentioned preclinical neuropathic pain models as it allows behavioral testing of intact cutaneous areas adjacent to injured denervated regions (Decosterd & Woolf, 2000). In addition to these three extensively used models (the Bennett chronic constriction injury model, the Selzer partial sciatic nerve ligation model and the Chung spinal nerve ligation model), other animal models based on photochemically induced ischaemia in the spinal cord have been described (Watson et al, 1986;Hao et al, 1991;Gazelius et al, 1996). All preclinical pain models have been developed in order to mimick clinical pain states in humans as closely as possible.…”

Mechanisms and Treatment of Spinal Cord Injury Pain: An Update

“…One model uses laser irradiation to produce an ischemic injury to the spinal cord (38,39). One uses intraspinal injections of an excitatory amino acid to produce an excitotoxic lesion (40).…”