A quantitative analysis of the microglial cell reaction in central primary sensory projection territories following peripheral nerve injury in the adult rat

Abstract

The time course of the microglial cell reaction in central nervous system primary sensory projection territories has been examined following peripheral nerve injury in the adult rat using qualitative and quantitative analysis of immunoreactivity with the monoclonal antibody OX-42, which recognises the complement receptor CR3. The regions examined included the gracile nucleus, the column of Clarke and the spinal cord dorsal horn (superficial and deep laminae separately) after unilateral sciatic nerve transection, and the spinal trigeminal nucleus following unilateral infraorbital nerve transection. In all territories examined a qualitative increase in OX-42 immunoreactivity was observed 24 h postlesion. Further, quantitative analysis revealed an exponential development of the OX-42 immunoreactivity, with a peak at one week postlesion, thereafter showing a slow exponential decline. Our results show that the signal (or signals) that induces the microglial cell response in primary sensory projection territories is rapid in comparison to previously described central degenerative changes following peripheral nerve lesions (transganglionic degeneration). These findings are compatible with the hypothesis that activated microglia play a pathogenetic role in the development of transganglionic degeneration.

Loss of Neurons from Laminas I-III of the Spinal Dorsal Horn Is Not Required for Development of Tactile Allodynia in the Spared Nerve Injury Model of Neuropathic Pain

“…This, together with their distribution in both gray and white matter, the fact that the great majority were Iba-1 immunoreactive (but none were labeled for NeuN, APC, or GFAP), and their occasional association with neurons, strongly suggests that the apoptotic cells are all microglia, as has been reported after complete transection of the sciatic nerve (Gehrmann and Banati, 1995). Microglia are known to proliferate in the spinal cord after peripheral nerve injury (Gehrmann et al, 1991;Eriksson et al, 1993), and apoptosis is thought to be a homeostatic mechanism to reduce their number after activation (Gehrmann and Banati, 1995).…”

ATP receptors gate microglia signaling in neuropathic pain

“…A progressive series of morphological changes in spinal microglia has been reported in rodent models of nerve injury caused by compression, ligation, or transection (Liu et al, 1995;Tsuda et al, 2003;Zhang and De, 2006). After peripheral nerve injury, microglia withdraw their thin processes and adopt an amoeboid-like structure (Eriksson et al, 1993). These morphological changes are often followed by an increase in the number and density of microglia in the ipsilateral spinal dorsal horn Echeverry et al, 2008;Gehrmann and Banati, 1995;Perry, 1994;Stoll and Jander, 1999).…”

Do glial cells control pain?

“…Microglia become activated by various stimuli. Microglia activation is also described in various ways , such as changes in morphology from ramified to amoeboid (Eriksson et al, 1993), increase in the expression of microglial markers [e.g., MHC II, CD 11b (Coyle, 1998;Eriksson et al, 1993;Liu et al, 1995)], and increase in the number of microglia (proliferation). These slow changes often take hours to days to manifest.…”