Neuropeptide Y and Y1 receptor like immunoreactivity in dorsal root ganglia and spinal cord after colchicine applicaton to the sciatic nerve in the rat.

CORONEL, M.F., J.B. AQUINO, T. HÖKFELT, HÖKFELT AND M.J. VILLAR

Congreso; 18th Biennial Meeting of the International Society for Neurochemsitry (ISN) and 32th Annual Meeting of the American Society for Neurochemistry (ASN); 2001

Under normal conditions, neuropeptide Y (NPY) is present in very few neurons in dorsal root ganglia (DRG) and in terminals of layers I-III of the spinal cord. However, following peripheral axotomy or crush, NPY is up regulated in small and, to a greater extent, large primary sensory neurons, as well as in the neuropil of the dorsal horn. NPY Y1 receptor (Y1r) is expressed in the soma of some small and medium sized primary sensory neurons in DRG and in layers II-III of the dorsal horn of the spinal cord. To determine a possible regulation of NPY and Y1r expression in DRG and spinal cord by a peripheral trophic factor, the immunoreactivity of both molecules was examined after the application of colchicine, a blocker of the fast axonal transport, to the intact sciatic nerve of adult male rats. Colchicine (5, 10, 20, 50 mM) or saline were either injected to the nerve or applied using a cotton bud. After different survival times the ipsilateral and contralateral DRG (L4-5), as well as the corresponding levels of the spinal cord were removed. The tissue was then processed for standard immunohistochemistry ABC and immunofluorescence techniques using NPY and Y1r antibodies. Application of colchicine to the sciatic nerve induced an increase in NPY-immunoreactive (IR) neurons of dorsal root ganglia L4-5 as well as in terminals in layers I-III of the dorsal horn of the lumbar spinal cord. On the other hand, colchicine showed a decrease in the number of neuronal profiles exhibiting Y1r-like immunoreactivity in DRGs. These effects were more pronounced in animals with a longer survival time (14 days) and/or a higher concentration of colchicine. NPY expression has been previously shown to be dependent on NGF. Our present results showing an increase of NPY-IR neurons after colchicine application to the sciatic nerve give further support to this idea. The mechanism by which peripheral administration of colchicine induced a reduction in the number of Y1r-IR neurons is unknown. However, a regulation by NGF should be further analysed. Nevertheless, a down regulation of the receptor as a consequence of the increase of its ligand cannot be discarded.