Sympathetic-correlated c-Fos expression in the neonatal rat spinal cord in vitro.
J Biomed Sci
; 16: 44, 2009 May 01.
Article
en En
| MEDLINE
| ID: mdl-19409080
ABSTRACT
An isolated thoracic spinal cord of the neonatal rat in vitro spontaneously generates sympathetic nerve discharge (SND) at ~25 degrees C, but it fails in SND genesis at < or = 10 degrees C. Basal levels of the c-Fos expression in the spinal cords incubated at < or = 10 degrees C and ~25 degrees C were compared to determine the anatomical substrates that might participate in SND genesis. Cells that exhibited c-Fos immunoreactivity were virtually absent in the spinal cords incubated at < or = 10 degrees C. However, in the spinal cords incubated at ~25 degrees C, c-Fos-positive cells were found in the dorsal laminae, the white matter, lamina X, and the intermediolateral cell column (IML). Cell identities were verified by double labeling of c-Fos with neuron-specific nuclear protein (NeuN), glial fibrillary acidic protein (GFAP), or choline acetyltransferase (ChAT). The c-Fos-positive cells distributed in the white matter and lamina X were NeuN-negative or GFAP-positive and were glial cells. Endogenously active neurons showing c-Fos and NeuN double labeling were scattered in the dorsal laminae and concentrated in the IML. Double labeling of c-Fos and ChAT confirmed the presence of active sympathetic preganglionic neurons (SPNs) in the IML. Suppression of SND genesis by tetrodotoxin (TTX) or mecamylamine (MECA, nicotinic receptor blocker) almost abolished c-Fos expression in dorsal laminae, but only mildly affected c-Fos expression in the SPNs. Therefore, c-Fos expression in some SPNs does not require synaptic activation. Our results suggest that spinal SND genesis is initiated from some spontaneously active SPNs, which are capable of TTX- or MECA-resistant c-Fos expression.
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1
Base de datos:
MEDLINE
Asunto principal:
Médula Espinal
/
Sistema Nervioso Simpático
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Proteínas Proto-Oncogénicas c-fos
Idioma:
En
Revista:
J Biomed Sci
Asunto de la revista:
MEDICINA
Año:
2009
Tipo del documento:
Article