RESUMO
The localization of the neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-4 (NT-4), and neurotrophin-3 (NT-3) was demonstrated immunohistochemically in discrete neuronal subsets of the human trigeminal ganglion at ages ranging from 23 weeks of gestation to adulthood. Neurotrophin-containing subpopulations partially overlapped with each other and with those immunoreactive for the relevant trk receptor. Glial elements could also be immunostained, labelled satellite cells being particularly abundant in NT-3 stained sections. These results suggest that the neurotrophins are of functional significance for the human trigeminal primary sensory neurones throughout life. Their localization in the ganglion cellular components supports their function as target-derived trophic factors and as molecules effective in autocrine/paracrine interactions.
Assuntos
Fatores de Crescimento Neural/análise , Neurônios/citologia , Receptores de Fator de Crescimento Neural/análise , Gânglio Trigeminal/citologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Envelhecimento , Fator Neurotrófico Derivado do Encéfalo/análise , Feminino , Humanos , Lactente , Recém-Nascido , Recém-Nascido Prematuro , Masculino , Pessoa de Meia-Idade , Neurotrofina 3 , Proteínas Proto-Oncogênicas/análise , Receptores Proteína Tirosina Quinases/análise , Receptor do Fator Neutrófico Ciliar , Receptor trkA , Receptor trkC , Gânglio Trigeminal/crescimento & desenvolvimentoRESUMO
Chemical kindling was induced in the rat by chronic treatment with pentylenetetrazol (PTZ, 30 mg/kg, IP, three times a week for eight weeks). PTZ kindling was associated with a reduction in central GABAergic function, as reflected by a significant decrease in the density of 35S-t-butylbicyclophosphorothionate (35S-TBPS) binding sites in the cerebral cortex. The pretreatment with the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 (1 mg/kg, IP, 40 min before each PTZ injection) prevented the development of kindling as well as the reduction in 35S-TBPS binding. The results suggest that NMDA receptors may play a role in the alterations of GABAergic function observed in PTZ-kindled rats.