Glutamate in the glomus cells of the cat carotid body: immunocytochemistry and in vitro release.

The identity of the postulated excitatory transmitter released by glomus cells is not known. Since our preliminary work on paraffin sections of the cat carotid body indicated that most glomus cells were intensely immunoreactive to glutamate, we decided to investigate whether glutamate might be such a transmitter, using two approaches. One approach was to make a quantitative immunogold analysis of ultrathin sections to assess the level of glutamate immunoreactivity of glomus cells relative to glia and to afferent axon terminals. The other approach was to measure the potassium-induced release of glutamate from carotid bodies superfused in vitro. We consistently found that glomus cell profiles had 50% more immunogold particles per unit of area than glial cell or axonal profiles. However, the levels of glutamate immunoreactivity of glomus cells were lower than those expected for glutamatergic terminals. We also found that glutamate was not released from in vitro carotid bodies stimulated with high concentrations of potassium. These findings indicate that the oxygen-sensitive glomus cells have a high concentration of glutamate, which is not released by superfusion with high potassium. Thus, glutamate is not the excitatory transmitter released by glomus cells. We speculate that the high concentrations of glutamate might instead be related to the known dependence of the "in vitro" chemosensory activity on metabolic substrates.

Propuesta de un indice pronostico en la enfermead de Hodgkin / proposal of a pronostic index in the Hodgkins disease

En este trabajo se ha comprobado la validez del índice pronóstico de la Enfermedad de Hodgkin calculado en 1983. La heterogeneidad de la serie ha sido una característica acusada, en cuanto a la procedencia de los enfermos y los tipos de tratamientos aplicados. Con ampliar la serie se ha pretendido aumentar su representatividad para generalizar el valor de los resultados. En este índice se considera la presencia de 13 factores implicados en la evolución postremisión completa de los pacientes con EH. Se asignó 1 punto a la presencia de síntomas generales; al tipo histológico celularidad mixta; estadio II-abdominal; III; afectación extraganglionar en los estadios I, ó III; afectación supraclavicular; esplenomegalia mayor de 5 cm; síndrome de cava inferior; síndrome mediastínico; y cuando el paciente es varón mayor de 40 años de edad. Se otorgan 2 puntos al tipo histológico depleción linfocítica; estadio IV; y al tiempo de evolución de los síntomas mayor de 6 meses. El pronóstico adverso que conllevan todos estos factores se confirma ampliamente en la literatura

Ultrastructural identification of satellite interneurons in the rat dorsal lateral geniculate nucleus.

Multiple injections of horseradish peroxidase (HRP) were placed in the occipital cortex of rats, including all striate and extrastriate visual areas, to examine with the electron microscope the population of retrogradely labeled and unlabeled cells in the dorsal lateral geniculate nucleus (LGN), for the purpose of ultrastructurally identifying geniculate interneurons. O-tolidine was used as chromogen in the histochemical procedure. EM analysis of LGN showed dense HRP reaction products diffusely distributed in the cytoplasm of virtually all large and medium size geniculate cells, identifying the geniculo-cortical relay cells. The classes of unlabeled cells distinguished in this study are oligodendrocytes, astrocytes, and other small cells whose glial or neural nature is difficult to assess in light microscopic semithin sections. In serial ultrathin sections, these small cells were seen to be presynaptic in somato-somatic synapses with relay cells, and to give origin to presynaptic dendrites. These neurons are cytologically identifiable by their small size, scant cytoplasm, characteristic chromatin clumps in nuclei that are not indented, and by having extended contacts with the cytologically different relay cells. We conclude that these neurons were not retrogradely labeled because of their intrinsic nature in LGN and, because of their common contacts with relay cells, we term them "satellite interneurons".