Distribution of NADPH-diaphorase in rat mesencephalon: a light and electron microscopical study

NADPH-diaphorase is a useful technique to reveal NO producing neurons at light microscopic level (LM). A modification of the technique using the tetrazolium salt BSPT as substrate, is useful to study the ultrastructure of NO neurons. The aim of this work was to perform a detailed analysis of NADPH-diaphorase reactive neurons in rat mesencephalon both at light and electron microscopic levels. NADPH-diaphorase reactive neurons were observed in superior colliculus, in central gray matter, in dorsal and medial raphe and in the pedunculopontine tegmental nucleus using two histochemical techniques at LM. Electron microscopy showed deposits on membranes of the endoplasmic reticulum, Golgi apparatus and nuclear envelope of dorsal raphe neurons. Presynaptic and postsynaptic terminals showed deposits on membranous elements but postsynaptic terminals also showed deposits on the inner surface of their membranes. Further physiological studies are needed to clarify the meaning of the ultrastructural findings such as the putative interaction of NOS with postsynaptic proteins, receptors or membranous channels.

Striatal cytomegalic neurons containing nitric oxide are associated with experimental perinatal asphyxia: implication of cold treatment

Neuropathological mechanisms triggered by excitatory aminoacids are Known to involve nitric oxide (NO). Neurons containing NO are histochemically reactive to nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), which labels NO synthase in CNS, Sprague-Dawley male rats subjected to perinatal asphyxia (PA) at 37 degreese Celsius, and PA plus 15 degreese Celsius hypothermia were evaluted when 6 months old by NADPH-d histochemical reaction. Computarized image analysis was used for quantification of stained sections. NADPH-d neurons in striatum from subsevere and severe PA showed a significant increment in soma size and dendritic process length versus control and hypothermic treated rats. Post-ischemic damage reurons are therefore involved in NO changes induced by PA that may be prevented by hypothermia treatment.