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      Localization of putative nitrergic neurons in peripheral chemosensory areas and the central nervous system of Aplysia californica.

      The Journal of Comparative Neurology
      Animals, Aplysia, cytology, metabolism, Biological Markers, Brain, Central Nervous System, Chemoreceptor Cells, Cilia, ultrastructure, Epithelial Cells, Feeding Behavior, physiology, Ganglia, Invertebrate, Histocytochemistry, Mouth, NADPH Dehydrogenase, Neurons, Afferent, Neuropil, Nitrergic Neurons, Nitric Oxide, Nitric Oxide Synthase, Peripheral Nervous System

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          Abstract

          The distribution of putative nitric oxide synthase (NOS)-containing cells in the opisthobranch mollusc Aplysia californica was studied by using NADPH-diaphorase (NADPH-d) histochemistry in the CNS and peripheral organs. Chemosensory areas (the mouth area, rhinophores, and tentacles) express the most intense staining, primarily in the form of peripheral highly packed neuropil regions with a glomerular appearance as well as in epithelial sensory-like cells. These epithelial NADPH-d-reactive cells were small and had multiple apical ciliated processes exposed to the environment. NADPH-d processes were also found in the salivary glands, but there was no or very little staining in the buccal mass and foot musculature. In the CNS, most NADPH-d reactivity was associated with the neuropil of the cerebral ganglia, with the highest density of glomeruli-like NADPH-d-reactive neurites in the areas of the termini and around F and C clusters. A few NADPH-d-reactive neurons were also found in other central ganglia, including paired neurons in the buccal, pedal, and pleural ganglia and a few asymmetrical neurons in the abdominal ganglion. The distribution patterns of NADPH-d-reactive neurons did not overlap with other known neurotransmitter systems. The highly selective NADPH-d labeling revealed here suggests the presence of NOS in sensory areas both in the CNS and the peripheral organs of Aplysia and implies a role for NO as a modulator of chemosensory processing. J. Comp. Neurol. 495:10-20, 2006. (c) 2006 Wiley-Liss, Inc.

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