Role Of Intrinsic Neurons Research Articles

Regional variations in the number distribution of intrinsic myenteric neurons and coinnervated motor endplates on the striated muscles in the rat esophagus.

The roles of intrinsic neurons and the significance of the coinnervated striated muscles in the esophagus are unclear. We examined the number distribution of intrinsic neurons and coinnervated motor endplates on the striated muscles in the rat esophagus using immunohistochemistry to investigate whether these neurons and coinnervated striated muscles may be relevant to the local control of esophageal motility. The number of PGP9.5-positive neurons was higher in the cervical esophagus (segment 1) and gradually decreased toward the aboral, with a moderate increase in the abdominal (segment 5). This pattern was similar to that of NOS-positive neurons, while the number of ChAT-positive neurons decreased toward the aboral, but it was not significantly different among segments 3 to 5. The number of ChAT-positive motor endplates increased toward the aboral, with the highest number in segment 5. The proportion of coinnervated motor endplates was approximately 80% in segments 1 to 4, but approximately 66% in segment 5. NPY-IR was localized in some nerve terminals among the smooth muscles of the muscularis mucosa and some NOS- or ChAT-positive esophageal intrinsic neurons. ENK-8-IR was found in some NOS- or ChAT-positive intrinsic neurons, and nerve terminals surrounding intrinsic neurons in the esophagus, but not in motor neurons at the NA or DMV. This study suggests that regional variations in the number of intrinsic neurons and coinnervated striated muscles in the rat esophagus may be involved in local regulations of esophageal motility, and that the rat esophageal intrinsic neurons may contain, at least, motor neurons and interneurons.

The role of intrinsic neurons in lateral hypothalamic self-stimulation

In this brief review, we summarize some of our recent work concerning the effect of a specific lesion of the intrinsic neurons located in the middle part of the lateral hypothalamus on electrical self-stimulation of this structure by electrodes implanted along the medial forebrain bundle. In a first experiment the neurons of the lateral hypothalamus were destroyed unilaterally by local injejction of ibotenic acid (4 μg in 0.5 μl). The contralateral side served as the sham-lesion control. Between 10 and 20 days later, electrodes were bilaterally implanted, one in the lesioned area, the other in the contralateral hypothalamus. Intracranial self-stimulation (ICSS) was obtained separately for each electrode, at various current intensities, using a nose-poke response. ICSS from electrodes implanted in the lesioned area was decreased in all cases, whereas ICSS of the sham-lesioned side was normal. In a second experiment, two groups of rats lesioned and implanted as above, received two additional electrodes either in the anterior hypothalamus or in the posterior hypothalamus. In rats with electrodes in the anterior hypothalamus, the lesion produced a large deficit in self-stimulation when stimulation was applied to the anterior electrode ipsilateral to the lesion. Only 3 of 6 rats showed a decrease in ICSS with stimulation of the posterior hypothalamic electrode ipsilateral to the lesion. These results suggest that ICSS in the anterior part of the medial forebrain bundle is sustained by long fibers originating in the middle part of the lateral hypothalamus, while ICSS in the posterior part of the lateral hypothalamus may not depend on the neurons located in the lesioned area.