No abstract

Acupuncture points are clinically described by their localization and sensation measuring skin resistance. As a morphological correlate, gap junctions and connexines (Cx) were postulated but up to now only few animal studies tried to identify these structures histologically. Immunohistochemical staining of acupuncture point Lu11 of 4 human donors (76-81 years of age) were stained with antibodies against Cx 26, 30, 32 and 43. A densitometric evaluation was performed using analySIS Software 3.2 (Olympus). In the region of the acupuncture point Lu11 the density of Cx 26 and Cx 43 was increased. This increase was not restricted to the epidermal layers but also included the dermis and subcutis. Our findings give evidence that there are persistent regions of increased Cx density in the human skin. They provide a morphological base for fast alterations in electrical skin resistance dependent on the functional stage of the Cxs by forming either gap junctions or hemi-channels.

Although the presence of an arrector pili smooth muscle is documented in many monkey species, its regional peculiarities are hitherto not well documented. We aimed to study this aspect in the face of rhesus monkeys with different areas of hair coat. Eight different regions of six monkeys (male and female) were studied using light microscopy and immunohistochemistry (antibody against smooth muscle alpha actin). We identified two regions (lips and eyelids) with vellus hairs that did not show an arrector pili muscle. In the eyelids, the hairs are rather small and short; in the lips, the vellus hairs were surrounded by striated muscle fibers from the orbicularis oris muscle. In all other regions (frontal region, forehead, cheek, chin), the vellus hairs contained an arrector pili muscle with comparable morphology. Only in the chin region, where additional striated muscles from the face muscles were present, the arrector pili muscles were thinner. All vibrissae showed a close relation to striated muscle fiber bundles of the facial muscles. They never developed smooth muscle bundles assigned as arrector pili equivalent.

NADPH diaphorase/neuronal nitric oxide synthase stained amacrine cells (NAC) are supposed to interact with the retinal vasculature. To study this hypothesis, the retinae of two different mouse strains and their controls were stained using the NADPH diaphorase technique labelling NAC and vessels. In the retina degeneration (rd) mouse, the total number of NAC in the first weeks during early retinal degeneration was slightly reduced. The number persisted in older animals and did not show the decrease described in normal mice. In the Norrie disease (nd) mouse, early vascular malformation lead to increased numbers of NAC. Although the progress of neural remodelling in the degenerated retina leads to a continuous loss of neurons in general, the NAC persist in higher numbers in parallel with a reduced vascular bed. Brief reportClose association between the retinal vasculature and NADPH diaphorase (NADPH-d)/nNOS stained amacrine cells (NAC) were reported for the rat and primate [1,2] and a regulatory function of these cells on retinal microcirculation discussed. This is supported by physiological findings concerning the intensity of relaxation measured in retinal vessels [3,4].To further study the interdependency between NOS positive amacrine cells and vasculature, two different kinds of retinal degeneration were investigated. One showed degenerative and neovascular processes after normal vascular development (rd mouse [5,6]), the other primary vascular irregularities (nd mouse [7]). Retina whole mounts from rd, nd, and C57BL/6 mice at various ages were stained for NADPH-d as described previously [8]. All animals were kept according to the Declaration of Helsinki and the local rules for animal research.In the rd mouse retina, first NAC somata were detected at P3 in the inner cytoblast layer similar to controls. At P14, the number of NAC was only 80% of that counted in control animals (Table 1). However, this number persisted during ageing resulting in an elevated number of NAC somata at 3 months of age and older (Table 2).First changes of the retinal vasculature were obvious at P14. The outer vascular layer continuously degenerated and was almost completely absent at 6 weeks of age. Sprouting vessels in the retinal pigment epithelium (RPE) layer were noted at four weeks of age, rising in number and size with age. From eight weeks on, RPE cells were found around vessels of the inner vascular layers indicating migration along the vasculature.Combining vascular and NAC alterations in the rd mouse, some relation between both structures can be stated. The first onset of retinal degeneration after P7 [5] lead to decreased numbers of NAC. Vascular degeneration paralleled stabilization of elevated NAC number during further retinal degeneration. Neovascularizations did not alter the increased NAC level.