[PubMed] [Google Scholar]Nurhidayat, Tsukamoto Y, Sigit K, Sasaki F. determine the neuronal contacts and cyto- and chemoarchitecture of the PVH in the popular C57BL/6J male mouse. Our findings reveal a distinct corporation in the mouse PVH that is substantially different from the PVH of male rats. The variations are particularly obvious with respect to the spatial relations of two principal neuroendocrine divisions (magnocellular and parvicellular) and three descending preautonomic populations in the PVH. We discuss these data in relation to what is known about PVH function and provide the work like a source for further studies of the neuronal architecture and function of the mouse PVH. (the PeM), which, together with the anterior commissural part (AC; related to the PVHam defined here and previously in rats by Swanson and Kuypers, 1980), is included in the accessory magnocellular neuroscretory neurons. In agreement with Swanson and Kuypers (1980), we consider the PVHmm as a major part of the PVH rather than an accessory to magnocellular neuroesecretory neurons. Indeed, the coronal aircraft containing both the PVHmm and the PVHpmm (level 61 in ARA; Figs. 3B, 5B,C) contains the largest quantity of OXY neurons in the mouse PVH. Next, the PVHpml, which consists of primarily VAS in both rats (Swanson and Kuypers, 1980) and mice (mainly because shown here), also displays very unique cellular organizational properties. In rats, the PVHpml is very prominent, in which VAS neurons are densely clustered in the center like a ball, surrounded by a ring composed of dispersed OXY neurons (Sawchenko et al., 1984b; Swanson, 1986, 1987; Simmons and Swanson, 2009). In the mouse mind, although VAS neurons in the PVHpml will also be clustered into a tightly packed ball, its relative size (relative to the overall size of the PVH at same coronal planes) is much smaller. Also, unlike in rats, only small numbers of OXY neurons are distributed medially to the VAS-positive ball and don’t form a ring surrounding the PVHpml. Finally, in rats, the PVHpmm, which consists of twice as many OXY neurons as VAS neurons (Simmons and Swanson, 2009), is located more rostrally than the PVHpml, and these two parts are not Amifampridine present at the same coronal levels. However, in mice, the PVHpmm and PVHpml are present at the same coronal levels for some a range throughout the PVH, along with the extension of the PVHmpd, which essentially sits between these two magnocellular parts. Nevertheless, these two magnocellular parts are not completely segregated. Instead, they may be more or less continued by quite a few magnocellular neurons (especially VAS neurons) across the PVHmpd. Several studies using immunohistochemical Amifampridine methods have also examined the neuronal morphology and distributions of OXY and VAS neurons in C57BL/6J mice (Kublaoui et al., 2008), albino house mice (the Oxford Amifampridine University or college strain; Castel and Morris, 1988), and ICR and mutant polydipsic (STR/N) strains (Ison et al., 1993). Despite different strains being utilized, the general Amifampridine distribution patterns of these two magnocellular populations in the mouse PVH are consistent with the present statement. Transgenic mice expressing the rat OXY gene also display mouse-like OXY immunoreactivity patterns in the PVH (Young et al., 1990b) rather than the OXY patterns explained for rats (Swanson and Kuypers, 1980). We estimate the mouse PVH consists of approximately 1,000C1,200 OXY neurons and fewer VAS neurons. These figures are less than those reported for additional strains of mice. For example, Kawamoto and Kawashima (1985) estimated 2,100 OXY and 1,600 VAS neurons in 3-month-old C57BLTw mice. Ison et al. (1993) estimated about 1,600 VAS neurons in mutant polydipsic (STR/N) mice and 1,300 VAS neurons in the PVH of ICR mice that were 6C12 weeks of age. These variations may be the result of variations in the mouse Kdr strains, variations in immunohistochemical methods (e.g., different antibodies, thickness of sections, and immunostaining methods), or variations in the methodologies for Amifampridine cell counting. Our figures typically look like lower than those reported in these additional studies, which is definitely consistent with the method we used to count positive neurons. Only cells with obvious DAPI-labeled nuclei through the entire z-stack were counted, and the Abercrombie element (1946) was applied, both of which.