Carbocyanine dye labeling reveals a new motor nucleus in octopus brain

1993 ◽  
Vol 328 (4) ◽  
pp. 485-500 ◽  
Author(s):  
J. David Robertson ◽  
Owen M. Schwartz ◽  
Psyche Lee
Development ◽  
1997 ◽  
Vol 124 (6) ◽  
pp. 1215-1226 ◽  
Author(s):  
S. Schneider-Maunoury ◽  
T. Seitanidou ◽  
P. Charnay ◽  
A. Lumsden

The vertebrate hindbrain is transiently segmented during its early development with the formation of reiterated bulges, the rhombomeres (r). The Krox-20 gene, which encodes a zinc finger transcription factor, has been shown previously to be implicated in the maintenance of r3 and r5 (Schneider-Maunoury, S., Topilko, P., Seitanidou, T., Levi, G., Cohen-Tannoudji, M., Pournin, S., Babinet, C. and Charnay, P. (1993) Cell 75, 1199–1214; Swiatek, P. J. and Gridley, T. (1993) Genes Dev. 7, 2071–2084. However, it was not clear from these analyses how extensive the deletion of r3 and r5 was and whether the overall segmentation and internal architecture of the hindbrain was affected. We have now reinvestigated these issues by analysis of rhombomere boundaries, using both morphological and molecular markers, and of the fate of specific motor neuron populations, using retrograde and anterograde carbocyanine dye tracing. We conclude that r3 and r5 and their derivatives are completely eliminated in Krox-20(−/−) embryos while overall hindbrain segmentation is maintained. In addition, we show that the disappearance of these territories has important consequences for even-numbered rhombomeres as well, in particular on axonal navigation: (i) a population of r6 motoneurons, presumably normally fated to join the glossopharyngeal nerve, has its axons misrouted toward the facial exit point in r4; (ii) the trigeminal motor axons are also misrouted, presumably because of the proximity of the trigeminal and facial exit points. They fasciculate with facial axons outside the neural tube and enter the second branchial arch instead of the first arch. This navigational error could explain the disappearance, at around 17.5 dpc, of the trigeminal motor nucleus in Krox-20(−/−) embryos by inadequate supply of essential, possibly arch-specific survival factors.


1991 ◽  
Vol 260 (1) ◽  
pp. R200-R207 ◽  
Author(s):  
H. R. Berthoud ◽  
N. R. Carlson ◽  
T. L. Powley

The gastrointestinal territories innervated by the gastric, celiac, and hepatic abdominal vagi were identified in rats with selective branch vagotomies by means of 1) anterograde tracing with the carbocyanine dye DiI injected into the dorsal motor nucleus and 2) measurement of cervical vagal stimulation-induced motility responses throughout the gut axis. Presence of DiI-labeled vagal terminals in the myenteric plexus and evoked motility responses were well correlated across the sampled gastrointestinal (GI) sites. In animals with only the two gastric branches intact, the entire stomach and the most proximal duodenum showed significant motility responses and were densely innervated, having DiI-labeled vagal terminals in almost every ganglion. The hepatic branch was found to primarily innervate the duodenum, with minor projections to the distal antral stomach and the intestines. The two celiac branches were found to almost exclusively innervate the jejunum, ileum, cecum and entire colon, and, together with the other vagal branches, the duodenum. Therefore, while there is some degree of specific innervation by the abdominal vagal branches of the oral-to-anal gut axis, which could be called "viscerotopic," the considerably overlapping innervation of the duodenum does not satisfy a viscerotopy criterion and needs further functional analysis.


Author(s):  
Linda C. Hassinger ◽  
James E. Crandall

We have begun to look directly at small numbers of afferent axons to early generated neurons that form the preplate in the developing mouse cortex. The carbocyanine dye Dil (1’1, dioctadecyl-3,3,3’3’-tetramethyl-indocarbocyanine) has proved especially useful for this goal. DiI labels axons and their terminals with greater sensitivity and without some of the disadvantages of axon filling with HRP. The increased sensitivity provided by labeling embryonic axons with DiI has given us new insights into the development of cortical afferents. For instance, we reported originally that afferents from the thalamus were present below the cortex as early as embryonic day 15 (E15) based on HRP injections into mouse embryos. By using DiI placements into the thalamus in aldehyde-fixed brains, we now know that thalamic fibers reach the cortex 24 hrs earlier.


Author(s):  
F. Sartucci ◽  
T. Bocci ◽  
M. Santin ◽  
P. Bongioanni ◽  
G. Orlandi

Abstract Background and rationale Histopathological studies revealed degeneration of the dorsal motor nucleus of the vagus nerve (VN) early in the course of idiopathic Parkinson’s disease (IPD). Degeneration of VN axons should be detectable by high-resolution ultrasound (HRUS) as a thinning of the nerve trunk. In order to establish if the VN exhibits sonographic signs of atrophy in IPD, we examined patients with IPD compared with age-matched controls. Material and methods We measured the caliber (cross-sectional area, CSA) and perimeter of the VN in 20 outpatients with IPD (8 females and 12 males; mean age 73.0 + 8.6 years) and in age-matched controls using HRUS. Evaluation was performed by blinded raters using an Esaote MyLab Gamma device in conventional B-Mode with an 8–19 MHz probe. Results In both sides, the VN CSA was significantly smaller in IPD outpatients than in controls (right 2.37 + 0.91, left 1.87 + 1.35 mm2 versus 6.0 + 1.33, 5.6 + 1.26 mm2; p <0.001), as well as the perimeter (right 5.06 + 0.85, left 4.78 + 1.74 mm versus 8.87 + 0.86, 8.58 + 0.97 mm; p <0.001). There were no significant correlations between VN CSA and age, the Hoehn and Yahr scale, L-dopa therapy, and disease duration. Conclusion Our findings provide evidence of atrophy of the VNs in IPD patients by HRUS. Moreover, HRUS of the VN represent a non-invasive easy imaging modality of screening in IPD patients independent of disease stage and duration and an interesting possible additional index of disease.


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