PubMed · 6462419
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A B Joseph. 1984. Startle disease.. https://doi.org/10.1097/00006123-198406000-00027
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
An immunohistochemically distinct zone was identified in the superficial aspect of trigeminal nucleus caudalis of the New World owl monkey that is not immunoreactive for substance P or serotonin, in stark contrast to the dense staining present in the surrounding laminae I and II. Thionin-stained sections in different planes showed that this is a subregion of lamina I containing clusters of neurons that appear to have pyramidal or polygonal somata. Extracellular microelectrode recordings in this region revealed clusters of thermoreceptive-specific (COLD) cells with nasal or labial receptive fields, whereas nociceptive neurons were found in the adjacent portions of lamina I. Anterograde tracer injections in this region produced trigeminothalamic terminal labeling in the site homologous to the lamina I spino-thalamo-cortical relay nucleus identified previously in the Old World macaque monkey and in humans. Retrograde tracer injections involving this thalamic site, where recordings of trigeminal COLD-like neurons were obtained, produced clusters of retrogradely labeled trigeminothalamic neurons in this immunohistochemically distinct subregion of lamina I, nearly all of which are pyramidal neurons. We conclude that the nocturnal owl monkey has a specialized perinasal thermoreceptive trigeminothalamic sensory pathway that is probably of behavioral significance during olfactory sniffing. In addition, these observations corroborate other findings that have indicated that lamina I COLD cells are pyramidal neurons and are not physiologically modulated by substance P or serotonin, in contrast to nociceptive neurons.
Adult rats received intracerebroventricular (i.c.v.) administration of either phosphate buffer (PBS) or 192 IgG-saporin (Toxin), 3.6 micrograms rat-1, a cholinergic immunotoxin. Six to eight weeks later, the animals received a continuous intravenous (i.v.) infusion of either physostigmine (4.2 micrograms kg-1 min-1) or saline, followed by measurement of cerebral cortical blood flow (CBF) with the autoradiographic Iodo-14C-antipyrine methodology in four groups of animals: Toxin i.c.v.+saline i.v. (n=9), Toxin i.c.v.+physostigmine i.v. (n=6), PBS i.c.v.+saline i.v. (n=6) and PBS i.c.v. +physostigmine i.v. (n=6). Choline acetyltransferase activity (ChAT) was assessed with Fonnum's method in samples of cortical tissue adjacent to the sites of CBF measurement. ChAT decreased in all regions of the Toxin groups when compared to PBS (% decrease: hippocampus=93%, neocortex=80-84%, entorhinal-piriform cortex=42%, amygdala=28%). CBF decreased globally in Toxin+SAL, most severely in posterior parietal and temporal regions (24-40% decrease from PBS+saline). Physostigmine enhanced CBF predominantly in these same areas both in PBS and Toxin animals although to a lesser extent in the latter. Our results demonstrate the importance of cholinergic mechanisms in the control of CBF. The similarity between the topography of CBF decrease following administration of the immunotoxin to that observed in Alzheimer's disease suggests that the CBF pattern observed in this disease may be the result of cholinergic deafferentation.
Fork head-5 (Fkh5; also known as Mf3 and TWH) is a transcription factor of the winged helix family. As part of an extended project to understand the function of this protein in the developing mouse brain, in the present work we have used Fkh5/Mf3 expression as a marker to study the development of the midbrain and hindbrain. In the midbrain, Fkh5/Mf3 is expressed in the superior colliculus, in the ventricular layer of the inferior colliculus and in the isthmus. In the superior colliculus, Fkh5/Mf3 is expressed by cells of layers 4a and 4c since early in development. In the hindbrain, Fkh5/Mf3 is a longitudinal marker (as opposed to a transverse or rhombomeric one), since it labels nuclei belonging to the somatic afferent zone (ventral cochlear nucleus, cuneate and external cuneate nuclei, principal and spinal nuclei of the trigeminal). In addition, Fkh5/Mf3 is expressed by the developing endopiriform nucleus and by the olivary pretectal nucleus. The results suggest that Fkh5/Mf3 has an early role in the lamination of the tectum and in the longitudinal differentiation of the hindbrain.