Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Jul 26;13:921470. doi: 10.3389/fphys.2022.921470

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2022 Dean and Stavitzski.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Locations of lesions in animal models that do not (1–3) versus do (4) abolish the seizures of CNS-OT. Removing the forebrain (lesions 1 and 2) and bisecting the corpus callosum (lesion 3) do not abolish seizure genesis when breathing HBO₂. A medullary pyramidal tractotomy does abolish seizure, however (lesion 4). Thus, the critical areas involved in seizure genesis must reside between lesions 2 and 4; that is, in the hind brain; i.e., brain stem plus cerebellum (light green shaded region). Nuclei postulated to function as “oxtox trigger nuclei” based on the early abnormal cardio-respiratory responses and nonconvulsive S/Sx that precede HBO₂-seizures are indicated, including CO₂-chemosensitive areas (golden yellow nuclei) and cranial nerve nuclei (blue nuclei). While neurons in CO₂-chemosenitive areas are reported to be stimulated during exposure to hypercapnic acidosis, to date, only CO₂-sensitive neurons in the cSC (green nuclei) are reported to be stimulated by exposure to hyperoxia and chemical oxidants in control O₂. CO₂-excited neurons in the other chemosensitive areas of the mCNS have not been studied yet to determine their sensitivity to increased oxygenation and cellular oxidation. The sagittal view presented is 0.40 mm lateral to midline in the rat brain, which was adapted from Figure 164 in the brain atlas of Paxinos and Watson (Paxinos and Watson 2007). The relative locations of cranial nerve nuclei III, IV, VI, VII, VIII and X and chemosensitive nuclei indicated come from sagittal views passing 0.18 through 2.4 mm lateral to midline (Figures 163–171 in the rat brain atlas). Recall that CN X is the dorsal motor nucleus of vagus, which with the nucleus tractus solitarius comprises the cSC. The purpose of the Figure 2 is to emphasize, based on lesion studies, the region of the mCNS that likely contains neurons involved in seizure genesis in CNS-OT; that is, the rostro-caudal distribution of nuclei postulated to function as “oxtox trigger nuclei”. Their locations presented here do not to accurately convey their true medial-to-lateral distributions. Abbreviations used: III, oculomotor nucleus; IV, trochlear nucleus; VI, abducens nucleus; VII, facial nucleus; VIII, vestibular-cochlear nuclei; ac, anterior commissure; APit, anterior pituitary; cc, corpus callosum; cSC, caudal Solitary Complex (= NTS and DMNV/CN X); Fast, fastigial nucleus of the cerebellum; HC, hippocampus; LC, locus coeruleus; LH, lateral hypothalamus; MR, medullary raphe; ox, optic chiasm; PBC, pre-Bötzinger Complex; RTN, retrotrapezoid nucleus; Thal, thalamus.