Document Detail

Infant brain stem is prone to the generation of spreading depression during severe hypoxia.
MedLine Citation:
PMID:  19261708     Owner:  NLM     Status:  MEDLINE    
Spreading depression (SD) resembles a concerted, massive neuronal/glial depolarization propagating within the gray matter. Being associated with cerebropathology, such as cerebral ischemia or hemorrhage, epileptic seizures, and migraine, it is well studied in cortex and hippocampus. We have now analyzed the susceptibility of rat brain stem to hypoxia-induced spreading depression-like depolarization (HSD), which could critically interfere with cardiorespiratory control. In rat brain stem slices, severe hypoxia (oxygen withdrawal) triggered HSD within minutes. The sudden extracellular DC potential shift of approximately -20 mV showed the typical profile known from other brain regions and was accompanied by an intrinsic optical signal (IOS). Spatiotemporal IOS analysis revealed that in infant brain stem, HSD was preferably ignited within the spinal trigeminal nucleus and then mostly spread out medially, invading the hypoglossal nucleus, the nucleus of the solitary tract (NTS), and the ventral respiratory group (VRG). The neuronal hypoxic depolarizations underlying the generation of HSD were massive, but incomplete. The propagation velocity of HSD and the associated extracellular K(+) rise were also less marked than in other brain regions. In adult brain stem, HSD was mostly confined to the NTS and its occurrence was facilitated by hypotonic solutions, but not by glial poisoning or block of GABAergic and glycinergic synapses. In conclusion, brain stem tissue reliably generates propagating HSD episodes, which may be of interest for basilar-type migraine and brain stem infarcts. The preferred occurrence of HSD in the infant brain stem and its propagation into the VRG may be of importance for neonatal brain stem pathology such as sudden infant death syndrome.
Frank Funke; Miriam Kron; Mathias Dutschmann; Michael Müller
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-03-04
Journal Detail:
Title:  Journal of neurophysiology     Volume:  101     ISSN:  0022-3077     ISO Abbreviation:  J. Neurophysiol.     Publication Date:  2009 May 
Date Detail:
Created Date:  2009-04-21     Completed Date:  2009-06-04     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0375404     Medline TA:  J Neurophysiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2395-410     Citation Subset:  IM    
Deutsche Forschungsgemeinschaft Research Center for Molecular Physiology of the Brain, Georg-August-Universität Göttingen, Göttingen, Germany.
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MeSH Terms
Age Factors
Animals, Newborn
Anoxia / pathology*,  physiopathology
Brain Stem / growth & development,  physiopathology*
Cortical Spreading Depression / drug effects,  physiology*
Dose-Response Relationship, Drug
Electric Stimulation / methods
Extracellular Fluid / drug effects,  physiology
Hypoglossal Nerve / drug effects,  physiopathology
Potassium / pharmacology
Rats, Sprague-Dawley
Reaction Time / drug effects,  physiology
Sensory Thresholds / physiology
Solitary Nucleus / drug effects,  physiopathology
Trigeminal Nucleus, Spinal / drug effects,  physiopathology
Reg. No./Substance:

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