Early changes in second messenger but not receptor binding sites after acute subdural hematoma

An in vitro autoradiographic study

Y. Kuroda, D. Dewar, Ross Bullock

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Neurotransmitter receptor-coupled mechanisms have been recently recognized as important determinants of cell damage after central nervous system (CNS) trauma and ischemia. Many of these receptors exert their intracellular effects via second messenger systems. This study used in vitro autoradiographic radioligand binding to measure β-adrenergic and muscarinic cholinergic receptors and adenylate cyclase and protein kinase C (PKC) binding sites two h after acute subdural hematoma in rats. Both β-adrenergic and cholinergic receptor binding sites were unchanged in comparison to controls, while adenylate cyclase binding significantly decreased in the ischemic cortex under the hematoma. These changes may constitute a major limiting factor on receptor-linked therapeutic strategies in trauma and ischemia. Protein kinase C activation significantly increased in the ischemic area under the hematoma in these studies. This appears to be a response to calcium flux, which may be in part glutamate mediated.

Original languageEnglish
Pages (from-to)47-55
Number of pages9
JournalJournal of Neurotrauma
Volume10
Issue number1
StatePublished - Jan 1 1993
Externally publishedYes

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Hematoma, Subdural, Acute
Second Messenger Systems
Cholinergic Receptors
Adenylyl Cyclases
Hematoma
Protein Kinase C
Ischemia
Binding Sites
Nervous System Trauma
Adenylate Kinase
Neurotransmitter Receptor
Muscarinic Receptors
Adrenergic Agents
Adrenergic Receptors
Glutamic Acid
Central Nervous System
Calcium
Wounds and Injuries
In Vitro Techniques
Therapeutics

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Early changes in second messenger but not receptor binding sites after acute subdural hematoma : An in vitro autoradiographic study. / Kuroda, Y.; Dewar, D.; Bullock, Ross.

In: Journal of Neurotrauma, Vol. 10, No. 1, 01.01.1993, p. 47-55.

Research output: Contribution to journalArticle

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