Effect of injury on the bi-affinity α1-adrenoreceptor binding in rat brain in vivo

S. Dyve, Y. J. Yang, M. McHugh, A. Gjedde, H. M. Pappius

Research output: Contribution to journalArticle

Abstract

Focal freezing lesions in rats cause a widespread decrease of cortical glucose utilization in the lesioned hemisphere, probably as a reflection of depressed cortical activity. The noradrenergic neurotransmitter system was implicated in these alterations when it was demonstrated that prazosin, a specific norepinephrine (NE) antagonist at α1-adrenergic receptors, prevented their development. In normal rat brain, specific binding of [125I]HEAT [(±)2-(3-[125I]iodo-4-hydroxyphenyl)-ethyl-aminomethyl- tetralone], another selective α1-adrenoreceptor ligand, was demonstrated in vivo at sites consistent with the α(1A)- and α(1B)-adrenoreceptor subtypes. In the present study, the effect of a freezing lesion on specific binding of [125I]HEAT in rat brain in vivo was determined three days after traumatization when cortical glucose use suggested the greatest degree of functional depression. The steady-state volumes of distribution of [125I]HEAT three days after injury were significantly increased in all the cortical areas of the lesioned hemisphere, but not in the subcortical structures. Injury did not modify the binding affinities for HEAT. However, a statistically significant increase in the number of low-affinity binding sites for this ligand was demonstrated in all cortical areas of the lesioned hemisphere, but not in subcortical structures. The traumatization did not modify B(max) estimates for the high-affinity binding of HEAT. The results support the hypothesis that changes in the noradrenergic system are of functional importance in brain injury and that at least some effects of injury are mediated by α(1B)-adrenergic receptors.

Original languageEnglish (US)
Pages (from-to)88-96
Number of pages9
JournalSynapse
Volume19
Issue number2
DOIs
StatePublished - 1995
Externally publishedYes

Fingerprint

Adrenergic Receptors
Freezing
Wounds and Injuries
Brain
Tetralones
Ligands
Glucose
Prazosin
Brain Injuries
Neurotransmitter Agents
Norepinephrine
Binding Sites
2-(beta-(3-iodo-4-hydroxyphenyl)ethylaminomethyl)tetralone

Keywords

  • α-adrenoreceptors
  • Brain injury
  • Noradrenergic neurotransmission

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology
  • Pharmacology

Cite this

Dyve, S., Yang, Y. J., McHugh, M., Gjedde, A., & Pappius, H. M. (1995). Effect of injury on the bi-affinity α1-adrenoreceptor binding in rat brain in vivo. Synapse, 19(2), 88-96. https://doi.org/10.1002/syn.890190204

Effect of injury on the bi-affinity α1-adrenoreceptor binding in rat brain in vivo. / Dyve, S.; Yang, Y. J.; McHugh, M.; Gjedde, A.; Pappius, H. M.

In: Synapse, Vol. 19, No. 2, 1995, p. 88-96.

Research output: Contribution to journalArticle

Dyve, S, Yang, YJ, McHugh, M, Gjedde, A & Pappius, HM 1995, 'Effect of injury on the bi-affinity α1-adrenoreceptor binding in rat brain in vivo', Synapse, vol. 19, no. 2, pp. 88-96. https://doi.org/10.1002/syn.890190204
Dyve, S. ; Yang, Y. J. ; McHugh, M. ; Gjedde, A. ; Pappius, H. M. / Effect of injury on the bi-affinity α1-adrenoreceptor binding in rat brain in vivo. In: Synapse. 1995 ; Vol. 19, No. 2. pp. 88-96.
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