Acute effects of lithium chloride on noradrenergic neurons from rat cerebral cortex |
| |
| Affiliation: | 1. MRC Laboratory of Molecular Biology, Neurobiology Division, Francis Crick Avenue, Cambridge CB2 0QH, UK;1. Epilepsy Center of Excellence, Veterans Affairs Puget Sound Healthcare System, Seattle, WA 98108, USA;2. Department of Physiology & Biophysics, University of Washington, Seattle, WA 98195, USA;3. Department of Neurology, University of Washington, Seattle, WA 98195, USA;1. Centre for Organismal Studies, University of Heidelberg, Heidelberg, Germany;2. Experimental Pain Research, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany;1. Department of Physiology, University of California, San Francisco, San Francisco, CA, USA;2. Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA, USA |
| |
| Abstract: | o- 1.1. Acute effects of lithium chloride upon the parameters of central noradrenergic function were assessed at either a therapeutic dose (2 m-equiv/kg) or a toxic one (10 m-equiv/kg) on rats.
- 2.2. Lithium chloride lacked a direct effect on tyrosine hydroxylase (TH), monoamine oxidase (MAO), or catechol-O-methyltransferase (COMT) in concentrations up to 2 mM.
- 3.3. A single i.p. injection of both studied doses inhibited MAO 1 hr later.
- 4.4. Endogenous NA levels in frontal cerebral cortex were increased by a therapeutic dose and slightly increased by a toxic dose.
- 5.5. Uptake of [3H]NA was increased in pretreated tissues at a therapeutic level but decreased by a toxic dose.
- 6.6. The unmetabolized [3H]NA was always increased over controls.
|
| |
| Keywords: | |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
