MAO-B Inhibition by a Single Dose of l-Deprenyl or Lazabemide Does Not Prevent Neuronal Damage Following Focal Cerebral Ischaemia in Rats
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چکیده
منابع مشابه
Inhibition of nitric oxide synthase activity improves focal cerebral damage induced by cerebral ischemia/reperfusion in normotensive rats
Introduction: Nitric oxide seems to play a dual role in ischemia/reperfusion injury. Few studies have investigated whether it exacerbates or improves brain edema. In the present study, we inhibited the activity of nitric oxide synthase by L-NAME and evaluated the cerebral infarct volume, tissue swelling and brain edema, alongside the measurement of blood flow of the ischemic region. Methods...
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Extracellular adenosine is dramatically increased during cerebral ischaemia and is considered to be neuroprotective due to its inhibitory effect on synaptic transmission mediated by the adenosine A1 receptor (A1R). We investigated the importance of the A1R in a mouse model of global ischaemia and in a murine hippocampal slice culture model of in vitro ischaemia, using mice with the A1R gene del...
متن کاملTest-retest reproducibility of [11C]-l-deprenyl-D2 binding to MAO-B in the human brain
BACKGROUND [11C]-L-deprenyl-D2 is a positron emission tomography (PET) radioligand for measurement of the monoamine oxidase B (MAO-B) activity in vivo brain. The estimation of the test-retest reproducibility is important for accurate interpretation of PET studies. RESULTS We performed two [11C]-L-deprenyl-D2 scans for six healthy subjects and evaluated the test-retest variability of this radi...
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Transient ischaemic depolarizations (IDs) are thought to play a key role in the pathogenesis of focal cerebral ischaemia. Most transient IDs are akin to spreading depression (SD), although a negative DC shift is not observed in half the cases. The other IDs may represent transient anoxic depolarizations. Using cortical DC and blood flow recordings, following middle cerebral artery occlusion in ...
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Background: Central renin angiotensin system has an important role on the cerebral microcirculation and metabolism. Our previous work showed that inhibition of angiotensin converting enzyme (ACE) activity prior to induction of ischemia protected the brain from severe ischemia/reperfusion (I/R) injuries. This study evaluated the impacts of post-ischemic inhibition of ACE, enalapril, on brain inf...
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ژورنال
عنوان ژورنال: Pharmacology & Toxicology
سال: 2008
ISSN: 0901-9928
DOI: 10.1034/j.1600-0773.2000.pto870509.x