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  • Neuroprotective Agents  (1)
  • Presynaptic alpha 2 receptor  (1)
  • 1
    Keywords: Medicine ; Biomedicine ; Toxicology ; Pharmacology ; Neurosciences ; Neurology ; Receptors, Nicotinic metabolism ; Signal Transduction physiology ; Neuroprotective Agents
    Description / Table of Contents: This open access book presents the roles and mechanisms of signal transduction triggered by nicotinic acetylcholine receptors (nAChRs) stimulation in neuroprotection against toxic effects of risk factors of neurodegenerative diseases. Accumulating evidence suggests that nAChRs in the CNS play important roles not only in excitatory neurotransmission but also in neuronal survival and related functions. Neuroprotection mediated by nAChRs in neurodegenerative diseases such as Alzheimer's disease is the major topic of this book. In response to rapidly evolving areas in clinical and laboratory neuropharmacology and neurochemistry, this volume provides in-depth coverage of neuroprotection in basic research and future developments in the clinical application of effective neuroprotective strategies in neurodegenerative diseases. This work appeals to both basic and clinical researchers in several fields, such as neuroscience, neurology, and pharmacology. This book is published with open access under a CC BY 4.0 license
    Type of Medium: Online Resource
    Pages: Online-Ressource (X, 191 p. 62 illus., 20 illus. in color, online resource)
    ISBN: 9789811084881
    Series Statement: SpringerLink
    Language: English
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  • 2
    ISSN: 1432-1912
    Keywords: Dog cerebral artery ; Sympathetic denervation ; Postsynaptic alpha 2 receptor ; Presynaptic alpha 2 receptor ; Alpha 1 receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The magnitude of the noradrenaline-induced contractions of dog middle cerebral arteries was less than that seen in the vertebral, common carotid, femoral and renal arteries. Noradrenaline and clonidine produced a similar magnitude of maximum contractions in the middle cerebral arteries, whereas methoxamine produced no significant contractions in the same arteries. In the extracranial arteries, noradrenaline and methoxamine produced significantly larger contractions than clonidine. Binding studies revealed no specific3H-prazosin binding sites in the cerebral arteries, though such binding sites were evident in the case of extracranial arteries.3H-Yohimbine binding studies revealed the presence of two classes of binding sites with high and low affinities in both cerebral and extracranial arteries. After superior cervical ganglionectomy, noradrenaline- and clonidine-induced contractions of the denervated middle cerebral arteries were not altered, compared with the control arteries. A3H-yohimbine binding study was also performed using the denervated cerebral arteries. This study revealed that there was a low affinity3H-yohimbine binding site, whereas high affinity3H-yohimbine binding site was not detectable. These results suggest the presence of two different binding sites with high and low affinity for alpha 2 adrenoceptors, which we are classifying into alpha 2H and alpha 2L subtypes. The high affinity sites, alpha 2H adrenoceptors, are presynaptically located while the low affinity sites, alpha 2L adrenoceptors, located postsynaptically. The noradrenaline-induced contractions are probably mediated by postsynaptic low affinity sites of alpha 2 adrenoceptors (alpha 2L adrenoceptors) in the cerebral arteries and mainly by alpha 1 adrenoceptors in the extracranial arteries.
    Type of Medium: Electronic Resource
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