China
Africa
Explore chapters and articles related to this topic
Specific Arterial Disease
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Headache in migraine is associated with and appears to be caused by dilatation of cerebral and extracerebral cranial arteries, sometimes with evidence of associated edema and inflammation (Iversen et al., 1990; Olesen, 1994; Raskin, 1994). In migraine with aura, headache with arterial vasodilatation follows a preliminary wave of “spreading depression” over the cerebral cortex. The mechanism is complex and not completely understood, but it appears to involve the release of serotonin from platelets at the beginning of the attack when vasoconstriction initially occurs. Sensory neuropeptides appear also to be involved and may be responsible for inflammation and the stimulation of pain receptors.
Improving the Old, Embracing the New: Implications of Alcohol Research for Future Practice
Published in Gary Rosenberg, Weissman Andrew, Behavioral and Social Sciences in 21st Century Health Care: Contributions and Opportunities, 2021
The role of various neuropeptides–substances in the brain which allow brain cells or neurons to communicate with one another–in the development of alcohol dependence is also under study. For example, neuropeptide Y (NPY), a transmitter in the brain, is known to stimulate appetitive behaviors. Recently, NIAAA-funded scientists reported that mice in whom the NPY gene had been “knocked out” consumed more alcohol and were less sensitive to the sedative effects of alcohol than controls. Conversely, mice genetically altered to produce abnormally high levels of NPY showed a lower preference for alcohol and were more sensitive to alcohol’s sedative effects. These findings suggest that NPY is part of the neural circuits involved in responses to alcohol. If NPY is found to play a key role in human alcohol-use disorders, NPY and its receptors become potential targets for medications to control alcohol intake.
Neuropeptide Receptor-Ion Channel Coupling in the Mammalian Brain
Published in Gerard O’Cuinn, Metabolism of Brain Peptides, 2020
The effector mechanisms underlying the actions of a number of other neuropeptides within the mammalian brain has been explored, albeit to a lesser degree than those previously mentioned. Usually this has led to the identification of the ionic current(s) which are modified but evidence for or against a direct link between receptor and ion channel is not available.
Stimulant use for self-management of pain among safety-net patients with chronic non-cancer pain
Published in Substance Abuse, 2022
Cathleen M. Beliveau, Vanessa M. McMahan, Justine Arenander, Martin S. Angst, Margot Kushel, Andrea Torres, Glenn-Milo Santos, Phillip O. Coffin
Our findings reveal a potential relationship between neuropathic pain and stimulant use to treat pain. Specifically, we observed an association between the number of neuropathic pain attributes used by participants to describe their pain and their use of stimulants to treat pain. A qualitative study15 documented methamphetamine use to treat neuropathic pain in a small cohort of HIV-positive men. Notably, in our sample half of the HIV-positive participants who used stimulants used stimulants to treat pain, suggesting that HIV-associated pain, which is neuropathic in nature, may be one reason for stimulant use. The previously described role of the neuropeptide CART in regulating neuropathic pain further supports the potential benefit of these agents in neuropathic pain syndromes.17,18 Patients who have pain with a greater number of neuropathic characteristics may be more likely to use stimulants as a strategy to self-manage pain, although further study is needed.
Developments in the discovery and design of intranasal antidepressants
Published in Expert Opinion on Drug Discovery, 2020
Małgorzata Panek, Paweł Kawalec, Andrzej Pilc, Władysław Lasoń
In the light of the promising results showing an antidepressant activity of intranasal oxytocin, also other neuropeptides are under investigation for possible antidepressant effects. Preclinical studies showed that intranasally administered neuropeptide Y reduced anxiety and depressive behavior in an animal model of posttraumatic stress disorder [83,84]. It was also reported that neuropeptide S administered via the nasal route reduced general anxiety and prolonged memory in rats [97]. Thyrotropin-releasing hormone (TRH) and TRH-like peptides are potential therapeutic agents for the treatment of major depression, anxiety, and bipolar disorder [98]. Intranasal application of TRH was shown to attenuate anxiety in rats [99]. Interestingly, ketamine modulated intranasally administered TRH and TRH-like peptide turnover in the brain and peripheral tissues of rats, which suggests that these peptides may be downstream mediators of the rapid antidepressant actions of ketamine [100].
Worms sleep: a perspective
Published in Journal of Neurogenetics, 2020
Each of the four worm sleep papers published in this edition of the Journal of Neurogenetics carries an important message. The van Buskirk lab paper (Goetting, et al, J. Neurogenet., in press) contributes to our understanding of the mechanism of SIS. They also describe a new trigger for SIS: skin injury, which is relevant to the human complaint of severe fatigue after an operation. The Bringmann lab paper (Busack et al, J. Neurogenet., in press) describes a method for long-term optogenetic manipulation of worms. Developing such methods is important because prior worm tools have been optimized for much shorter durations of manipulation and observations. The Nelson lab describes the role of orcokinins, neuropeptides conserved among molting animals, in regulating sleep (Honer et al, J. Neurogenet., in press). This study again emphasizes the important, but complex roles of neuropeptides in behavioral state modulation. Finally, the Hart lab paper reminds us that not all that stops moving is sleep and that we must remain self-skeptical as a field. They suggest that cessation of swimming is better explained by neuromuscular fatigue than by sleep (Schuch et al, J. Neurogenet., in press).