ORCID Profile
0000-0002-6250-1594
Current Organisation
Macquarie University
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Publisher: Wiley
Date: 10-2013
DOI: 10.1111/BPH.12329
Publisher: Hindawi Limited
Date: 2016
DOI: 10.1155/2016/9247057
Abstract: Endocannabinoids are important retrograde modulators of synaptic transmission throughout the nervous system. Cannabinoid receptors are seven transmembrane G-protein coupled receptors favoring G i / o protein. They are known to play an important role in various processes, including metabolic regulation, craving, pain, anxiety, and immune function. In the last decade, there has been a growing interest for endocannabinoids in the retina and their role in visual processing. The purpose of this review is to characterize the expression and physiological functions of the endocannabinoid system in the visual system, from the retina to the primary visual cortex, with a main interest regarding the retina, which is the best-described area in this system so far. It will show that the endocannabinoid system is widely present in the retina, mostly in the through pathway where it can modulate neurotransmitter release and ion channel activity, although some evidence also indicates possible mechanisms via amacrine, horizontal, and Müller cells. The presence of multiple endocannabinoid ligands, synthesizing and catabolizing enzymes, and receptors highlights various pharmacological targets for novel therapeutic application to retinal diseases.
Publisher: Informa Healthcare
Date: 22-02-2008
Abstract: In this study, we explored the analgesic and antihyperalgesic properties of a synthetic cannabinoid (nabilone) on experimental heat pain in men and women, as well as its effects on descending pain inhibitory systems. A double-blind, placebo controlled, crossover study of nabilone single doses of 0.5 and 1 mg was conducted. Excitatory systems were elicited using a temporal summation test (tonic heat pain evoked by a Peltier thermode) administered before and after activation of descending inhibitory control (triggered using a counter-irritation procedure). These tests were given before and after drug treatment. Primary outcome measures included average heat pain, temporal summation of heat pain, and drug-induced changes in the strength of descending analgesia. Possible adverse reactions were monitored throughout treatment. Seven men (mean age = 22.5 years, SD = +/- 1.5) and 10 women (mean age = 23.2 years, SD = +/- 2.8) completed this study. Nabilone (1 mg and 0.5 mg) did not reduce the global pain intensity experienced during tonic heat pain (all values of p > 0.18). It also failed to potentiate the strength of descending inhibitory responses (all values of p > 43). Nevertheless, at the highest dose (1 mg), and only for women, nabilone significantly (p = 0.003) d ened the temporal summation experienced during the last portion of the tonic heat pulse test (i.e., the period of time during which temporal summation is greatest). This antihyperalgesic effect was not observed for men (at either 0.5 mg or 1 mg dose), suggesting that the antihyperalgesic properties of cannabinoids are greater for women than for men. Adverse reactions encountered were generally mild and did not provoke the cessation of testing. Nabilone failed to produce analgesic effects and it did not interact with descending pain inhibitory systems. However, we found that a single 1 mg dose of nabilone reduced temporal summation for women but not men. Although a titration regime and a larger s le of subjects might have provided more robust effects, these preliminary results suggest that nabilone appears effective at relieving hyperalgesic responses in women. Possible neurobiological mechanisms and clinical implications are further discussed.
Publisher: Frontiers Media SA
Date: 2018
Publisher: Springer Science and Business Media LLC
Date: 24-08-2020
Publisher: Association for Research in Vision and Ophthalmology (ARVO)
Date: 31-08-2017
DOI: 10.1167/17.10.437
Publisher: Springer Science and Business Media LLC
Date: 28-08-2019
Publisher: Elsevier BV
Date: 04-2007
Publisher: Springer Science and Business Media LLC
Date: 04-12-2020
Publisher: Wiley
Date: 09-2014
DOI: 10.1002/PRP2.79
Publisher: Springer Science and Business Media LLC
Date: 19-03-2021
DOI: 10.1038/S41593-020-00779-0
Abstract: A Correction to this paper has been published: 0.1038/s41593-020-00779-0.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 07-2007
DOI: 10.1016/J.PAIN.2006.11.011
Abstract: Changes in pain produced by psychological factors (e.g., placebo analgesia) are thought to result from the activity of specific cortical regions. However, subcortical nuclei, including the periaqueductal gray and the rostroventral medulla, also show selective activation when subjects expect pain relief. These brainstem regions send inhibitory projections to the spine and produce diffuse analgesic responses. Regrettably the precise contribution of spinal mechanisms in predicting the strength of placebo analgesia is unknown. Here, we show that expectations regarding pain radically change the strength of spinal nociceptive responses in humans. We found that contrary to expectations of analgesia, expectations of hyperalgesia completely blocked the analgesic effects of descending inhibition on spinal nociceptive reflexes. Somatosensory-evoked brain potentials and pain ratings further confirmed changes in spino-thalamo-cortical responses consistent with expectations and with changes in the spinal response. These findings provide direct evidence that the modulation of pain by expectations is mediated by endogenous pain modulatory systems affecting nociceptive signal processing at the earliest stage of the central nervous system. Expectation effects, therefore, depend as much about what takes place in the spine as they do about what takes place in the brain. Furthermore, complete suppression of the analgesic response normally produced by descending inhibition suggests that anti-analgesic expectations can block the efficacy of pharmacologically valid treatments which has important implications for clinical practice.
Publisher: Wiley
Date: 17-11-2015
DOI: 10.1111/BPH.13341
Publisher: PeerJ
Date: 28-01-2014
DOI: 10.7717/PEERJ.248
Publisher: Frontiers Media SA
Date: 2019
No related grants have been discovered for William John Redmond.