Publications by authors named "Daniel McQueen"

21 Publications

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Evolutionary Considerations on the Emerging Subculture of the E-psychonauts and the Novel Psychoactive Substances: A Comeback to the Shamanism?

Curr Neuropharmacol 2017 ;15(5):731-737

Psychopharmacology, Drug Misuse and Novel Psychoactive Substances Research Unit, School of Life and Medical Sciences, College Lane Campus, University of Hertfordshire, Hatfield, Herts, AL10 9AB. United Kingdom.

Background: Evolutionary research on drug abuse has hitherto been restricted to proximate studies, considering aetiology, mechanism, and ontogeny. However, in order to explain the recent emergency of a new behavioral pattern (e.g. 'the e-psychonaut style') of novel psychoactive substances' (NPS) intake, a complementary evolutionary model may be needed.

Objective: A range of evolutionary interpretations on the 'psychonaut style' and the recent emergency of NPS were here considered.

Method: The PubMed database was searched in order to elicit evolutionary theory-based documents commenting on NPS/NPS users/e-psychonauts.

Results: The traditional 'shamanic style' use of entheogens/plant-derived compounds may present with a range of similarities with the 'e-psychonauts' use of mostly of hallucinogen/psychedelic NPS. These users consider themselves as 'new/technological' shamans.

Conclusion: Indeed, a range of evolutionary mechanisms, such as: optimal foraging, costly signaling, and reproduction at the expense of health may all cooperate to explain the recent spread and diffusion of the NPS market, and this may represent a reason of concern.
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http://dx.doi.org/10.2174/1570159X15666161111114838DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5771049PMC
March 2018

Classical and novel psychoactive substances: rethinking drug misuse from an evolutionary psychiatric perspective.

Hum Psychopharmacol 2013 Jul;28(4):394-401

Hertsmere Community Mental Health Team, Hertfordshire Partnership Foundation Trust, Borehamwood, UK.

In this article, ontogenetic and phylogenetic causes of drug abuse and links to human emotional development are considered. Some evolutionary perspectives (e.g. that under certain conditions, consumption of otherwise toxic alkaloids may confer both physical and cultural advantages) are reviewed. As described in the 'mismatch theory', the capacity of the human genome to evolve defences against toxins has been outstripped by the pace of cultural change and technological development, such as purposeful fermentation of alcohol and more recently distillation of alcohol; purification and chemical manipulation of plant alkaloids; and the engineering of entirely novel psychoactive substances (NPS). The functions of the neurobiological substrates that mediate substance misuse and dependence are reviewed. Reasons are given why NPSs present greater cause for concern than plant-derived substances of abuse. We argue that evolutionary biology provides an important orientation for the research agenda in substance misuse.
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http://dx.doi.org/10.1002/hup.2303DOI Listing
July 2013

Placebo effects: a new paradigm and relevance to psychiatry.

Int Psychiatry 2012 Feb 1;9(1):1-3. Epub 2012 Feb 1.

General Adult Psychiatrist, Hertfordshire Partnership Foundation Trust, UK, email

Systematic evaluations show that placebo treatments can have large effects, sometimes larger than those of 'evidence-based treatments'. This is the 'efficacy paradox'. The neurobiology of placebo effects is being mapped out. Placebo effects are no less real or, in some illnesses, clinically important than the effects of direct biomechanical or pharmacological interventions. The technical model of medicine seeks impersonal technologies that can be applied independently of context and person. This approach has had spectacular success in the treatment of but meaning, cultural context, interpersonal effects, personal preferences and values are enormously important in the treatment of . The study of placebo reveals aspects of the biology of interpersonal relationships and the social environment. The evidence demonstrates that interpersonal healing (sometimes called placebo) in illness is just as real, scientific and biological as technological healing. This is a paradigm shift.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6735047PMC
February 2012

eDrugCalc: an online self-assessment package to enhance medical students' drug dose calculation skills.

Br J Clin Pharmacol 2010 Oct;70(4):492-9

Departments of Neuroscience, Learning Technology Section and Clinical Pharmacology Unit, University of Edinburgh, College of Medicine and Veterinary Medicine, Edinburgh, UK.

Aims: Dose calculation errors can cause serious life-threatening clinical incidents. We designed eDrugCalc as an online self-assessment tool to develop and evaluate calculation skills among medical students.

Methods: We undertook a prospective uncontrolled study involving 1727 medical students in years 1-5 at the University of Edinburgh. Students had continuous access to eDrugCalc and were encouraged to practise. Voluntary self-assessment was undertaken by answering the 20 questions on six occasions over 30 months. Questions remained fixed but numerical variables changed so each visit required a fresh calculation. Feedback was provided following each answer.

Results: Final-year students had a significantly higher mean score in test 6 compared with test 1 [16.6, 95% confidence interval (CI) 16.2, 17.0 vs. 12.6, 95% CI 11.9, 13.4; n= 173, P < 0.0001 Wilcoxon matched pairs test] and made a median of three vs. seven errors. Performance was highly variable in all tests with 2.7% of final-year students scoring < 10/20 in test 6. Graduating students in 2009 (30 months' exposure) achieved significantly better scores than those in 2007 (only 6 months): mean 16.5, 95% CI 16.0, 17.0, n= 184 vs. 15.1, 95% CI 14.5, 15.6, n= 187; P < 0.0001, Mann-Whitney test. Calculations based on percentage concentrations and infusion rates were poorly performed. Feedback showed that eDrugCalc increased confidence in calculating doses and was highly rated as a learning tool.

Conclusions: Medical student performance of dose calculations improved significantly after repeated exposure to an online formative dose-calculation package and encouragement to develop their numeracy. Further research is required to establish whether eDrugCalc reduces calculation errors made in clinical practice.
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http://dx.doi.org/10.1111/j.1365-2125.2010.03609.xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950984PMC
October 2010

Medicine, affect and mental health services.

World Psychiatry 2010 Feb;9(1):35-6

Barnet Enfield and Haringey Mental Health NHS Trust, Edgware, UK.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2816910PMC
http://dx.doi.org/10.1002/j.2051-5545.2010.tb00264.xDOI Listing
February 2010

Neurohawks fight back.

Authors:
Daniel McQueen

Br J Psychiatry 2009 Sep;195(3):269; author reply 269-70

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http://dx.doi.org/10.1192/bjp.195.3.269DOI Listing
September 2009

Changes in the expression of NaV1.7, NaV1.8 and NaV1.9 in a distinct population of dorsal root ganglia innervating the rat knee joint in a model of chronic inflammatory joint pain.

Eur J Pain 2008 Jul 18;12(5):564-72. Epub 2007 Oct 18.

Division of Neuroscience, University of Edinburgh, Medical College, 1 George Sq., Edinburgh EH8 9JZ, UK.

Voltage-gated sodium channels play an essential role in regulating the excitability of nociceptive primary afferent neurones. In particular the tetrodotoxin-sensitive (TTX-S) Na(V)1.7 and the tetrodotoxin-resistant (TTX-R) Na(V)1.8 and Na(V)1.9 channels have been suggested to play a role in inflammatory pain. Previous work has revealed acute administration of inflammatory mediators, such as Freund's complete adjuvant (FCA) or carrageenan caused an upregulation in the levels of Na(V)1.7 and Na(V)1.8 protein in DRG (dorsal root ganglia) tissue up to 4 days post-insult. In the present study, the expression of Na(V)1.7, Na(V)1.8 and Na(V)1.9 was examined over a 28 day timecourse during a rat model of FCA-induced chronic inflammatory joint pain. Using the retrograde tracer Fast Blue (FB) and specific Na(V)1.7, Na(V)1.8 and Na(V)1.9 sodium channel antibodies, immunohistochemical staining techniques were used to study sodium channel expression in a distinct population of L3-L5 knee joint afferent DRGs. In the ganglia, counts were made of positively labelled cells in the FB population. The results demonstrate that, following FCA injection, Na(V)1.9 expression is upregulated at days 14, 21 and 28 post-FCA, with Na(V)1.7 and Na(V)1.8 showing increased channel expression at days 14 and 28. These observations are accompanied by a unilateral joint hypersensitivity in the FCA-injected knee indicated by a behavioural shift in weight distribution measured using an incapacitance tester. The increased presence of these channels suggests that Na(V)1.7, Na(V)1.8 and Na(V)1.9 play a role, at least in part, in the maintenance of chronic inflammatory pain several weeks after the initial insult.
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http://dx.doi.org/10.1016/j.ejpain.2007.09.001DOI Listing
July 2008

Demonstration of a novel technique to quantitatively assess inflammatory mediators and cells in rat knee joints.

J Inflamm (Lond) 2007 Jun 13;4:13. Epub 2007 Jun 13.

Division of Neuroscience, University of Edinburgh, Medical College, 1 George Sq, Edinburgh, EH8 9JZ, UK.

Background: The inflammation that accompanies the pain and swelling associated with osteo- and rheumatoid arthritis is mediated by complex interactions of inflammatory mediators. Cytokines play a pivotal role in orchestrating many of these processes, including inflammatory cell recruitment, adhesion and activation. In addition, prostaglandins are secreted into the synovial cavity and are involved in perpetuation of local inflammation, vasodilatation and vasoconstriction, and also with bone resorption. Pre-clinical models have been developed in order to correlate to the human disease and principle among these is the adjuvant-induced arthritis model in the rat.

Methods: We have developed a technique to quantitatively assess the contents of synovial fluid samples from rat joints. Two needles joined together are inserted into the knee joint of anaesthetised rats and connected to a Watson-Marlow perfusion pump. Sterile saline is infused and withdrawn at 100 microl min-1 until a 250 microl sample is collected.

Results: Our results demonstrate up to 125 fold increases in synovial IL1alpha and IL1beta concentrations, approximately 30 fold increases in levels of IL6 and IL10 and a 200-300 fold elevation in synovial concentrations of TNFalpha during FCA-induced experimental arthritis. Finally, this novel technique has demonstrated a dose-response relationship between FCA and the total cell counts of synovial perfusates.

Conclusion: In summary, this new technique provides a robust method for quantifying inflammatory mediators and cells from the synovial cavity itself, thereby detailing the inflammatory processes from within the capsule and excluding those processes occurring in other tissues surrounding the entire articulation.
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http://dx.doi.org/10.1186/1476-9255-4-13DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1919375PMC
June 2007

Pressure application measurement (PAM): a novel behavioural technique for measuring hypersensitivity in a rat model of joint pain.

J Neurosci Methods 2007 Jun 20;163(1):67-75. Epub 2007 Feb 20.

Division of Neuroscience, University of Edinburgh, Medical College, 1 George Square, Edinburgh EH8 9JZ, UK.

Chronic joint pain affects physical well being and can lead to severe psychological and social problems, therefore successful long-term management is highly sought-after. No current behavioural measures of pain used in pre-clinical models mimic the clinical dolorimeter, which provides an objective measure of joint hypersensitivity. In this study we aim to use a novel behavioural readout alongside an established measure to mimic the multifactorial measurements taken in the clinic. Using the pressure application measurement (PAM) device a gradually increasing squeeze was applied across the knee joint of rats until the animal gave an indication of pain or discomfort. PAM and the incapacitance tester were used to detect joint hypersensitivity in a well-established rodent model of adjuvant-induced arthritis. Subsequently, the analgesic effects of prednisolone (1, 3 or 10 mg kg(-1)), morphine (3 mg kg(-1)) and celecoxib (15 mg kg(-1)) were assessed. Both PAM and the incapacitance tester detected a reversal of hypersensitivity 1h post-drug administration. Furthermore, the two readouts were highly correlated, and power analysis indicated that PAM was highly reproducible. In conclusion, PAM provides a novel, accurate behavioural tool for detecting a primary mechanical hypersensitivity in a rat model of chronic inflammatory joint pain.
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http://dx.doi.org/10.1016/j.jneumeth.2007.02.012DOI Listing
June 2007

Histamine H4 receptor antagonists are superior to traditional antihistamines in the attenuation of experimental pruritus.

J Allergy Clin Immunol 2007 Jan 13;119(1):176-83. Epub 2006 Oct 13.

Johnson & Johnson Pharmaceutical Research & Development, LLC, San Diego, CA 92121, USA.

Background: Histamine is a potent mediator of itch in humans, yet histamine H(1) receptor antagonists have been shown to be of limited use in the treatment of certain chronic pruritic diseases. The histamine H(4) receptor is a recently described histamine receptor, expressed on hematopoietic cells, linked to the pathology of allergy and asthma.

Objective: The contribution of the novel histamine H(4) receptor to histaminergic and allergic pruritus was investigated.

Results: Histamine and a selective histamine H(4) receptor agonist caused scratching responses in mice, which were almost completely attenuated in histamine H(4) receptor knockout mice or by pretreatment with the selective histamine H(4) receptor antagonist, JNJ 7777120. Pruritus induced by allergic mechanisms was also potently inhibited with histamine H(4) receptor antagonist treatment or in histamine H(4) receptor knockout mice. In all cases, the inhibitory effect of histamine H(4) receptor antagonist was greater than those observed with histamine H(1) receptor antagonists. The histamine H(4) receptor-mediated pruritus was shown to be independent of mast cells or other hematopoietic cells and may result from actions on peripheral neurons.

Conclusion: These results demonstrate that the histamine H(4) receptor is involved in pruritic responses in mice to a greater extent than the histamine H(1) receptor.

Clinical Implications: Histamine H(4) receptor antagonists may have therapeutic utility for treating chronic pruritic diseases in humans where histamine H(1) receptor antagonists are not effective.
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http://dx.doi.org/10.1016/j.jaci.2006.08.034DOI Listing
January 2007

eDrug: a dynamic interactive electronic drug formulary for medical students.

Br J Clin Pharmacol 2006 Dec 19;62(6):673-81. Epub 2006 Oct 19.

Clinical Pharmacology Unit, University of Edinburgh, Queen's Medical Research Institute, Royal Infirmary of Edinburgh, Edinburgh, UK.

Aims: Prescribing drugs is a key responsibility of a doctor and requires a solid grounding in the relevant scientific disciplines of pharmacology and therapeutics (PT). The move away from basic science disciplines towards a more system-based and integrated undergraduate curriculum has created difficulties in the delivery of PT teaching in some medical schools. We aimed to develop a web-based strategy to overcome these problems and improve the PT learning experience.

Methods: We designed and introduced 'eDrug', a dynamic interactive web-based student formulary, as an aid to teaching and learning of PT throughout a 5-year integrated medical curriculum in a UK medical school of 1300 students. This was followed by a prospective observational study of student-reported views about its impact on their PT learning experience.

Results: eDrug was rated highly by students and staff, with the main benefits being increased visibility of PT in the curriculum, clear identification of core drugs, regular sourcing of drug information via direct links to accredited sources including the British National Formulary, prioritization of learning, immediate access and responsiveness. It has also served as a focus of discussion concerning core PT learning objectives amongst staff and students.

Conclusions: Web-based delivery of PT learning objectives actively supports learning within an integrated curriculum.
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http://dx.doi.org/10.1111/j.1365-2125.2006.02777.xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1885184PMC
December 2006

An animal model of chronic inflammatory pain: pharmacological and temporal differentiation from acute models.

Eur J Pain 2006 Aug 30;10(6):537-49. Epub 2005 Sep 30.

Department of Pain Research, Neurology and Gastrointestinal CEDD, GlaxoSmithKline Research and Development Ltd., Harlow, Essex, UK.

Clinically, inflammatory pain is far more persistent than that typically modelled pre-clinically, with the majority of animal models focussing on short-term effects of the inflammatory pain response. The large attrition rate of compounds in the clinic which show pre-clinical efficacy suggests the need for novel models of, or approaches to, chronic inflammatory pain if novel mechanisms are to make it to the market. A model in which a more chronic inflammatory hypersensitivity phenotype is profiled may allow for a more clinically predictive tool. The aims of these studies were to characterise and validate a chronic model of inflammatory pain. We have shown that injection of a large volume of adjuvant to the intra-articular space of the rat knee results in a prolonged inflammatory pain response, compared to the response in an acute adjuvant model. Additionally, this model also results in a hypersensitive state in the presence and absence of inflammation. A range of clinically effective analgesics demonstrate activity in this chronic model, including morphine (3mg/kg, t.i.d.), dexamethasone (1mg/kg, b.i.d.), ibuprofen (30mg/kg, t.i.d.), etoricoxib (5mg/kg, b.i.d.) and rofecoxib (0.3-10mg/kg, b.i.d.). A further aim was to exemplify the utility of this chronic model over the more acute intra-plantar adjuvant model using two novel therapeutic approaches; NR2B selective NMDA receptor antagonism and iNOS inhibition. Our data shows that different effects were observed with these therapies when comparing the acute model with the model of chronic inflammatory joint pain. These data suggest that the chronic model may be more relevant to identifying mechanisms for the treatment of chronic inflammatory pain states in the clinic.
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http://dx.doi.org/10.1016/j.ejpain.2005.08.003DOI Listing
August 2006

Inflammation alters somatostatin mRNA expression in sensory neurons in the rat.

Eur J Neurosci 2005 Jan;21(1):135-41

Department of Physiology, University of Bristol School of Medical Sciences, University Walk, Bristol, UK.

Proinflammatory neuropeptides, such as substance P and calcitonin gene-related peptide, are up-regulated in primary afferent neurons in acute and chronic inflammation. While these neuropeptides have been intensively studied, potentially anti-inflammatory and/or anti-nociceptive neuropeptides such as somatostatin (SS) have been less widely investigated. Endogenous somatostatin is thought to exert a tonic antinociceptive effect. Exogenous SS is anti-inflammatory and antinociceptive and is thought to exert these actions through inhibition of proinflammatory neuropeptide release. In this study we have compared the expression of somatostatin in two inflammatory models: arthritis, a condition associated with increased nociception, and periodontitis, in which there is little evidence of altered nociceptive thresholds. In acute arthritis (< 24 h) SS mRNA was down-regulated in ipsilateral dorsal root ganglia (DRG; 52 +/- 7% of control, P < 0.05), and up-regulated in contralateral DRG (134 +/- 10% of control; P < 0.05). In chronic arthritis (14 days) this pattern of mRNA regulation was reversed, with SS being up-regulated ipsilaterally and down-regulated contralaterally. In chronic mandibular periodontitis (7-10 days), SS mRNA was up-regulated in only the mandibular division of the ipsilateral trigeminal ganglion (TG) (day 7, 219 +/- 9% and day 10, 217 +/- 12% of control; P < 0.02) but showed no change in other divisions of the trigeminal ganglion or in the mesencephalic nucleus. These data show that antinociceptive and anti-inflammatory neuropeptides are also regulated in inflammation. It is possible that the degree of inflammation and nociception seen may depend on the balance of pro- and anti-inflammatory and nociceptive peptide expression in a particular condition.
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http://dx.doi.org/10.1111/j.1460-9568.2004.03854.xDOI Listing
January 2005

Perivascular nerves induce cardiorespiratory reflexes in response to algogens in anaesthetised rats.

Neurosci Res 2004 Nov;50(3):271-81

Division of Neuroscience, College of Medicine and Veterinary Medicine, The University of Edinburgh, George Square, Edinburgh EH8 9JZ, UK.

In the present study we measured cardiovascular and respiratory reflexes evoked by administration of bradykinin and capsaicin into the hindlimb vasculature of anaesthetised rats, whilst simultaneously recording activity of sensory afferents on the adventitial surface of femoral arteries and veins. Bradykinin (0.9 nmol) and capsaicin (0.3 nmol) caused a rapid reflex fall in mean arterial pressure (delta mmHg: -37 +/- 8 and -28 +/- 3, respectively; P < 0.01) and an increase in respiratory minute volume (delta ml min(-1): 180.0 +/- 39.2 and 156.1 +/- 24.5, respectively; P < 0.01), associated with an increase in neural discharge in arterial afferents (from basal 0.4 +/- 0.3 to 8.5 +/- 2.9 impulses s(-1) following intra-arterial administration of bradykinin, P < 0.05, n = 7; from basal 0.2 +/- 0.1 to 7.5 +/- 3.7 impulses s(-1) with capsaicin, P < 0.01, n = 18). The antagonists FR173657 and capsazepine confirmed bradykinin B2 and vanilloid VR1 receptors mediated the responses to bradykinin and capsaicin, respectively. Topical administration of algogen to the vessel surface, and electrical stimulation of the adventitia also evoked cardiovascular and respiratory responses. These data support the hypothesis that stimulation of sensory nerve endings within the hindlimb vasculature contributes to systemic cardiorespiratory reflexes in the rat.
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http://dx.doi.org/10.1016/j.neures.2004.07.006DOI Listing
November 2004

A robust model of adjuvant-induced chronic unilateral arthritis in two mouse strains.

J Neurosci Methods 2004 Oct;139(2):281-91

Department of Neuroscience, University of Edinburgh, 1 George Square, Edinburgh, EH8 9JZ, UK.

We have developed a model of unilateral adjuvant-arthritis that is reproducible across two mouse strains. DBA/1 and C57BL/6 male mice were injected intra-articularly into a stifle joint with FCA (5 microg in 5 microl) once per week for 4 weeks. Measurements of joint diameter and joint histopathology were used to monitor the course of the arthritis. Inflammatory hyperalgesia was assessed as the pressure causing a limb withdrawal. FCA injection into the mouse stifle joint caused a pronounced increase in joint diameter when compared to the contralateral limb or vehicle controls. There was also a significant decrease in the pressure required to elicit a withdrawal of the injected limb. Histology showed arthritic changes, including synovial hypertrophy and polymorphonuclear neutrophil infiltration. In established chronic inflammation, seven days of treatment with either indomethacin (NSAID) or prednisolone (steroid) caused a significant decrease in joint inflammation and associated hyperalgesia. FCA induces a long-lasting joint inflammation in DBA/1 and C57BL/6 mice, which is restricted to the injected joint and exhibits some of the pathology associated with an arthritic condition. This model will be useful in examining the effect of joint inflammation on nociceptor sensitisation in both normal and transgenic mice.
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http://dx.doi.org/10.1016/j.jneumeth.2004.05.003DOI Listing
October 2004

Cannabidiol lacks the vanilloid VR1-mediated vasorespiratory effects of capsaicin and anandamide in anaesthetised rats.

Eur J Pharmacol 2004 May;491(2-3):181-9

Division of Neuroscience, College of Medicine and Veterinary Medicine, University of Edinburgh, 1 George Square, Edinburgh EH8 9JZ, Scotland, UK.

The results of vasorespiratory studies in rats anaesthetised with pentobarbital show that (+/-) cannabidiol, a cannabinoid that lacks psychotropic actions and is inactive at cannabinoid (CB) receptors, does not affect respiration or blood pressure when injected (1-2000 microg; 3.2-6360 nmol i.a.). Cannabidiol in doses up to 2 mg (6360 nmol) i.a. or i.v. did not affect the fall in mean blood pressure or the increase in ventilation (respiratory minute volume) caused by capsaicin and high doses of anandamide, responses that are mediated by activation of vanilloid VR1 (TRPV1) receptors in this species. Similar results were obtained with (-) cannabidiol (30-100 microg i.a.; 95-318 nmol). It has previously been shown using human embryonic kidney (HEK) cells over-expressing vanilloid human VR1 (hVR1) receptors that cannabidiol is a full agonist at vanilloid VR1 receptors in vitro. However, in the intact rat cannabidiol lacked vanilloid VR1 receptor agonist effects. We conclude that there are substantial functional differences between human and rat vanilloid VR1 receptors with respect to the actions of cannabidiol as an agonist at vanilloid VR1 receptors. Studies in vivo show that cannabidiol lacks any significant effect on mean blood pressure or respiratory minute volume when injected i.a. or i.v., and that this cannabinoid does not modulate the vanilloid VR1 receptor-mediated cardiovascular and ventilatory changes reflexly evoked by capsaicin or anandamide in rats anaesthetised with pentobarbital.
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http://dx.doi.org/10.1016/j.ejphar.2004.03.045DOI Listing
May 2004
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