糖心原创

Contact

• workRoom B208 South Laboratory
  Sutton Bonington Campus
  Sutton Bonington
  Leicestershire
  LE12 5RD
  UK
• work0115 951 6316
• fax0115 951 6099
• john.harris@nottingham.ac.uk

Biography

Dr John Harris

Assistant Professor in Neurophysiology

John's research investigates mechanisms behind acute and chronic pain by measuring spinal reflexes using electrophysiological recording and motion analysis techniques. Current research includes:

• How individual muscles in a limb are organized in producing a withdrawal reflex
• How this organization changes in acute and chronic pain states
• The mechanisms underlying excitability changes in the spinal cord ('central sensitization') in pain
• Pain in rheumatoid and osteoarthritis and development of more effective analgesics
• The treatment of osteoarthritis in dogs

Teaching Summary

Teaching Commitments

I am the Programme Director and Theme Lead for the Animal Science 3 year BSc and 4 year MSci degrees. In addition I am the module convenor for the third year 40 credit Undergraduate Research Project module BIOS3040 which covers projects by students on Agriculture, Animal Science, Biotechnology, Food Sciences, Miicrobiology and Plant Biology courses. I am also the Animal Sciences project co-ordinator for these projects. Furthermore I am the module convenor and a primary contributor (lectures and practical classes) to neurophysiology modules taught as part of BSc degrees offered within the School of Biosciences. I additionally contribute lectures to various other modules within the School of Biosciences.

Level 1: BIOS1066 - Animal Physiology & Anatomy (Module convenor; lectures and practical classes)

Level 1: BIOS1029 - Essential 糖心原创 Skills (Tutor groups; Writing development)

Level 1: BIOS1067 - Sustainable Agriculture, Food & Nutrition (Presentation assessment)

Level 2: BIOS2033 - Physiology of Electrically Excitable Tissues (Module convenor; lectures and practical classes)

Level 2: BIOS2083 - Research Skills for Animal Scientists (Lectures)

Level 3: BIOS3100 - Musculoskeletal Physiology (Module convenor; lectures and practical classes)

Level 3: BIOS3095 - Systems Neurophysiology (Module convenor; lectures and practical classes)

Level 3: BIOS3040 - Undergraduate Research Project (Module convenor; and Project co-ordinator for Animal Sciences; also supervise 6 - 10 students per year)

Teaching Awards/Recognition

Awarded Physiological Society poster prize in 2012 (Education & Teaching theme) for presentation "On-line discussion groups as a tool for enhancing student understanding following practical-based teaching". Proc. Physiol. Soc., 27: PC276.

Nominated for Lord Dearing Award in 2012

Nominated for University Staff Oscar - Teaching: Best All Rounder (2014)

Nominated for University Staff Oscar - Teaching: Makes best use of technology to enhance learning (2015)

Nominated for University Staff Oscar - Supervisor: Best Dissertation Supervisor (2015)

Nominated for University Staff Oscar - Teaching: Best All Rounder (2016)

Won School of Biosciences Best Teaching Award 2016

Nominated for University Staff Oscar - Personal Tutors: Difficult Issue (2017)

Won Lord Dearing Award in 2017

Current additional administrative roles

Committee member of Student-Staff Forum

Committee member of Learning & Teaching Strategy Group

Committee member and chair of Extenuating Circumstances panel

Committee member and deputy chair of Biosciences Research Ethics Committee

Animal Sciences Disability Champion

Research Summary

Withdrawal reflexes are the simplest centrally-organized responses to painful stimuli hence they are often used for the study of nociception, however few studies examine the withdrawal response in… read more

Selected Publications

• KELLY, S., DOBSON, K.L. and HARRIS, J., 2013. Osteoarthritis and Cartilage. 21(9), 1327-1335
• DOBSON, K.L. and HARRIS, J., 2012. Experimental Physiology. 97(6), 693-698
• MCCLYMONT, D.W., HARRIS, J. and MELLOR, I.R., 2012. European Journal of Pharmacology. 686(1-3), 22-31
• POTTERTON, S.L., GREEN, M.J., HARRIS, J., MILLAR, K.M., WHAY, H.R. and HUXLEY, J.N., 2011. Journal of Dairy Science. 94(6), 2952-2963

• View all publications

Current Research

Withdrawal reflexes are the simplest centrally-organized responses to painful stimuli hence they are often used for the study of nociception, however few studies examine the withdrawal response in any detail. The organization of limb withdrawal was first described by Charles Sherrington at the start of the 20^th century, who proposed that withdrawal to a transient stimulus was a stereotypical response involving excitation of all flexor muscles in a limb with concomitant inhibition of extensor muscles: the 'flexor reflex'. However recent studies on the organization of withdrawal reflexes suggest they produce the most appropriate movement depending on the site of the stimulus and that each hind limb muscle has an excitatory receptive field overlying the area withdrawn by contraction of that muscle. The total movement generated by a noxious stimulus is therefore the result of collective activation of reflexes to those muscles that have excitatory receptive fields overlapping the point of stimulation. This 'modular theory', first proposed by Jens Schouenborg, means extensors as well as flexors can act as the primary movers. Studies in the Harris laboratory have recently focused on how reflex responses are (re-)organized following injurious peripheral stimuli. Injurious stimuli augment the protective function of reflexes by enhancing (sensitizing) reflexes that protect the injured site and inhibiting those reflexes that might exacerbate the site of injury. The group has shown that the areas from which a reflex can be sensitized closely match those from which the reflex itself can be evoked, provided the spinal cord is intact. If descending pathways are interrupted, sensitization can be evoked from a much wider area. Thus whether the reflex is sensitized or inhibited after an injury depends on the relationship between the site of the injury and its relationship to the movement made by the reflex. The nature of the pathways that control these 'sensitization fields' is also of great interest to the group. Major projections from the brain to the spinal cord contain the neurotransmitters noradrenaline or 5-hydroxytryptamine (5-HT, serotonin) hence these pathways are prime candidates to study pharmacologically in order to tap into endogenous systems towards the possible benefit of pain relief.

My previous research has been particularly targeted towards the potential sensitization and reorganization of reflex responses in arthritic pain states and the influence of descending pathways. Osteoarthritis (OA) is a degenerative joint disease affecting almost 40% of the population aged over 60 as well as being a major debilitating disease in animals, leading to chronic pain and disability. Understanding the mechanisms that drive and maintain OA pain is therefore critical for the rational development of effective therapies. Evidence suggests that plasticity within the central nervous system ('central sensitization') contributes to the maintenance of OA pain. In collaboration with veterinary researchers in Bristol (UK) and North Carolina State University (USA) I have translated some of my techniques and findings to a clinical setting by studying reflex responses in dogs with arthritis, in the hope of developing better diagnostic capability and a more targeted treatment regime.

Past Research

Measurement of limb movements during reflex withdrawal

All previous work on the organisation and re-organisation of withdrawal reflexes had been based on the measurement of electrical signals rather than the actual movements made. Thus, the primary objective of these studies was to quantify the movements generated in withdrawal reflexes, by measuring 3-dimensional position changes (Codamotion庐) of a limb evoked by mechanical stimulation of selected parts of the same limb. Once the "normal" organisation of reflex movements was mapped, we examined how reflexes were altered by (i) acute noxious stimulation of strategically-selected parts of the foot; (ii) analgesic drugs, (iii) disruption of endogenous control systems; and (iv) acute and chronic inflammation. This was the first time that the stimulus site-dependence of the movements generated in response to cutaneous stimulation had been studied.

Pharmacology of 'central sensitization'

We have also investigated some of the neurotransmitters behind (central) sensitization of reflex responses. In agreement with others, we have confirmed the importance of the NMDA subtype of glutamate receptor in central sensitization however we found no evidence for a role of Group I metabotropic glutamate receptors in this process. Simultaneous blockade of all tachykinin receptors was required to reveal their role in central sensitization of reflexes. Simultaneous block of tachykinin and GluN2B-subunit containing NMDA receptors indicated that a combined pharmacological approach offers a potential way forward for the development of new anti-hyperalgesic agents.

Opioids as analgesics

Opioids are important analgesics in animals and man but their effectiveness can be radically altered in some chronic pain states. Against inflammatory pain they are generally found to be more potent compared to use in acute pain, however for the treatment of pain following nerve injury (neuropathic pain), opioids can be completely ineffective. Research into the mode of action of opioids is therefore of major importance. A crucial site at which the inhibitory effect of opioids is mediated is the spinal cord (as evidenced by their effectiveness following epidural application), however opioids also have an action in the brain, where it is thought they cause disinhibition (i.e. an overall facilitation) of inhibitory pathways to the spinal cord thereby suppressing the transmission of nociceptive information. Thus one possible explaination for the reduction in efficacy of opioids in neuropathic states is the breakdown of opioid-activated descending inhibition to the spinal cord. Our previous studies therefore looked further at the involvement of these pathways from the brain in determining the potency of opioids, and how their interaction might change in inflammatory and neuropathic conditions. Studies such as these aid in the design of analgesic strategies for long-term pain states.

• HUNT JR, KNAZOVICKY D, HARRIS J, KELLY S, KNOWLES TG, MURRELL JC and LASCELLES BDX, 2025. Frontiers in Pain Research. 6, 1505064
• HUNT JR, KNAZOVICKY D, GOFF M, HARRIS J, KNOWLES TG, ENOMOTO M, MENDL M, WHAY B, LASCELLES BDX and MURRELL JC, 2025. Quantitative sensory testing in dogs with spontaneous osteoarthritis Frontiers in Pain Research. (In Press.)
• WHITE, K., ALDURDUNJI, M., HARRIS, J., ORTORI, C. and PAINE, S., 2022. Alfaxalone population pharmacokinetics in the rat: Model application for pharmacokinetic and pharmacodynamic design in inbred and outbred strains and sexes Pharmacology Research & Perspectives. 10(6), e01031
• J.R. HUNT, M. GOFF, H. JENKINS, J. HARRIS, T.G. KNOWLES, B.D.X. LASCELLES, M. MENDL, B. WHAY and J.C. MURRELL, 2019. Clinical measurements performed during alfaxalone total intravenous anaesthesia for radiography and neurophysiological investigations in dogs Veterinary Anaesthesia & Analgesia. 46, 483-487
• K. WHITE, M. TARGETT and J. HARRIS, 2018. The Veterinary Journal. 237, 16 - 25
• J.R. HUNT, M. GOFF, H. JENKINS, J. HARRIS, T.G. KNOWLES, B.D.X. LASCELLES, M. ENOMOTO, M. MENDL, H.R. WHAY and J.C. MURRELL, 2018. Electrophysiological characterisation of central sensitisation in canine spontaneous osteoarthritis Pain. 159, 2318-2330
• HARRIS, J., 2016. European Journal of Neuroscience. 43, 834-845
• HUNT, J., MURRELL, J., KNAZOVICKY, D., HARRIS, J., KELLY, S., KNOWLES, T.G. and LASCELLES, B.D.X., 2016. PLOS ONE. 11(7), e0158990
• WHITE, K., PAINE, S. and HARRIS, J., 2016. Veterinary Anaesthesia and Analgesia. 44, 865-875
• KELLY, S., DOBSON, K.L. and HARRIS, J., 2013. Osteoarthritis and Cartilage. 21(9), 1327-1335
• DOBSON, K.L. and HARRIS, J., 2012. Experimental Physiology. 97(6), 693-698
• MCCLYMONT, D.W., HARRIS, J. and MELLOR, I.R., 2012. European Journal of Pharmacology. 686(1-3), 22-31
• POTTERTON, S.L., GREEN, M.J., HARRIS, J., MILLAR, K.M., WHAY, H.R. and HUXLEY, J.N., 2011. Journal of Dairy Science. 94(6), 2952-2963
• POTTERTON, S.L., GREEN, M.J., MILLAR, K.M., BRIGNELL, C.J., HARRIS, J., WHAY, H.R. and HUXLEY, J.N., 2011. Veterinary Record. 169(24), 634
• HARRIS, J. and CLARKE, R.W., 2007. Brain Research. 1131, 106-111
• HARRIS, J., WATERFALL, A.H. and CLARKE, R.W., 2006. The contribution of extension to withdrawal reflexes in the anaesthetised rabbit measured by movement analysis Proceedings of the Physiological Society. 3, PC54
• LO, W.C., HARRIS, J. and CLARKE, R.W., 2005. The contribution of descending pathways to the inhibitory effect of intravenous morphine on spinal reflexes in the decerebrated rabbit Journal of Physiology. 565.P, PC118
• LO, W.C., HARRIS, J. and CLARKE, R.W., 2005. The inhibitory effect of intracerebroventricular morphine on a withdrawal reflex in the decerebrated rabbit does not involve spinal alpha 2-adrenoceptors Journal of Physiology. 567.P, PC204
• HARRIS, J., JOULES, C., STANLEY, C., THOMAS, P. and CLARKE, R.W., 2004. Experimental Physiology. 89(2), 187-198
• LO, W.C., JACKSON, E., MERRIMAN, A., HARRIS, J. and CLARKE, R.W., 2004. Pain. VOL 109(NUMBER 1-2), 162-171
• JENKINS, S., WORTHINGTON, M., HARRIS, J. and CLARKE, R.W., 2004. Brain Research. VOL 1012(NUMBER 1-2), 146-153
• LO, W.C., HARRIS, J. and CLARKE, R.W., 2004. Modulation of fentanyl induced inhibition of spinal reflexes by blockade of alpha 2-adrenoceptors: effects of acute inflammation Journal of Physiology. 557.P, C93
• CLARKE, R.W. and HARRIS, J., 2004. The organisation of motor responses to noxious stimuli Comparative Biochemistry and Physiology. Part A: Physiology. 137A((3/Suppl.)), S107
• HARRIS, J. and CLARKE, R.W., 2004. Organisation of sensitisation of hind limb withdrawal reflexes during the development of acute antigen-induced inflammation in the anaesthetised rabbit Journal of Physiology. 555.P, C88
• CLARKE, R.W. and HARRIS, J., 2004. Brain Research Reviews. VOL 46(NUMBER 2), 163-172
• HARRIS, J. and CLARKE, R.W., 2003. Journal of Physiology. 546(1), 251-265
• CLARKE, R.W., BROWN-REID, K., KASHER, P. and HARRIS, J., 2003. Experimental Physiology. 88(1), 13-18
• LO, W.C., HARRIS, J. and CLARKE, R.W., 2003. Neuroscience Letters. 340, 95-98
• LO, W.C., MERRIMAN, A., HARRIS, J. and CLARKE, R.W., 2003. Blockade of spinal nicotinic receptors reduces descending inhibition of spinal reflexes evoked by intraventricular administration of fentanyl in the decerebrated rabbit Journal of Physiology. 551.P, C19
• HARRIS, J., PATEL, R. and CLARKE, R.W., 2003. Alpha 2-adrenoceptors mediate inhibition of withdrawal reflexes after remote noxious stimuli in the anaesthetised rabbit Journal of Physiology. 551.P, C20
• HARRIS, J., STANLEY, C., THOMAS, P. and CLARKE, R.W., 2003. Tachykinin receptors involved in central sensitisation in the decerebrated rabbit Journal of Physiology. 547.P, C84
• CLARKE, R.W. and HARRIS, J., 2002. RX 821002 as a tool for physiological investigation of alpha 2-adrenoceptors CNS Drug Reviews. 8, 177-193
• HARRIS, J. and CLARKE, R.W., 2002. Diffuse organization of central sensitization of withdrawal reflexes in the decerebrated, spinalized rabbit Journal of Physiology. 539, 109P-110P
• CLARKE, R.W., HARRIS, J., KASHER, P. and BROWN-REID, K., 2002. Temporal summation in reflexes evoked by selective stimulation of sural nerve C-fibres in the decerebrated rabbit Pflugers Archiv - European Journal of Physiology. 443(Suppl 2), S315
• HARRIS, J. and CLARKE, R.W., 2002. Organization of central sensitization of withdrawal reflexes in the anaesthetized rabbit. Abstracts: 10th World Congress on Pain. 16
• PATEL, A., HARRIS, J. and CLARKE, R.W., 2002. Involvement of L-type calcium channels in temporal summation of a spinal reflex in the decerebrated rabbit. Journal of Physiology. 543.P, 111P
• CLARKE, R.W., EVES, S., HARRIS, J., PEACHEY, J.E. and STUART, E., 2002. Neuroscience. 112(3), 555-571
• HARRIS, J., JOULES, C. and CLARKE, R.W., 2002. Glutamate receptors involved in central sensitisation of withdrawal reflexes in the decerebrated rabbit. Journal of Physiology. 544.P, 36P
• CLARKE, R.W., HARRIS, J., JENKINS, S. and WITTON, S.K, 2001. Neuropharmacology. 40(4), 570-577
• CLARKE, R.W. and HARRIS, J., 2001. European Journal of Pain. VOL 5(PART 2), 175-186
• CLARKE, R.W., HARRIS, J. and HOUGHTON, A.K., 2001. Neuroscience Letters. VOL 308(NUMBER 3), 189-192
• CLARKE, R.W., WYCH, B.E. and HARRIS, J., 2001. Neuroscience Letters. VOL 304(NUMBER 1-2), 120-122
• CLARKE, R.W., BROWN-REID, K. and HARRIS, J., 2001. Selective block of A fibre conduction by tetrodotoxin in rabbit sural nerve. Journal of Physiology. 536.P, 39P-40P
• STUART, E., HARRIS, J. and CLARKE, R.W., 2001. The role of glutamate N-methyl-D-aspartate (NMDA) receptors in temporal summation in a withdrawal reflex pathway in the decerebrated rabbit. Journal of Physiology. 531.P, 143P
• STUART, E., HARRIS, J. and CLARKE, R.W., 2001. Selective descending inhibition of N-methyl-D-aspartate (NMDA) receptor-mediated components of spinal reflexes in the decerebrated rabbit. Journal of Physiology. 531.P, 146P-147P
• HARRIS, J., JENKINS, S. and CLARKE, R.W., 2001. Site-specific central sensitization of withdrawal reflexes in the decerebrated rabbit. Journal of Physiology. 536.P, 44P
• CLARKE, R.W., HARRIS, J. and OGILVIE, J., 2000. Neuropharmacology. 39(10), 1904-1912
• DREW, L.J., HARRIS, J., MILLNS, P.J., KENDALL, D.A. and CHAPMAN, V., 2000. European Journal of Neuroscience. 12(6), 2079-2086
• HARRIS, J., DREW, L.J. and CHAPMAN, V., 2000. NeuroReport. 11(12), 2817-2819
• HARRIS, J. and CHAPMAN, V., 2000. Spinal administration of the endocannabinoid anandamide inhibits C-fibre evoked post-discharge responses of dorsal horn neurones in carrageenan inflamed rats British Journal of Pharmacology. VOL 129(SUPP/1), 140P
• BRIERLEY, M., HARRIS, J., MELLOR, I., MINARINI, A., BOLOGNESI, M.L., MELCHIORRE, C. and USHERWOOD, P., 1999. Antagonism of rat cortical cell NMDAR by a series of methoctramine analogues: an assessment of their potential as neuroprotectants. British Neuroscience Association Abstracts. 15, 124
• HARRIS J., MILLNS, P.J., KENDALL, D.A. and CHAPMAN, V., 1999. The effect of cannabinoid ligands on [S-35]GTP gamma S binding in spinal cord slices of non-inflamed and inflamed rats. British Journal of Pharmacology. 128, 290P
• SHAO, Z., MELLOR, I.R., BRIERLEY, M.J., HARRIS, J. and USHERWOOD, P.N.R., 1998. Potentiation and inhibition of nicotinic acetylcholine receptors by spermine in the TE671 human muscle cell line Journal of Pharmacological and Experimental Therapeutics. 286, 1269-1276
• CLARKE, R.W., HARRIS, J. and HOUGHTON, A.K., 1998. Experimental Brain Research. 120, 18-24
• GREEN, A.C., HARRIS J., SNOWDON, E. and USHERWOOD, P.N.R., 1998. Polyamine-induced neurotoxicity: indirect involvement of N-methyl-D-aspartate receptors in cortical neuronal cell culture. Human & Experimental Toxicology. 17(1), 55
• GREEN, A.C., CHATHA, T., HARRIS J. and USHERWOOD, P.N.R., 1998. Neurotoxicity triggered by chelation of intracellular zinc: possible involvement of an endonuclease? Human & Experimental Toxicology. 17(1), 50
• TOMLINSON, S., KERWIN, S., MELLOR, I., HARRIS, J., MUNDEY, M., BRIERLEY, M., BELL, D.R and USHERWOOD, P.N.R., 1997. Interaction of a polyamine amide wasp toxin with cloned and mutant glutamate receptors. Biochemical Society Transactions. 25, 551S
• CLARKE, R.W., HARRIS, J. and HOUGHTON, A.K., 1996. Spinal 5-HT receptors and tonic modulation of transmission through a withdrawal reflex pathway in the decerebrated rabbit British Journal of Pharmacology. 119, 167-176
• SOLOVIEV, M.M., BRIERLEY, M.J., SHAO, Z.Y., MELLOR, I.R., VOLKOVA, T.M., KAMBOJ, R., ISHIMARU, H., SUDAN, H., HARRIS, J., FOLDES, R.L., GRISHIN, E.V., USHERWOOD, P.N.R. and BARNARD, E.A., 1996. Journal of Biological Chemistry. 271, 32572-32579
• HARRIS, J., MUNDEY, M., TOMLINSON, S., MELLOR, I., NAKANISHI, K., BELL, D. and USHERWOOD, P.N.R., 1996. Toxicon. 34, 730-731
• HARRIS, J. and CLARKE, R.W., 1993. European Journal of Pharmacology. 237(2-3), 323-328
• CLARKE, R.W., FORD, T.W. and HARRIS, J., 1993. Changes in a spinal reflex and arterial blood pressure in the decerebrated rabbit after intrathecal RX 821029, a selective ligand for imidazoline binding sites. Journal of Physiology. 467, 199P
• HARRIS, J., NOBLE, E., HOUGHTON, A.K. and CLARKE, R.W., 1993. Interactions between noradrenaline and 5-HT in the spinal cord of the rabbit. Brain Research Association Abstracts. 10, 15
• HARRIS, J., WHITE, D.P. and CLARKE, R.W., 1992. The roles of 5-HT in modulating a spinal reflex in the decerebrated rabbit. Neuroscience Letters. S14
• HARRIS, J. and CLARKE, R.W., 1992. Experimental Brain Research. 92(2), 310-317
• CLARKE, R.W., HARRIS, J. and HOUGHTON, A.K., 1992. Modulation by endogenous opioids of reflexes evoked by mechanical stimulation of the heel in the decerebrated and spinalized rabbit. Journal of Physiology. 452, 241P
• CLARKE, R.W., HARRIS, J. and FORD, T.W., 1992. Seeking a role for cholecystokinin in the control of spinal reflexes. In: DOURISH, C.T., COOPER, S.J., IVERSEN, S.D. and IVERSEN, L.L., eds., Multiple cholecystokinin receptors in the CNS Oxford University Press. 522-528
• CLARKE, R.W., GALLOWAY, F.J., HARRIS, J., TAYLOR, J.S. and FORD, T.W., 1992. Opioidergic inhibition of flexor and extensor reflexes in the rabbit. Journal of Physiology. 449, 493-501
• CLARKE, R.W., HARRIS, J. and FORD, T.W., 1992. Cholecystokinin (CCK), endogenous opioids and spinal reflexes in the rabbit. Neuroscience Letters. S58
• CLARKE, R.W., FORD, T.W. and HARRIS, J., 1992. Fentanyl depresses a spinal reflex in the rabbit via spinal and supraspinal actions. Neuroscience Letters. S26
• CLARKE, R.W., HARRIS, J., FORD, T.W. and TAYLOR, J.S., 1992. Pain. 49(1), 65-70
• CLARKE, R. W., ISHERWOOD, S.G. and HARRIS, J., 1991. Excitability changes in hindlimb flexor reflexes after intense afferent barrage in the decerebrated and spinalized rabbit. Journal of Physiology. 438, 197P
• HARRIS, J., FORD, T.W. and CLARKE, R.W., 1991. Opioidergic modulation of reflexes evoked by mechanical stimulation of the heel in the rabbit. Society for Neuroscience Abstracts. 17, 465
• TAYLOR, J.S., NEAL, R.I., HARRIS, J., FORD, T.W. and CLARKE, R.W., 1991. Prolonged inhibition of a spinal reflex after intense stimulation of distant peripheral nerves in the decerebrated rabbit. Journal of Physiology. 437, 71-83
• FORD, T.W., HARRIS, J. and TAYLOR, J.S., 1991. The effects of naloxone on spinal neurones with an excitatory input from the sural nerve in the decerebrated and spinalized rabbit. Journal of Physiology. 435, 61P
• CLARKE, R.W., HARRIS, J., FORD, T.W. and TAYLOR, J.S., 1991. Opioidergic inhibition of reflexes evoked by selective stimulation of sural nerve C fibres in the rabbit. Experimental Physiology. 76(6), 987-90
• CLARKE, R.W., FORD, T.W., HARRIS, J. and TAYLOR, J.S., 1990. Transmitters modulating spinal withdrawal reflexes. Neuroscience Letters. S21
• CLARKE, R.W., FORD, T.W., HARRIS, J. and TAYLOR, J.S., 1990. Long lasting facilitation of the sural gastrocnemius reflex caused by noxious stimulation of the heel in the decerebrated and spinalized rabbit. Journal of Physiology. 420, 35P
• CLARKE, R.W., FORD, T.W., HARRIS, J., PETTIT, J.S. and TAYLOR, J.S., 1990. Pain. S97
• TAYLOR, J.S., PETTIT, J.S., HARRIS, J., FORD, T.W. and CLARKE, R.W., 1990. Brain Research. 531(1-2), 263-268
• HARRIS, J., FORD, T.W. and CLARKE, R.W., 1990. The effects of intrathecal application of alpha-adrenoceptor antagonists on the sural-gastrocnemius reflex in the decerebrate rabbit. Journal of Physiology. 429, 130P
• CLARKE, R.W., FORD, T.W., HARRIS, J. and TAYLOR, J.S., 1988. The effects of direct spinal application of idazoxan and prazosin on a spinal reflex in the decerebrated rabbit. Neuroscience Letters. S32-S33