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Professor Ian Kitchen

Associate Dean (Research)

Email:
Phone: Work: 01483 68 9734
Room no: 07 AY 02

Office hours

Please contact Helen Auld for an appointment.

Further information

Biography

As Associate Dean, Professor Kitchen is responsible for leading the research strategy of the Faculty of Health & Medical Sciences.  Appointed as a Professor of Neuropharmacology in 1997, he was formerly Head of the Pharmacology group and Deputy Head of School in Biomedical and Molecular Sciences at Surrey.  He graduated with a 1st Class honours degree in 1977, and gained his PhD in 1980 from the University of London.


In 2006 he was elected a Fellow of the British Pharmacological Society and in 2010 elected a Fellow of the Society of Biology.  His primary area of research for over 30 years has been in opioid neuropharmacology and he has been a major academic contributor to the opioid field in the UK and world-wide.  Surrey has gained international recognition for work on opioid system development in the brain and for neuroanatomical studies in opioid gene knockout mice in relation to furthering our understanding of pain and drug addiction.  In collaboration with molecular genetics groups in France we were the first to publish the phenotype of an opioid receptor knockout mouse (Nature 383, 819-823, 1996), and Professor Kitchen has led Euorpean consortia funded by substantial EC grants studying the genomics of drug addiction. At a national level he is Co-Chair of the UK Heads of Pharmacology and Therapeutics and has served on MRC advisory and grant boards.  


He has been a sub-panel member on two UK research assessment exercises; on Allied Health Professions and Studies in RAE 2008 and on Allied Health Professions, Dentistry, Nursing and Pharmacy for REF 2014. At an international level he is founder and was President of the European Opioid Conference until 2011, has served three elected terms on the Executive Committee of the International Narcotics Research Conference, and is a member of the IUPHAR opioid receptor nomenclature sub-committee.

Research Interests

Professor Kitchen’s current research projects are listed below.  He has supervised over 30 PhD students and is actively looking for prospective PhD students interested in these project areas.  Students that are on line for a first or upper second class honours degree in one of the biomedical sciences, or equivalent, should send their cv by e-mail:

Gene Knockout and drug addiction

In collaboration with groups in France, Germany, Spain and the US we are characterising the phenotype and neuroanatomy of transgenic mice deficient in opioid receptor, opioid peptide and dopamine receptor genes, as part of a major EC funded project (8.1million Euro) studying the genetics of drug addiction.  The application of transgenic technology to our understanding of opioid receptor heterogeneity is currently being studied with knockouts of all four opioid receptors (MOP, DOP, KOP and NOP receptor and the endogenous peptide ligands (enkephalins, dynorphins and nociceptin) which act at these receptors.  In addition we are carrying out behavioural studies and measures of neurotransmitter release using microdialysis in gene knockout mice to characterise the neurobiological changes that occur in response to addictive drugs.  

Heterodimerisation of Receptors in the CNS

G-protein coupled receptors (GPCRs) are targets for many drugs and it was thought they existed as single units, but there is recent evidence from studies in cell systems that some of these receptors can form complexes known as heterodimers.  If these heterodimers exist under physiological conditions, this would be very important as the heterodimer sees drugs differently from the monomer forms, and this could give us novel drug targets.  Two of these receptors, the KOP and DOP opioid receptors, have been proposed to heterodimerise in cell systems.  We are using a completely novel approach to determine if this happens in brain tissue.  It uses brains taken from single and double opioid receptor gene knockout mice, where either only monomer or heterodimer forms can exist.  By measuring the receptor labelling we will be able to determine whether opioid compounds interact with a monomer or heterodimer form of the KOP and DOP receptor.  This technique, we call subtraction autoradiography, has the potential to be used to distinguish monomer or heterodimeric interaction of any new drug that can be labelled, and where appropriate gene knockout mouse tissue is available.

Neurobiological mechanisms of nicotine addiction

The focus of this investigation is on the psychological and neurobiological mechanisms involved in the modulation of nicotine cravings by exercise and the role of stress in mediating nicotine withdrawal.  During the human component of the project, cigarette cravings, CO levels, and exercise are being be monitored in humans in the laboratory using standards assessment methods.  The in vivo animal component of the project includes the investigation of mechanism of nicotine craving with the use of gene knockout models of addiction and neurochemical techniques including in vivo microdialysis, electrophysiology and receptor autoradiography.  A related project is investigating the role of a7 nicotinic subunits in cocaine and opioid addictive processes with the use of well characterised addictive related behavioural tests (e.g. conditioned place preference, behavioural sensitization, locomotion) in wild type andtransgenic animals.  The neurochemical effect of a7 nicotinic subunits in opioid and cocaine addiction is being investigated with the use of quantitative autoradiography and freely moving microdialysis.

Publications

Highlights

  • Metaxas A, Bailey A, Barbano MF, Galeote L, Maldonado R, Kitchen I. (2010) 'Differential region-specific regulation of alpha 4 beta 2*nAChRs by self-administered and non-contingent nicotine in C57BL/6J mice'. WILEY-BLACKWELL PUBLISHING, INC ADDICT BIOL, 15 (4), pp. 464-479.
    doi: 10.1111/j.1369-1600.2010.00246.x
    Full text is available at: http://epubs.surrey.ac.uk/285490/

    Abstract

    Neuronal nAChR upregulation is the hallmark of chronic nicotine exposure. Neuroplasticity to abused drugs, however, depends on whether their administration is forced by the experimenter or is under the control of the experimental animal. Neuroadaptation to chronic nicotine self-administration was examined with a yoked-control paradigm, using nose-poking as the operating procedure. Freely moving C57BL/6J mice that responded for 0.03 mg/kg/infusion of intravenous nicotine under a continuous schedule of reinforcement (FR-1), had control over the rate and amount of drug intake that a yoked littermate passively received (n = 11). The impact of response dependency on neurobiological changes in nicotinic and dopaminergic systems was subsequently assessed using quantitative autoradiography. Cytisine-sensitive [125I]epibatidine binding, [3H]SCH23390, [3H]raclopride and [3H]mazindol were used to label nAChRs with 4β2* subtype properties, D1 and D2 dopaminergic receptors, and dopamine transporters, respectively. During a period of 12 days, self-administration was reliably initiated and maintained in animals receiving response-contingent nicotine. Region specific changes in the density of 4β2* nAChRs were found to be dependent on the contingency of nicotine treatment. Higher levels of 4β2* receptor binding were observed in the dorsal lateral geniculate nucleus and the ventral tegmental area of self-administering mice, compared to non-contingent animals. Moreover, response-independent increases in D2 binding were observed following chronic nicotine administration. No change in D1 and DAT binding was observed among groups. These findings indicate regional specific alterations in the regulation of the nicotinic cholinergic system following contingent and non-contingent nicotine exposure, and underline the importance of response dependency on the development of nicotine addiction.

  • Bailey A, Metaxas A, Al-Hasani R, Keyworth HL, Forster DM, Kitchen I. (2010) 'Mouse strain differences in locomotor, sensitisation and rewarding effect of heroin; association with alterations in MOP-r activation and dopamine transporter binding'. WILEY-BLACKWELL PUBLISHING, INC EUROPEAN JOURNAL OF NEUROSCIENCE, 31 (4), pp. 742-753.
    doi: 10.1111/j.1460-9568.2010.07104.x
    Full text is available at: http://epubs.surrey.ac.uk/7455/
  • Castane A, Wells L, Soria G, Hourani S, Ledent C, Kitchen I, Opacka-Juffry J, Maldonado R, Valverde O. (2008) 'Behavioural and biochemical responses to morphine associated with its motivational properties are altered in adenosine A(2A) receptor knockout mice'. WILEY-BLACKWELL BRITISH JOURNAL OF PHARMACOLOGY, 155 (5), pp. 757-766.
    doi: 10.1038/bjp.2008.299
    Full text is available at: http://epubs.surrey.ac.uk/185381/
  • Lena I, Bradshaw S, Pintar J, Kitchen I. (2008) 'Adaptive changes in the expression of central opioid receptors in mice lacking the dopamine D2 receptor gene'. PERGAMON-ELSEVIER SCIENCE LTD NEUROSCIENCE, 153 (3), pp. 773-788.
    doi: 10.1016/j.neuroscience.2008.02.070

Journal articles

  • Foster JD, Kitchen I, Bettler B, Chen Y. (2012) 'GABA(B) Receptor Subtypes Differentially Modulate Synaptic Inhibition in the Dentate Gyrus to Enhance Granule Cell Output.'. Br J Pharmacol,
    doi: 10.1111/bph.12073
  • Yoo JH, Kitchen I, Bailey A. (2012) 'The endogenous opioid system in cocaine addiction: what lessons have opioid peptide and receptor knockout mice taught us?'. Br J Pharmacol, England: 166 (7), pp. 1993-2014.
    doi: 10.1111/j.1476-5381.2012.01952.x
  • Metaxas A, Keyworth H, Yoo J, Chen Y, Kitchen I, Bailey A. (2012) 'The stereotypy-inducing and OCD-like effects of chronic 'binge' cocaine are modulated by distinct subtypes of nicotinic acetylcholine receptors.'. Br J Pharmacol, England: 167 (2), pp. 450-464.
    doi: 10.1111/j.1476-5381.2012.02023.x
  • Hussey MJ, Clarke GD, Ledent C, Kitchen I, Hourani SM. (2012) 'Deletion of the adenosine A(2A) receptor in mice enhances spinal cord neurochemical responses to an inflammatory nociceptive stimulus.'. Neurosci Lett, Ireland: 506 (2), pp. 198-202.
    doi: 10.1016/j.neulet.2011.11.004
    Full text is available at: http://epubs.surrey.ac.uk/24873/

    Abstract

    Knockout mice lacking the adenosine A(2A) receptor are less sensitive to nociceptive stimuli, and this may be due to the presence of pronociceptive A(2A) receptors on sensory nerves. In support of this hypothesis, we have recently shown that in A(2A) receptor knockout mice there are marked reductions in the changes of two markers of spinal cord neuronal activity, [(3)H]MK801 binding to NMDA receptors and uptake of [(14)C]-2-deoxyglucose, in response to formalin injection. We now report that following a more prolonged inflammatory stimulus, consisting of intraplantar injections of PGE(2) and paw pressure, there was in contrast an increase in [(3)H]MK801 binding and [(14)C]-2-deoxyglucose uptake in the spinal cords of the A(2A) receptor knockout mice which was much greater than in the wild-type mice. This increase suggests that when there is a pronounced inflammatory component to the stimulus, loss of inhibitory A(2A) receptors on inflammatory cells outweighs the loss of pronociceptive A(2A) receptors on peripheral nerves so that overall there is an increase in nociceptive signalling. This implies that although A(2A) antagonists have antinociceptive effects they may have only limited use as analgesics in chronic inflammatory pain.

  • Wells L, Opacka-Juffry J, Fisher D, Ledent C, Hourani S, Kitchen I. (2011) 'In vivo dopaminergic and behavioral responses to acute cocaine are altered in adenosine A(2A) receptor knockout mice.'. Synapse, United States: 66 (5), pp. 383-390.
    doi: 10.1002/syn.21527
  • Al-Hasani R, Foster JD, Metaxas A, Ledent C, Hourani SM, Kitchen I, Chen Y. (2011) 'Increased desensitization of dopamine D(2) receptor-mediated response in the ventral tegmental area in the absence of adenosine A(2A) receptors.'. Elsevier Neuroscience, United States: 190, pp. 103-111.
    doi: 10.1016/j.neuroscience.2011.05.068
    Full text is available at: http://epubs.surrey.ac.uk/7454/

    Abstract

    G-protein coupled receptors interact to provide additional regulatory mechanisms for neurotransmitter signaling. Adenosine A(2A) receptors are expressed at a high density in striatal neurons, where they closely interact with dopamine D(2) receptors and modulate effects of dopamine and responses to psychostimulants. A(2A) receptors are expressed at much lower densities in other forebrain neurons but play a more prominent yet opposing role to striatal receptors in response to psychostimulants in mice. It is, therefore, possible that A(2A) receptors expressed at low levels elsewhere in the brain may also regulate neurotransmitter systems and modulate neuronal functions. Dopamine D(2) receptors play an important role in autoinhibition of neuronal firing in dopamine neurons of the ventral tegmental area (VTA) and dopamine release in other brain areas. Here, we examined the effect of A(2A) receptor deletion on D(2) receptor-mediated inhibition of neuronal firing in dopamine neurons in the VTA. Spontaneous activity of dopamine neurons was recorded in midbrain slices, and concentration-dependent effects of the dopamine D(2) receptor agonist, quinpirole, was compared between wild-type and A(2A) knockout mice. The potency of quinpirole applied in single concentrations and the expression of D(2) receptors were not altered in the VTA of the knockout mice. However, quinpirole applied in stepwise escalating concentrations caused significantly reduced maximal inhibition in A(2A) knockout mice, indicating an enhanced agonist-induced desensitization of D(2) receptors in the absence of A(2A) receptors. The A(2A) receptor agonist, CGS21680, did not exert any effect on dopamine neuron firing or response to quinpirole, revealing a novel non-pharmacological interaction between adenosine A(2A) receptors and dopaminergic neurotransmission in midbrain dopamine neurons. Altered D(2) receptor desensitization may result in changes in dopamine neuron firing rate and pattern and dopamine release in other brain areas in response to persistent dopamine release and administration of psychostimulants.

  • Smith SR, Pochani N, Al-Hasani R, Hourani S, Wells L, Kitchen I, Bailey A. (2011) 'Metabotropic mGluR5-and adenosine A(2A)-receptor interactions in opioid addiction'. POLISH ACAD SCIENCES INST PHARMACOLOGY PHARMACOLOGICAL REPORTS, 63 (1), pp. 225-225.
  • Zanos P, Alshehri M, Sahabandu T, Winsky-Sommerer R, Kitchen I, Bailey A. (2011) 'Persistent brain region-specific upregulation of vasopressin (V1ar) and oxytocin receptors in chronic intermittent escalating dose morphine administration in mice'. POLISH ACAD SCIENCES INST PHARMACOLOGY PHARMACOLOGICAL REPORTS, 63 (1), pp. 252-252.
  • Metaxas A, Bailey A, Barbano MF, Galeote L, Maldonado R, Kitchen I. (2010) 'Differential region-specific regulation of alpha 4 beta 2*nAChRs by self-administered and non-contingent nicotine in C57BL/6J mice'. WILEY-BLACKWELL PUBLISHING, INC ADDICT BIOL, 15 (4), pp. 464-479.
    doi: 10.1111/j.1369-1600.2010.00246.x
    Full text is available at: http://epubs.surrey.ac.uk/285490/

    Abstract

    Neuronal nAChR upregulation is the hallmark of chronic nicotine exposure. Neuroplasticity to abused drugs, however, depends on whether their administration is forced by the experimenter or is under the control of the experimental animal. Neuroadaptation to chronic nicotine self-administration was examined with a yoked-control paradigm, using nose-poking as the operating procedure. Freely moving C57BL/6J mice that responded for 0.03 mg/kg/infusion of intravenous nicotine under a continuous schedule of reinforcement (FR-1), had control over the rate and amount of drug intake that a yoked littermate passively received (n = 11). The impact of response dependency on neurobiological changes in nicotinic and dopaminergic systems was subsequently assessed using quantitative autoradiography. Cytisine-sensitive [125I]epibatidine binding, [3H]SCH23390, [3H]raclopride and [3H]mazindol were used to label nAChRs with 4β2* subtype properties, D1 and D2 dopaminergic receptors, and dopamine transporters, respectively. During a period of 12 days, self-administration was reliably initiated and maintained in animals receiving response-contingent nicotine. Region specific changes in the density of 4β2* nAChRs were found to be dependent on the contingency of nicotine treatment. Higher levels of 4β2* receptor binding were observed in the dorsal lateral geniculate nucleus and the ventral tegmental area of self-administering mice, compared to non-contingent animals. Moreover, response-independent increases in D2 binding were observed following chronic nicotine administration. No change in D1 and DAT binding was observed among groups. These findings indicate regional specific alterations in the regulation of the nicotinic cholinergic system following contingent and non-contingent nicotine exposure, and underline the importance of response dependency on the development of nicotine addiction.

  • Hussey MJ, Clarke GD, Ledent C, Kitchen I, Hourani SMO. (2010) 'Genetic deletion of the adenosine A(2A) receptor in mice reduces the changes in spinal cord NMDA receptor binding and glucose uptake caused by a nociceptive stimulus'. ELSEVIER IRELAND LTD NEUROSCIENCE LETTERS, 479 (3), pp. 297-301.
    doi: 10.1016/j.neulet.2010.05.084
    Full text is available at: http://epubs.surrey.ac.uk/7457/
  • Yoo J-H, Bailey A, Ansonoff M, Pintar JE, Matifas A, Kieffer BL, Kitchen I. (2010) 'Lack of Genotype Effect on D1, D2 Receptors and Dopamine Transporter Binding in Triple MOP-, DOP-, and KOP-Opioid Receptor Knockout Mice of Three Different Genetic Backgrounds'. WILEY-LISS SYNAPSE, 64 (7), pp. 520-527.
    doi: 10.1002/syn.20757
  • Bailey A, Metaxas A, Al-Hasani R, Keyworth HL, Forster DM, Kitchen I. (2010) 'Mouse strain differences in locomotor, sensitisation and rewarding effect of heroin; association with alterations in MOP-r activation and dopamine transporter binding'. WILEY-BLACKWELL PUBLISHING, INC EUROPEAN JOURNAL OF NEUROSCIENCE, 31 (4), pp. 742-753.
    doi: 10.1111/j.1460-9568.2010.07104.x
    Full text is available at: http://epubs.surrey.ac.uk/7455/
  • Fan L, Sawbridge D, George V, Teng L, Bailey A, Kitchen I, Li J-M. (2009) 'Chronic Cocaine-Induced Cardiac Oxidative Stress and Mitogen-Activated Protein Kinase Activation: The Role of Nox2 Oxidase'. AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 328 (1), pp. 99-106.
    doi: 10.1124/jpet.108.145201
  • Castane A, Wells L, Soria G, Hourani S, Ledent C, Kitchen I, Opacka-Juffry J, Maldonado R, Valverde O. (2008) 'Behavioural and biochemical responses to morphine associated with its motivational properties are altered in adenosine A(2A) receptor knockout mice'. WILEY-BLACKWELL BRITISH JOURNAL OF PHARMACOLOGY, 155 (5), pp. 757-766.
    doi: 10.1038/bjp.2008.299
    Full text is available at: http://epubs.surrey.ac.uk/185381/
  • Bailey A, Metaxas A, Yoo JH, McGee T, Kitchen I. (2008) 'Decrease of D-2 receptor binding but increase in D-2-stimulated G-protein activation, dopamine transporter binding and behavioural sensitization in brains of mice treated with a chronic escalating dose 'binge' cocaine administration paradigm'. BLACKWELL PUBLISHING EUR J NEUROSCI, 28 (4), pp. 759-770.
    doi: 10.1111/j.1460-9568.2008.06369.x
    Full text is available at: http://epubs.surrey.ac.uk/7456/

    Abstract

    Understanding the neurobiology of the transition from initial drug use to excessive drug use has been a challenge in drug addiction. We examined the effect of chronic 'binge' escalating dose cocaine administration, which mimics human compulsive drug use, on behavioural responses and the dopaminergic system of mice and compared it with a chronic steady dose (3 x 15 mg/kg/day) 'binge' cocaine administration paradigm. Male C57BL/6J mice were injected with saline or cocaine in an escalating dose paradigm for 14 days. Locomotor and stereotypy activity were measured and quantitative autoradiographic mapping of D(1) and D(2) receptors, dopamine transporters and D(2)-stimulated [(35)S]GTPgammaS binding was performed in the brains of mice treated with this escalating and steady dose paradigm. An initial sensitization to the locomotor effects of cocaine followed by a dose-dependent increase in the duration of the locomotor effect of cocaine was observed in the escalating but not the steady dose paradigm. Sensitization to the stereotypy effect of cocaine and an increase in cocaine-induced stereotypy score was observed from 3 x 20 to 3 x 25 mg/kg/day cocaine. There was a significant decrease in D(2) receptor density, but an increase in D(2)-stimulated G-protein activity and dopamine transporter density in the striatum of cocaine-treated mice, which was not observed in our steady dose paradigm. Our results document that chronic 'binge' escalating dose cocaine treatment triggers profound behavioural and neurochemical changes in the dopaminergic system, which might underlie the transition from drug use to compulsive drug use associated with addiction, which is a process of escalation.

  • Lena I, Bradshaw S, Pintar J, Kitchen I. (2008) 'Adaptive changes in the expression of central opioid receptors in mice lacking the dopamine D2 receptor gene'. PERGAMON-ELSEVIER SCIENCE LTD NEUROSCIENCE, 153 (3), pp. 773-788.
    doi: 10.1016/j.neuroscience.2008.02.070
  • Ribe D, Sawbridge D, Thakur S, Hussey M, Ledent C, Kitchen I, Hourani S, Li J-M. (2008) 'Adenosine A(2A) receptor signaling regulation of cardiac NADPH oxidase activity'. ELSEVIER SCIENCE INC FREE RADICAL BIOLOGY AND MEDICINE, 44 (7), pp. 1433-1442.
    doi: 10.1016/j.freeradbiomed.2007.12.035
  • Bailey A, Yoo JH, Racz I, Zimmer A, Kitchen I. (2007) 'Preprodynorphin mediates locomotion and D-2 dopamine and mu-opioid receptor changes induced by chronic 'binge' cocaine administration'. BLACKWELL PUBLISHING JOURNAL OF NEUROCHEMISTRY, 102 (6), pp. 1817-1830.
    doi: 10.1111/j.1471-4159.2007.04661.x
    Full text is available at: http://epubs.surrey.ac.uk/242873/
  • Cabello J, Bailey A, Kitchen I, Prydderch M, Clark A, Turchetta R, Wells K. (2007) 'Digital autoradiography using room temperature CCD and CMOS imaging technology'. IOP PUBLISHING LTD PHYSICS IN MEDICINE AND BIOLOGY, 52 (16), pp. 4993-5011.
    doi: 10.1088/0031-9155/52/16/019
  • Hussey MJ, Clarke GD, Ledent C, Hourani SMO, Kitchen I. (2007) 'Reduced response to the formalin test and lowered spinal NMDA glutamate receptor binding in adenosine A(2A) receptor knockout mice'. ELSEVIER SCIENCE BV PAIN, 129 (3), pp. 287-294.
    doi: 10.1016/j.pain.2006.10.014
  • Godfrey L, Bailey I, Toms NJ, Clarke GD, Kitchen I, Hourani SMO. (2007) 'Paracetamol inhibits nitric oxide synthesis in murine spinal cord slices'. ELSEVIER SCIENCE BV EUROPEAN JOURNAL OF PHARMACOLOGY, 562 (1-2), pp. 68-71.
    doi: 10.1016/j.ejphar.2007.01.075
    Full text is available at: http://epubs.surrey.ac.uk/185433/
  • Hammers A, Asselin M-C, Hinz R, Kitchen I, Brooks DJ, Duncan JS, Koepp MJ. (2007) 'Upregulation of opioid receptor binding following spontaneous epileptic seizures'. OXFORD UNIV PRESS BRAIN, 130, pp. 1009-1016.
    doi: 10.1093/brain/awm012
  • Godfrey L, Yan L, Clarke GD, Ledent C, Kitchen I, Hourani SMO. (2006) 'Modulation of paracetamol antinociception by caffeine and by selective adenosine A(2) receptor antagonists in mice'. ELSEVIER SCIENCE BV EUROPEAN JOURNAL OF PHARMACOLOGY, 531 (1-3), pp. 80-86.
    doi: 10.1016/j.ejphar.2005.12.004
    Full text is available at: http://epubs.surrey.ac.uk/185970/
  • Connor M, Kitchen I. (2006) 'Has the sun set on kappa(3)-opioid receptors?'. NATURE PUBLISHING GROUP BRITISH JOURNAL OF PHARMACOLOGY, 147 (4), pp. 349-350.
    doi: 10.1038/sj.bjp.0706603

Conference papers

  • Fan L, Sawbridge D, Bailey A, Kitchen I, Li J-M. (2008) 'The mechanism of chronic cocaine exposure on cardiac reactive oxygen species production and mitogen-activated protein kinase activation'. B M J PUBLISHING GROUP HEART, Manchester, ENGLAND: Annual Scientific Conference of the British-Cardiovascular-Society/British-Society-for-Cardiovascular-Research 94, pp. A115-A115.
  • Fan L, Sawbridge D, Bailey A, Kitchen I, Li J-M. (2008) 'The role of NADPH oxidase in cocaine-induced cardiac oxidative stress and redox signalling'. ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, Athens, GREECE: 28th Annual Meeting of the European Section of the International-Society-for-Heart-Research 44 (4), pp. 713-713.
    doi: 10.1016/j.yjmcc.2008.02.007
  • Ferre S, Diamond I, Goldberg SR, Yao L, Hourani SMO, Huang ZL, Urade Y, Kitchen I. (2007) 'Adenosine A(2A) receptors in ventral striatum, hypothalamus and nociceptive circuitry - Implications for drug addiction, sleep and pain'. PERGAMON-ELSEVIER SCIENCE LTD PROGRESS IN NEUROBIOLOGY, Boston, MA: International Research Conference on Targeting Adenosine A2A Receptons in Parkinson's Disease and other CNS Disorders 83 (5), pp. 332-347.
    doi: 10.1016/j.pneurobio.2007.04.002
  • Cabello J, Wells K, Metaxas A, Bailey A, Kitchen I, Clark A, Prydderch A, Turchetta R. (2007) 'Digital Autoradiography imaging using CMOS technology: First Tritium Autoradiography with a back-thinned CMOS detector and comparison of CMOS imaging performance with autoradiography film'. IEEE 2007 IEEE NUCLEAR SCIENCE SYMPOSIUM CONFERENCE RECORD, VOLS 1-11, Honolulu, HI: IEEE Nuclear Science Symposium/Medical Imaging Conference, pp. 3743-3746.
    doi: 10.1109/NSSMIC.2007.4436936
  • Cabello J, Wells K, Bailey A, Kitchen I. (2007) 'Semi-automatic elastic registration applied to a beta-autoradiography brain atlas'. IEEE 2007 IEEE NUCLEAR SCIENCE SYMPOSIUM CONFERENCE RECORD, VOLS 1-11, Honolulu, HI: IEEE Nuclear Science Symposium/Medical Imaging Conference, pp. 4303-4307.
    doi: 10.1109/NSSMIC.2007.4437068
  • Cabello J, Wells K, Bailey A, Kitchen I, Clark A, Crooks J, Halsall R, Key-Charriere M, Martin S, Prydderch M, Turchetta R. (2007) 'Digital autoradiography using CCD and CMOS imaging technology'. IEEE Nuclear Science Symposium Conference Record, 4, pp. 2607-2612.
    doi: 10.1109/NSSMIC.2006.354442
  • Kitchen I. (2006) 'Gene knockouts and the neuroscience of addiction'. BLACKWELL PUBLISHING ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, Sydney, AUSTRALIA: World Congress on Alcohol Research 30 (9), pp. 45A-45A.
  • Kitchen I. (2006) 'Opioid receptors: What, where and how?'. BLACKWELL PUBLISHING EPILEPSIA, Helsinki, FINLAND: 7th European Congress on Epileptology 47, pp. 222-223.

Teaching

Prof Kitchen has taught CNS pharmacology to undergraduate and postgraduate students on Biochemistry, Pharmacology, Neuroscience, Nursing and Toxicology degree programmes at Surrey. 

Departmental Duties

  • Associate Dean, Faculty of Health and Medical Sciences
  • University Warden of Sports Colours
  • Director, Experimental Biology Unit

Affiliations

  • 1980-Present British Pharmacological Society (Elected Fellow in 2006)
  • 2011-Present Society of Biology (Elected Fellow)