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Opioids and Neuropathic Pain Laboratory

Head of laboratory

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Overview of research program

Humans often experience long periods of pain as an unwanted legacy of injury and disease. Unfortunately this chronic pain continues even when there is complete recovery from the underlying condition that triggered the pain in the first place. Our group studies biological mechanisms in the nervous system that either sustain or intensify pain for long periods, or reduce the pain-relieving properties of opioids and other analgesic drugs. We are especially interested in how chronic pain is caused by neuronal plasticity associated with pathological changes in the functioning or structure of nerve cells in pain circuits.

We are currently engaged in non-human research investigating:

  1. pain in the context of spinal cord and peripheral nerve injury,
  2. pelvic pain and the role of circulating estrogens,
  3. opioid-induced hyperalgesia, and
  4. mechanisms of opioid receptor desensitization.

Pain research is inherently multidisciplinary and this is reflected by our use of electrophysiological recording, functional anatomical mapping, advanced cellular imaging methods and behavioral testing in our research. Various combination of these techniques have been used to study cell lines transfected with opioid receptors, cultured sensory neurons, spinal cord and brain slices, and for whole-animal studies.

Our recent research outcomes include:

  • Publication of the most extensive analysis to date of how an injury to the spinal cord affects the organization of the sensory circuits above the site of injury. This provides a new basis for understanding causes of at-level neuropathic pain.
  • Identification of a link between the central amygdala, which is part of the emotional brain circuitry, and anomalous increases in pain elicited by brief exposures to morphine.
  • First demonstration of an overlap involving the major endogenous dynorphin/kappa-opioid receptor brain system, and the amygdala CRH (corticotrophin releasing hormone) system that facilitates fear, stress and anxiety.
  • Demonstration of a novel inhibitory effect of estrogen on the capsaicin receptor TRPV1 in female rat dorsal root ganglia sensory neurons. This identifies a biological mechanism by which a drop in circulating estrogens could lead to increased activity of this major pain transducer. This is consistent with clinical observations that pelvic pain is facilitated by menopause and other conditions that reduce circulating estrogens.
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Major funding sources

  • National Institutes of Health (US)
  • NSW Office of Science and Medical Research (Spinal Cord Injury and Related Neurological Conditions Program)
  • Australia and New Zealand College of Anaesthetists
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Selected publications

Xu S, Cheng Y, Keast JR, Osborne PB. 17beta-estradiol activates estrogen receptor beta-signalling and inhibits transient receptor potential vanilloid receptor 1 activation by capsaicin in adult rat nociceptor neurons. Endocrinology 2008 149:5540-5548.

Marchant NJ, Densmore VS, Osborne PB (2007) Coexpression of prodynorphin and corticotrophin-releasing hormone in the rat central amygdala: evidence of two distinct endogenous opioid systems in the lateral division. Journal of Comparative Neurology 2007 504:702-715.

Kalous A, Osborne PB, Keast JR. Acute and chronic changes in dorsal horn innervation by primary afferents and descending supraspinal pathways after spinal cord injury. Journal of Comparative Neurology. 2007 504:238-253.

Hamlin AS, McNally GP, Osborne PB. Induction of c-Fos and zif268 in the nociceptive amygdala parallel abstinence hyperalgesia in rats briefly exposed to morphine. Neuropharmacology. 2007 53:330-343.

Chieng BC, Christie MJ, Osborne PB. Characterization of neurons in the rat central nucleus of the amygdala: cellular physiology, morphology, and opioid sensitivity. Journal of Comparative Neurology. 2006 497:910-927.

Buller KM, Hamlin AS, Osborne PB. Dissection of peripheral and central endogenous opioid modulation of systemic interleukin-1beta responses using c-fos expression in the rat brain. Neuropharmacology. 2005 49:230-242.

Borgland SL, Connor M, Osborne PB, Furness JB, Christie MJ. Opioid agonists have different efficacy profiles for G protein activation, rapid desensitization, and endocytosis of mu-opioid receptors. Journal of Biological Chemistry. 2003 278:18776-18784.

Kanjhan R, Osborne PB, Ouyang M, Keast JR. Postnatal maturational changes in rat pelvic autonomic ganglion cells: a mixture of steroid-dependent and -independent effects. Journal of Neurophysiology 2003 89:315-323.

Hamlin A, Buller KM, Day TA, Osborne PB. Peripheral withdrawal recruits distinct central nuclei in morphine-dependent rats. Neuropharmacology 200141:574-581.

Osborne PB, Vaughan CW, Wilson HI, Christie MJ. Opioid inhibition of rat periaqueductal grey neurones with identified projections to rostral ventromedial medulla in vitro. Journal of Physiology. 1996 490:383-389.

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Major collaborations

  • Professor Robert Callister and Dr Brett Graham, University of Newcastle
  • Dr Stephen Petrou, Howard Florey Institute
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Research project opportunities

Supervised by Dr Peregrine Osborne

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