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Hammond Laboratory

Donna Hammond

Donna Hammond, PhD
Professor and Vice Chair for Research

Research Interests

The overall goal of our research is to gain a better understanding of the neuroanatomy, neurophysiology and neuropharmacology of the central nervous system pathways that convey pain, as well as the bulbospinal pathways that modulate the transmission of nociceptive information. Our studies emphasize a systems-level approach that uses many different methodologies in concert, including behavioral pharmacology in normal, transgenic or knockout animals, neuroanatomical tract tracing, immunocytochemical labeling of neurons, measurement of neurotransmitter release by push-pull perfusion or microdialysis, patch clamp recordings from neurons in slices of the spinal cord or brainstem and elementary molecular biology. We are particularly interested in the role that inhibitory neurotransmitters, such as gamma-aminobutyric acid (GABA) or the endogenous opioid peptides, play in the modulation of nociceptive sensitivity at the level of the spinal cord and brainstem. Our very early studies focused on how these neurotransmitter systems dictate responses to acute or transient nociception. Our current investigations focus on the role of these neurotransmitters in the response of the central nervous system to peripheral injury and the subsequent development of persistent pain. Our results indicate that persistent pain can lead to long-term changes in the pharmacology and physiology of both the afferent pathways that convey pain, as well as the efferent pathways that suppress pain. These changes have significant consequences for the ability of drugs to produce analgesia and for the body to invoke its own homeostatic mechanisms to control pain. The mechanisms that underlie the plasticity of central nervous system pathways in response to persistent neuropathic and inflammatory pain will continue to be a focus of our work in the future.


  • Zhang, L. & Hammond, D.L. (2009). Substance P enhances excitatory synaptic transmission to spinally projecting neurons in the rostral ventromedial medulla after inflammatory injury. J Neurophysiol; 102:1139-1151.  [PubMed]
  • Jongeling, A.C., Johns, M.E., Murphy, A.Z., & Hammond, D.L. (2009). Persistent inflammatory pain decreases the antinociceptive effects of the mu opioid receptor agonist DAMGO in the locus coeruleus of male rats. Neuropharmacology; 56(6-7):1017-1026. [PubMed]
  • Price, T.J., Cervero, F., Gold, M.S., Hammond, D.L., & Prescott, S.A. (2009). Chloride regulation in the pain pathway. Brain Res Rev. 2009;60(1):149-70. [PubMed]
  • Sykes, K.T., White, S.R., Hurley, R.W., Mizoguchi, H., Tseng, L.F., & Hammond, D.L. (2007). Mechanisms responsible for the enhanced antinociceptive effects of micro-opioid receptor agonists in the rostral ventromedial medulla of male rats with persistent inflammatory pain. J Pharmacol Exp Ther; 322(2):813-21. [PubMed]