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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, and electrophysiological
recordings from neurons in slices of the spinal cord or brainstem. 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 early studies focused on how these neurotransmitter
systems dictate responses to acute or transient nociception. More recent
investigations have focused on the role of these neurotransmitters in
the response of the central nervous system to peripheral injury and
the occurrence of persistent pain in either the neonate or the adult.
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
for the control of pain. 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.
Representative publications:
Zhang, L., Sykes, K.T., Buhler, A.V., Hammond, D.L.: Electrophysiological heterogeneity of spinally projecting serotonergic and nonserotonergic neurons in the rostral ventromedial medulla. J Neurophysiol. 95(3):1853-1863, 2006.
Hammond,
D.L., Ackerman, L., Holdsworth, R., Elzey, B.: Effects of spinal nerve
ligation on Immunohistochemically identified neurons in the L4 and L5
dorsal root ganglia of the rat. J. Comp. Neurol. 475:575-589,
2004.
Hurley,
R.W. and Hammond, D.L.: Contribution of endogenous enkephalins to the
enhanced analgesic effects of supraspinal mu opioid receptor agonists
after inflammatory injury. J. Neurosci. 21:2536-2545,
2001.
Oh,
S.B., Tran, P.B., Gillard, S.E., Hurley, R.W., Hammond, D.L. and Miller,
R.J.: Chemokines and glycoprotein120
produce pain hypersensitivity by directly exciting primary nociceptive
neurons. J. Neurosci. 21:5027-5035,
2001.
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here to see a list of additional publications
Center and Program affiliations:
Biosciences
Program
Medical Scientist Training Program
Interdisciplinary Graduate
Program in Neurosciences |
