Hammond Laboratory

Research Focus

The primary goal of my 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.