Joel Austin Black PhD

Research Scientist in Neurology; Associate Director, Yale Center for Neuroscience and Regeneration Research

Research Interests

Membrane structure in normal and pathological neurons and glia; Ion channel expression in normal and injured neurons; Neuro-glial interactions; Cell biology of neurological disease

Current Projects

  • Transplantation-Based Approaches toward Remyelination
  • Strategies for Neuroprotection following Brain and Spinal Cord Injury
  • Neuropathic Pain Syndromes Associated with Nerve and Spinal Cord Injuries
  • Molecular Basis for Restoration of Impulse Conduction within the Injured

Research Summary

Research in our laboratory is directed towards understanding the mechanisms that regulate and modulate the localization of ionic channels and pumps within the plasmalemma of neurons and glial cells, as the non-random distribution of these membrane proteins greatly influences the physiological properties of these cells. Currently, the laboratory is focused on determining the factors that govern the expression and spatial organization of voltage-sensitive sodium channels within astrocytes and Schwann cells, with the goal of establishing the molecular pathway(s) for the incorporation and stabilization of these channels in specific membrane regions. The laboratory is also interested in determining the relationship between astrocyte and Schwann cell processes and the distribution of specific molecules within axonal membranes. These studies utilize immuno-electron and indirect fluorescence microscopic techniques with in vivo and in vitro tissues.

Extensive Research Description

The Center's research is propelled by the dedication and hard work of its staff of established basic and clinical neuroscientists, as well as that of young investigators— MD/PhD students, graduate students, medical students—who choose to obtain training within the Center. Trainees are carefully mentored by senior investigators at the Center to become independent thinkers capable of tackling tough and challenging questions facing the field.

Major research projects include:

  • Transplantation-Based Approaches toward Remyelination
Spinal cord injury can result in necrosis of the spinal cord, but often white matter tracts outside of the necrotic core become demyelinated. In the absence of myelin, these damaged axons are unable to conduct nerve impulses just as if they have been severed. Loss of myelin leading to impaired conduction also occurs in multiple sclerosis, an inflammatory disease of the CNS that alone affects approximately 35,000 US veterans today. Center scientists are investigating transplantation of myelin-forming cells into the site of injury as an approach to induce remyelination of demyelinated axons and thereby restore impulse conduction.
  • Strategies for Neuroprotection following Brain and Spinal Cord Injury
Secondary degeneration of neural tissue, initially spared but adjacent to irreversibly damaged tissue, can lead to further, and often, irreversible neurological damage after the initial injury to the brain and spinal cord, via a process of secondary injury. We are studying a number of different approaches, both cell-based and pharmacological, that can limit secondary degeneration and preserve neurological function following trauma to the brain and spinal cord.
  • Neuropathic Pain Syndromes Associated with Nerve and Spinal Cord Injuries
One of the key disabling consequences of nerve and spinal cord injury is an excruciating form of pain called neuropathic pain. It is brought upon by the reprogramming of injured spinal sensory neurons such that they become hyperexcitable, abnormally firing away electrical impulses when they should not be. In over fifty percent of individuals with nerve injuries, neuropathic pain significantly impacts quality of life; existing medications are in many cases ineffective, or are only partially effective. We are investigating neuropathic pain, particularly the role of sodium channels and associated molecules/mechanisms in neuropathic pain, with the goal of identifying effective treatments.
  • Molecular Basis for Restoration of Impulse Conduction within the Injured
CNSPatients with the relapsing-remitting form of MS experience symptom-free intervals that sometimes range in the order of years, despite the persistence of demyelinated lesions along their axons. Such a recovery of function after injury to the brain and spinal cord, even in the absence of myelin, is called a remission, and it is due to a molecular reorganization within the axons such that transmission of nerve signals is restored. The Center’s goal is to induce remissions in all people with nerve injuries and is therefore investigating the phenomenon of molecular reorganization in MS, particularly the reorganization of sodium channels which serve as molecular batteries in generating and transmitting signals along axons.


Selected Publications

  • Dib-Hajj SD, Black JA, Waxman SG. Voltage-gated sodium channels: therapeutic targets for pain. Pain Med. 2009 Oct;10(7):1260-9.
  • Dib-Hajj SD, Choi JS, Macala LJ, Tyrrell L, Black JA, Cummins TR, Waxman SG. Transfection of rat or mouse neurons by biolistics or electroporation. Nat Protoc. 2009;4(8):1118-26. Epub 2009 Jul 9.

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