Patients suffering from chronic pain often report that pain onset was preceded by an acute episode of peripheral inflammation or trauma. Previous findings demonstrate peripheral challenge can result in long-term changes in central nervous system astrocytes and microglia, possibly indicative of glial priming. By definition, primed cells can respond in an exaggerated manner to subsequent challenge. If priming were to occur in spinal cord glia, chronic pain may result on account of enhanced release of glial inflammatory products. In the current series of experiments, evidence for spinal glial priming was evaluated in two different animal models: subcutaneous inflammation via intraplantar injection of formalin and peripheral injury/inflammation associated with abdominal surgery (laparotomy). Evidence for spinal glial priming was assessed in each model following secondary challenge (2 weeks later) with intrathecal HIV-1 gp120, to directly stimulate spinal glia and induce glially-mediated pain enhancement. Changes in glial proinflammatory cytokine production and behavioral response thresholds to tactile stimuli were examined. Prior laparotomy followed by a later challenge does indeed lead to enhanced proinflammatory cytokine protein levels in the spinal cord. Examination of prior laparotomy on response thresholds are ongoing. Bilateral enhancement of pain behavior was seen in response to gp120 subsequent to unilateral subcutaneous inflammation 2 weeks before. Analyses of glial activation markers are underway to determine whether prior laparotomy or formalin result in exaggerated microglial and/or astrocytic response to gp120 injection. Taken together, these data suggest that spinal cord glia may be primed for extended periods of by a variety of stimuli, possibly leading to subsequent over-response to challenge.

A number of experiments have shown that hydrogen molecules can migrate on films of solid hydrogen. This was thought to be a diffusive process but recent experimental findings have led others to a different conclusion, so a question remains about the process by which the hydrogen molecules migrate over their own solid surface. We report new measurements using a hole-burning technique which confirm these recent experiments but we interpret them differently. We have developed a model for the recovery of the hydrogen which accounts for these results and shows that the H2 does move diffusively. The diffusion is thermally activated and we have determined the diffusion constant, D0=4.03×10−4±2.5×10−5 m2s−1, and the activation energy, E=43±7 K, for hydrogen.

We describe a method to determine the flow impedance of a submonolayer of a normal4He film on a strong binding substrate. The flow impedance should be a characteristic of the substrate and we hope to use it to detect surface changes that occur at low temperatures. We describe preliminary measurements of the flow rate as a function of the chemical potential difference, Δμ, along the flow path. The differential flow impedance changes radically with Δμ which we ascribe to the thickness of the free liquid layer going to zero at one end of the flow path.