Long-lasting hyperexcitability induced by depolarization in the absence of detectable Ca2+ signals.

Learning and memory depend on neuronal alterations induced by electrical activity. Most examples of activity-dependent plasticity, as well as adaptive responses to neuronal injury, have been linked explicitly or implicitly to induction by Ca(2+) signals produced by depolarization. Indeed, transient Ca(2+) signals are commonly assumed to be the only effective transducers of depolarization into adaptive neuronal responses. Nevertheless, Ca(2+)-independent depolarization-induced signals might also trigger plastic changes. Establishing the existence of such signals is a challenge because procedures that eliminate Ca(2+) transients also impair neuronal viability and tolerance to cellular stress. We have taken advantage of nociceptive sensory neurons in the marine snail Aplysia, which exhibit unusual tolerance to extreme reduction of extracellular and intracellular free Ca(2+) levels. The axons of these neurons exhibit a depolarization-induced memory-like hyperexcitability that lasts a day or longer and depends on local protein synthesis for induction. Here we show that transient localized depolarization of these axons in an excised nerve-ganglion preparation or in dissociated cell culture can induce short- and intermediate-term axonal hyperexcitability as well as long-term protein synthesis-dependent hyperexcitability under conditions in which Ca(2+) entry is prevented (by bathing in nominally Ca(2+) -free solutions containing EGTA) and detectable Ca(2+) transients are eliminated (by adding BAPTA-AM). Disruption of Ca(2+) release from intracellular stores by pretreatment with thapsigargin also failed to affect induction of axonal hyperexcitability. These findings suggest that unrecognized Ca(2+)-independent signals exist that can transduce intense depolarization into adaptive cellular responses during neuronal injury, prolonged high-frequency activity, or other sustained depolarizing events.

The experience and meaning of injury among migrant farmworkers from Starr County, Texas

Occupational injuries suffered by migrant farmworkers in the United States continue to be a significant byproduct of the hazards of the agricultural work sector. Although the fields of study involving occupational health and safety have helped to further an understanding of the importance of injury prevention in the workplace, farmworkers have typically not been the beneficiaries of significant improvement in working conditions; similarly, public health policies have generally not been successful in significantly improving their protection. The primary objective of this research was to examine more closely, through in-depth interviews, the underlying reasons attributed by migrant farmworkers to their having suffered occupational injuries. By re-contacting and re-interviewing migrant farmworkers who had reported injuries in a study entitled A Cohort Study of Injuries in Migrant Farmworker Families in South Texas, the current research study employed qualitative research methods and determined several reasons that may help to explain why this specific group has suffered injuries and may not have reported such injuries, as well as to consider what their experiences may say about injury prevention within the context of public health.^