Discordance of Gross and Histologic Findings in Estimating the Range of Fire of Gunshot Wounds.

Forensic pathologist use soot and/or stippling surrounding entrance gunshot wounds in categorizing range of fire. If absent, some pathologists suggest utilizing histology when the range is diagnostically critical. This study investigates the concordance of macroscopic and microscopic findings in estimating range of fire by evaluating gunshot entrance and exit wounds made through human tissue analogs at defined distances using two handgun calibers.

Effect of electrical field stimulation on dorsal root ganglion neuronal function.

Objectives: Neural stimulation may provide analgesia for a variety of painful conditions. Activation of primary sensory neurons, which underlies pain relief by spinal cord stimulation, also may be achieved by stimulation at the level of the dorsal root ganglion (DRG). The DRG also is a site of pain pathogenesis, particularly in neuropathic pain.

Failure of action potential propagation in sensory neurons: mechanisms and loss of afferent filtering in C-type units after painful nerve injury.

The T-junction of sensory neurons in the dorsal root ganglion (DRG) is a potential impediment to action potential (AP) propagation towards the CNS. Using intracellular recordings from rat DRG neuronal somata during stimulation of the dorsal root, we determined that the maximal rate at which all of 20 APs in a train could successfully transit the T-junction (following frequency) was lowest in C-type units, followed by A-type units with inflected descending limbs of the AP, and highest in A-type units without inflections. In C-type units, following frequency was slower than the rate at which AP trains could be produced in either dorsal root axonal segments or in the soma alone, indicating that the T-junction is a site that acts as a low-pass filter for AP propagation.

Ca²⁺-dependent regulation of Ca²⁺ currents in rat primary afferent neurons: role of CaMKII and the effect of injury.

Currents through voltage-gated Ca²⁺ channels (I(Ca)) may be regulated by cytoplasmic Ca²⁺ levels ([Ca²⁺](c)), producing Ca²⁺-dependent inactivation (CDI) or facilitation (CDF). Since I(Ca) regulates sensory neuron excitability, altered CDI or CDF could contribute to pain generation after peripheral nerve injury. We explored this by manipulating [Ca²⁺](c) while recording I(Ca) in rat sensory neurons.

Store-operated Ca2+ entry in sensory neurons: functional role and the effect of painful nerve injury.

Painful nerve injury disrupts levels of cytoplasmic and stored Ca(2+) in sensory neurons. Since influx of Ca(2+) may occur through store-operated Ca(2+) entry (SOCE) as well as voltage- and ligand-activated pathways, we sought confirmation of SOCE in sensory neurons from adult rats and examined whether dysfunction of SOCE is a possible pathogenic mechanism. Dorsal root ganglion neurons displayed a fall in resting cytoplasmic Ca(2+) concentration when bath Ca(2+) was withdrawn, and a subsequent elevation of cytoplasmic Ca(2+) concentration (40 ± 5 nm) when Ca(2+) was reintroduced, which was amplified by store depletion with thapsigargin (1 μm), and was significantly reduced by blockers of SOCE, but was unaffected by antagonists of voltage-gated membrane Ca(2+) channels.

Calcium signaling in intact dorsal root ganglia: new observations and the effect of injury.

Background: Ca is the dominant second messenger in primary sensory neurons. In addition, disrupted Ca signaling is a prominent feature in pain models involving peripheral nerve injury. Standard cytoplasmic Ca recording techniques use high K or field stimulation and dissociated neurons.