PubMed · 15034555
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Dominique Debanne. 2004. Information processing in the axon.. https://doi.org/10.1038/nrn1397
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The aim of the present study was to investigate how prostaglandin E2 (PGE2) affects the excitability of trigeminal root ganglion (TRG) neurons, projecting onto the superficial layer of the cervical dorsal horn, using fluorescence retrograde tracing and perforated patch-clamp techniques. TRG neurons were retrogradely labeled with fluorogold (FG). The cell diameter of FG-labeled neurons was small (< 30 microm). Under the voltage-clamp mode, application of PGE2 (0.01-10 microM) concentration-dependently increased the magnitude of the peak tetrodotoxin-resistant sodium current (TTX-R I(Na)) and this current was maximal at a concentration of 1 microM. One micromolar PGE2 application caused a hyperpolarizing shift of 8.3 mV in the activation curve for TTX-R I(Na). In the current-clamp mode, the PGE2 (1 microM) application significantly increased the number of action potentials during the depolarizing step pulses as well as the level of overshoot but had no significant effect on the resting membrane potential. These results suggest that the excitability of small diameter TRG neurons seen after 1 microM PGE2 application is involved in an increase in the
The flexor carpi ulnaris is a useful local muscle flap in the forearm and elbow. It is, however, an important palmar flexor and ulnar deviator of the wrist, and functional loss may arise from the use of this muscle in its entirety. The flexor carpi ulnaris is made up of two distinct neuromuscular compartments. This arrangement allows for splitting of the muscle and the potential use of the larger ulnar compartment as a local muscle flap while maintaining the humeral compartment as an ulnar deviator and palmar flexor of the wrist. We report two cases illustrating the clinical use of the split flexor carpi ulnaris as a local muscle flap.
Ocular dominance plasticity is enhanced by sleep and reduced by sleep deprivation or when all neural activity in the sleeping visual cortex is reversibly inhibited. These latter findings demonstrate that the mechanisms responsible for the effects of sleep on cortical plasticity are activity dependent. To better isolate this activity dependent mechanism, we investigated the role of postsynaptic activity by inactivating the sleeping visual cortex after a period of monocular deprivation with the gamma-amino-n-butyric acid agonist muscimol. Microelectrode recordings showed that ocular dominance plasticity was significantly reduced in cortices reversibly silenced during sleep compared with cortices infused with vehicle only. These findings demonstrate that postsynaptic activity during sleep is required for the consolidation of experience-dependent cortical plasticity.