RESUMEN
The noise-delayed decay (NDD) phenomenon emerges when the first-spike latency of a periodically forced stochastic neuron exhibits a maximum for a particular range of noise intensity. Here, we investigate the latency response dynamics of a single Hodgkin-Huxley neuron that is subject to both a suprathreshold periodic stimulus and a background activity arriving through dynamic synapses. We study the first-spike latency response as a function of the presynaptic firing rate f. This constitutes a more realistic scenario than previous works, since f provides a suitable biophysically realistic parameter to control the level of activity in actual neural systems. We first report on the emergence of classical NDD behavior as a function of f for the limit of static synapses. Second, we show that when short-term depression and facilitation mechanisms are included at the synapses, different NDD features can be found due to their modulatory effect on synaptic current fluctuations. For example, an intriguing double NDD (DNDD) behavior occurs for different sets of relevant synaptic parameters. Moreover, depending on the balance between synaptic depression and synaptic facilitation, single NDD or DNDD can prevail, in such a way that synaptic facilitation favors the emergence of DNDD whereas synaptic depression favors the existence of single NDD. Here we report the existence of the DNDD effect in the response latency dynamics of a neuron.
RESUMEN
A 55-year-old woman was seen in the Plastic and Reconstructive Surgery Clinic because of a nonhealing wound on her left leg of approximately 2 months' duration. She had an 8-month history of multiple wounds appearing on her arms and legs. The patient noted that the majority of the wounds had been treated and healed with the use of topical medications. One wound on her left leg had continued to enlarge rapidly despite topical treatments. Therefore, hyperbaric oxygen therapy had been administered for 15 sessions. No additional healing had occurred with this treatment. Skin grafting was performed on the affected area. She developed ulcers and blistering lesions at surgical and nonsurgical sites after skin grafting. The patient was referred to the Dermatology Department. Dermatologic examination revealed a deep, necrotic ulcer, 30 cm x 10 cm, with surrounding violaceous erythema on the donor area, ulceration (18 cm x 8 cm) on the graft area, a hemorrhagic bullous plaque (5 cm x 15 cm) over the right malleolus, scattered ecchymotic lesions and small hemorrhagic bullae on both legs, and small pustules around the staplers (Fig. 1a,b). Cutaneous biopsy of a new lesion revealed a focal, dense neutrophilic infiltrate, liquefaction degeneration in the center, lymphocytic and mild plasmacytic infiltration around the venules, and fibrinoid deposits in the walls and lumen of the vessels (Fig. 2a). In addition, excessive polymorphonuclear leukocytes and extravasated erythrocytes were present in the papillary and reticular dermis (Fig. 2b). The patient had a 14-year history of asthma bronchiale. Physical examination did not reveal any abnormality, except for crackling rales at the base of each lung. Laboratory examinations were within normal limits, except for the sedimentation rate (55 mm/h). Protein electrophoresis, peripheral blood smear, abdominal ultrasound, and thorax and abdominopelvic computed tomography scans were all normal. Swab cultures from the ulcers were negative. Bullous pyoderma gangrenosum was diagnosed on clinical and histopathologic grounds. Prednisolone 80 mg/day was started. Rapid epithelialization was observed within 2 months of treatment. The dose of prednisolone was gradually decreased to 20 mg/day, and was used as a maintenance dose for an additional 6 months. Complete improvement was achieved in 8 months. The patient has been followed up for approximately 1 year. There were no side effects observed during the treatment and in addition no new lesions developed at the follow-up.
