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Habitat requirements of wild boar in the northern Apennines (N. Italy): a multi-level approach.
No full textIdentification of delayed potassium and calcium currents in the rat sympathetic neurone under voltage clamp
No full textPost-ganglionic neurones of the isolated rat superior cervical ganglion were studied at 37 degrees C under two-electrode voltage-clamp conditions. Membrane depolarization beyond -40 mV from holding levels between -50 and -100 mV produced a delayed outward current which exhibited no inactivation within this voltage range. The current is carried primarily by K+ ions and its instantaneous I-V relation is linear. The total outward current could be separated into two distinct components on the basis of ion-substitution experiments. A voltage-dependent component of the delayed current, termed IK(V), is activated by membrane depolarization beyond -40 mV when Ca2+ fluxes are selectively blocked by Cd2+ or in Ca2+-free solution. IK(V) develops following first-order kinetics and rises to a peak with a voltage-dependent delay (239 ms at -30 mV and 23 ms at +10 mV). GK(V) attains a saturating value of the order of 17 mS/cm2 at about +20 mV and can be described in terms of a simple Boltzmann distribution for a single gating particle with a valency equal to +2.5. A second component of the delayed outward current, termed IK(Ca), depends on Ca2+ entry for its activation and was isolated as difference current before and after block of Ca2+ movements across the membrane. IK(Ca) is larger and faster than IK(V): it is strictly related to Ca2+ influx and also depends on membrane potential depolarization. A distinct Ca2+ current, ICa, was recorded from the neurone exposed to Na+-free or tetrodotoxin solution. ICa was activated by membrane depolarization beyond -30 mV and reached a maximum value near 0 mV. Its activation agrees with fourth-order kinetics and becomes faster with increasing depolarization. The Ca2+ current developed with a voltage-dependent time to peak of 2.9-1.8 ms and thereafter completely inactivated. The relationship between ICa and IK(Ca) is discussed. The Ca2+-k+ repolarizing system is expected to be mainly associated with action potentials arising from a depolarized neurone, whereas the IA current (Belluzzi, Sacchi & Wanke, 1985) dominates the repolarization mechanism at the normal membrane potential. The effect of muscarine was examined. Muscarine (10-50 microM) produced a fall in conductance with a voltage dependence similar to that exhibited by GK(Ca) and was ineffective when removing extracellular Ca2+ or adding Cd2+. A partial suppression of ICa by muscarine is demonstrated. It is suggested that the decrease of the outward current magnitude in the presence of muscarine may be accounted for qualitatively by the reduction in ICa
Post-tetanic spontaneous spike activity in rat sympathetic neurons exposed to low potassium ion concentration.
No full textPreganglionic tetanic stimulation (30 sec at 50/sec) of rat superior cervical ganglia, performed in the presence of reduced external potassium concentration (0-1 mM), is followed by a long-lasting postganglionic afterdischarge which fails to appear if stimulation is repeated in normal (5.6 mM) postassium solution. Intracellular recordings revealed that tetanus is followed by 15-30 mV membrane hyperpolarization when the neuron is exposed to normal concentrations of potassium. Conversely, after the ganglion is soaked in low potassium, stimulation results in long-lasting depolarization of the nerve cell with the consequent appearance of spontaneous spikes. This effect is reversed on returing to normal external potassium. Spontaneous activity also occurs after antidromic activation of the cell. It is suggested that tetanus causes sodium loading of the neuron, which leads to stimulation of an electrogenic sodium pump. If potassium is available, the membrane will hyperpolarize, whereas depolarization and pacemaker activity ensues if external potassium is removed. The electrogenic sodium pump thus endows. the rat sympathetic neuron with a mechanism which enables it excitability to be controlled
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Participation of a Chloride Conductance in the Subthreshold Behavior of the Rat Sympathetic Neuron
No full textELECTROPHYSIOLOGICAL EFFECTS OF A NEUROTOXIN EXTRACTED FROM THE SKIN OF THE AUSTRALIAN FROG PSEUDOPHRYNE-CORIACEA
No full text1. The electrophysiological effects of a pumiliotoxin-B-like alkaloid extracted from the skin of the Australian frog Pseudophryine coriacea (PsC) have been studied in rat superior cervical ganglia at 37-degrees-C. 2. PsC (50 mg/ml) elicits a broadening of the evoked compound action potential and, at rest, the appearance of spontaneous spike discharge at 10-20 Hz. Action potentials presumably originate far away from the soma, which is invaded in a typical IS-SD sequence. 3. The toxin effect is not related to any direct action on the preganglionic fibers of the sympathetic trunk, and does not involve synaptic mechanisms. 4. Two-electrode voltage-clamp experiments showed that the main properties of the major voltage-dependent ionic currents are apparently unaffected by the toxin, while the cell input resistance is considerably reduced. 5. The data are consistent with the hypothesis that PsC elicits a cationic permeability increase generating a pacemaker current in a region close to the cell soma
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