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F F Weight

Publications and source records attributed to F F Weight.

115 records · Page 7Linked to original sources
PubMed1970

Slow synaptic excitation in sympathetic ganglion cells: evidence for synaptic inactivation of potassium conductance.

The slow excitatory postsynaptic potential (EPSP) was investigated in frog sympathetic ganglion cells. In contrast to the increased conductance associated with other known EPSP's, during the slow EPSP resting membrane conductance was decreased. Electrical depolarization of the membrane potentiated the slow EPSP, whereas progressive hyperpolarization decreased its size and then reversed it to a hyperpolarizing potential (the opposite of the effect of membrane polarization on other EPSP's). The reversal potential of the slow EPSP was close to the potassium equilibrium potential. We propose that the slow EPSP, in contrast to classical EPSP's, is generated by an inactivation of resting potassium conductance.

Animals↗
PubMedDate not supplied

Detection of intracellular Ca2+ transients in sympathetic neurones using arsenazo III.

Changes in cytosolic calcium ion concentration ([Ca2+]i) have been implicated in a wide variety of cellular stimulus--transduction roles. In nerve cells, it is believed that electrical activity raises [Ca2+]i by allowing influx of Ca2+ through voltage-dependent channels in the surface membrane. Elevation of neuronal [Ca2+]i may also occur due to release of Ca2+ from intracellular storage sites. Transient increases in [Ca2+]i are thought to trigger neurotransmitter release, and to modulate axonal transport, energy metabolism and growth cone movement. Intracellular Ca2+ also appears to regulate membrane potassium channels and thereby to regulate electrical excitability. Although [Ca2+]i transients have been measured in a few giant invertebrate neurones, detection of such transients in a vertebrate neurone has not been previously reported. We have measured [Ca2+]i in bullfrog sympathetic neurones by photometry of a microinjected calcium indicator dye, arsenazo III (refs 14-16), and report here that action potentials and voltage-clamped depolarizations cause long-lasting increases in [Ca2+]i. Aslo, exposure to the drug theophylline can cause spontaneous periodic increases in [Ca2+]i. Comparisons of [Ca2+]i signals with simultaneous intracellular recordings of membrane potential suggest that the kinetics of the post-tetanic hyperpolarization (PTH) following a series of action potentials or the spontaneous hyperpolarizations induced by theophylline directly reflect the kinetics of the [Ca2+]i transient.

Action Potentials↗