| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Departamento de Fisiología Médica y Biofísica, Facultad de Medicina, Universidad de Sevilla, Spain.
1. Action potentials of neurones of the ventral part of the guinea-pig periaqueductal grey (PAG) were studied by intracellular recording in a mesencephalic slice preparation maintained in vitro. 2. Fast spikes spontaneously fired last 2.8 +/- 0.6 ms (mean +/- S.D.) and have an amplitude of 72.3 +/- 5.3 mV (n = 28). The neurones could be antidromically activated from the neighbouring white matter and these spikes show an initial segment component that triggers the soma-dendritic spike. These two components were dissociated by hyperpolarization. Action potentials are Na+ dependent and a Ca2+ conductance is responsible for the hump on the falling phase. Hyperpolarization makes the hump disappear and a faster rate of rise and fall are seen. Accommodation of the firing threshold is observed in response to depolarizing ramps, which is eliminated with hyperpolarization. 3. High-threshold Ca2+ spikes are evoked in either Na(+)-free solution or in the presence of tetrodotoxin (TTX). These presumed dendritic action potentials display a fast repolarization and a large after-hyperpolarization (AHP) that prevent repetitive firing. This AHP is mainly generated by Ca(2+)-dependent K+ conductances. 4. The repolarization of fast action potentials depends on the activation of K+ conductances as well as a Na+ inactivation process. A fast-activated tetraethyl-ammonium (TEA)-sensitive K+ conductance, that could be Ca2+ dependent, and a K+ conductance blocked by apamin seem to be involved in the repolarization. 5. Each fast action potential is followed by a pronounced AHP with two components, an initial fast and a slow decaying phase. Membrane hyperpolarization around -60 mV eliminated the first component and the AHP acquired a plateau-like shape. At -90 mV the AHP was nullified. The slow phase was Ca2+ dependent and an apamin-sensitive K+ conductance is involved in its generation. This conductance may be active during the early part of the AHP, but a fast-activated TEA-sensitive K+ conductance and other voltage-dependent K+ conductances might also be present. A Ca2+ conductance is hypothesized to account for the fast depolarizing change after the AHP peak. 6. A delayed return to the baseline is observed after hyperpolarizing pulses. It is generated by the activation of a transient voltage-dependent K+ conductance that is inactive at resting membrane potential (RMP, around -50 mV). This transient hyperpolarization is abolished by Ca2+ channel blockers and insensitive to high external concentrations of 4-aminopyridine, TEA and Cs+.(ABSTRACT TRUNCATED AT 400 WORDS)
This article has been cited by other articles:
|
|
 |
|
  G. M. Drew, V. A. Mitchell, and C. W. Vaughan Glutamate Spillover Modulates GABAergic Synaptic Transmission in the Rat Midbrain Periaqueductal Grey via Metabotropic Glutamate Receptors and Endocannabinoid Signaling J. Neurosci., January 23, 2008; 28(4): 808 - 815. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. H. Li, H.-M. Hwang, P. P. Tan, T. Wu, and H.-L. Wang Neurotensin Excites Periaqueductal Gray Neurons Projecting to the Rostral Ventromedial Medulla J Neurophysiol, April 1, 2001; 85(4): 1479 - 1488. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. D. Bevan and C. J. Wilson Mechanisms Underlying Spontaneous Oscillation and Rhythmic Firing in Rat Subthalamic Neurons J. Neurosci., September 1, 1999; 19(17): 7617 - 7628. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
