Norepinephrine activates potassium conductance in neurons of the turtle cerebral cortex. Blanton, K J & Kriegstein, A R Brain Res, 570(1-2):42–48, Netherlands, January, 1992. abstract bibtex Whole-cell voltage and current clamp recordings were obtained from cortical neurons of the pond turtle, Pseudemys scripta elegans. Norepinephrine (NE) induced an outward current in 50% of pyramidal neurons. This current had a reversal potential of -88.3 +/- 3.2 mV, consistent with a K+ conductance increase, and had a mean amplitude of 18.3 +/- 7.2 pA at -40 mV. The ionic dependence and pharmacological analyses are both consistent with alpha 2 adrenergic receptor stimulation. Inhibition of Na(+)-dependent action potentials with TTX did not diminish the NE-induced K+ conductance, indicating that NE acts directly on the postsynaptic neuron. In addition to effects on postsynaptic conductance, NE dramatically decreased the amplitude of spontaneous inhibitory postsynaptic currents (IPSCs) in 55% of pyramidal neurons. The decrease in spontaneous IPSCs was observed both in those neurons which exhibited an increase in K+ conductance in response to NE administration (81%) and in those which did not (33%). Thus, NE modulates neuronal excitability both directly by activating a postsynaptic K+ conductance and indirectly by decreasing spontaneous IPSCs.
@ARTICLE{Blanton1992-as,
title = "Norepinephrine activates potassium conductance in neurons of the
turtle cerebral cortex",
author = "Blanton, K J and Kriegstein, A R",
abstract = "Whole-cell voltage and current clamp recordings were obtained
from cortical neurons of the pond turtle, Pseudemys scripta
elegans. Norepinephrine (NE) induced an outward current in 50\%
of pyramidal neurons. This current had a reversal potential of
-88.3 +/- 3.2 mV, consistent with a K+ conductance increase, and
had a mean amplitude of 18.3 +/- 7.2 pA at -40 mV. The ionic
dependence and pharmacological analyses are both consistent with
alpha 2 adrenergic receptor stimulation. Inhibition of
Na(+)-dependent action potentials with TTX did not diminish the
NE-induced K+ conductance, indicating that NE acts directly on
the postsynaptic neuron. In addition to effects on postsynaptic
conductance, NE dramatically decreased the amplitude of
spontaneous inhibitory postsynaptic currents (IPSCs) in 55\% of
pyramidal neurons. The decrease in spontaneous IPSCs was observed
both in those neurons which exhibited an increase in K+
conductance in response to NE administration (81\%) and in those
which did not (33\%). Thus, NE modulates neuronal excitability
both directly by activating a postsynaptic K+ conductance and
indirectly by decreasing spontaneous IPSCs.",
journal = "Brain Res",
volume = 570,
number = "1-2",
pages = "42--48",
month = jan,
year = 1992,
address = "Netherlands",
language = "en"
}
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