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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