cAMP modulates an S-type K+ channel coupled to GABAB receptors in mammalian respiratory neurons.
Premotor respiratory neurons from neonatal rats express a Ba(2+)-insensitive outward rectifying K+ channel (KOR) which is activated by gamma-aminobutyric acid acting at its beta receptor. The biophysical properties of KOR are similar to those described for the S-channel (KS) which underlies simple forms of non-associative learning in the marine mollusc Aplysia. We show here that KOR, like the S-channel, is inhibited by cAMP. In addition, we demonstrate that this inhibition is due to a change in closed time kinetics. Our data suggests that the ionic and biochemical substrates underlying synaptic plasticity in Aplysia have been phylogenetically conserved in mammalian motor circuits such as that controlling rhythmic breathing movements.
Wagner
P G
PG
Department of Medicine, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick 08903-0019, USA.
Dekin
M S
MS
D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology*; D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D002478:Cells, Cultured; D018755:GABA Agonists / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects*; D015221:Potassium Channels / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018080:Receptors, GABA-B / Q000187:drug effects*; D012137:Respiratory System / Q000187:drug effects* / Q000294:innervation
D018755:GABA Agonists; D015221:Potassium Channels; D018080:Receptors, GABA-B; D015124:8-Bromo Cyclic Adenosine Monophosphate; D001418:Baclofen