Serotonin modulates N- and P-type calcium currents in neocortical pyramidal neurons via a membrane-delimited pathway

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Abstract

1. The effects of serotonin (5HT) on neocortical pyramidal neurons were studied using whole cell and ON-cell patch-clamp recordings from acutely dissociated neurons. 2. 5HT decreased high voltage-activated calcium channel currents in a dose-dependent and reversible manner in acutely dissociated neocortical pyramidal neurons. The maximum block was 30% of the peak whole cell current (at -10 mV). 3. The 5HT modulation was mimicked by 5HT(1A) agonists and was reduced by 5HT(1A) antagonists. 5HT2 antagonists had no effect on the modulation. These data suggest that the 5HT effects were mediated by 5HT(1A) receptors. 4. The 5HT(1A) modulation was reduced in the presence of the specific N-type blocker ω-conotoxin GVIA (CgTx) and by the P-type channel blocker ω-agatoxin IVA (AgTx), but not by the L-type blocker nifedipine. 5HT did not modulate the slowed tail currents in the presence of the dihydropyridine agonist Bay K 8644. These data suggest that N- and P- type channels (but not L-type channels) were targeted by 5HT. 5. The modulation involved G proteins and utilized a membrane-delimited pathway. The modulation was rapid in onset (τ ~600 ms) and offset. About 50% of the reduction in current by 5HT(1A) agonists was overcome by prepulses to 120 mV. 6. Slowing of current onset kinetics in response to 5HT(1A) agonists was seen rarely in neocortical pyramidal neurons (11% of cases). The presence of slowing depended on agonist concentration, being evident only with high micromolar doses.

Original languageEnglish (US)
Pages (from-to)648-659
Number of pages12
JournalJournal of Neurophysiology
Volume75
Issue number2
DOIs
StatePublished - Jan 1 1996

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Pyramidal Cells
Serotonin
Calcium
Membranes
Agatoxins
Conotoxins
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
Calcium Channels
Nifedipine
GTP-Binding Proteins
Neurons

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Physiology

Cite this

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title = "Serotonin modulates N- and P-type calcium currents in neocortical pyramidal neurons via a membrane-delimited pathway",
abstract = "1. The effects of serotonin (5HT) on neocortical pyramidal neurons were studied using whole cell and ON-cell patch-clamp recordings from acutely dissociated neurons. 2. 5HT decreased high voltage-activated calcium channel currents in a dose-dependent and reversible manner in acutely dissociated neocortical pyramidal neurons. The maximum block was 30{\%} of the peak whole cell current (at -10 mV). 3. The 5HT modulation was mimicked by 5HT(1A) agonists and was reduced by 5HT(1A) antagonists. 5HT2 antagonists had no effect on the modulation. These data suggest that the 5HT effects were mediated by 5HT(1A) receptors. 4. The 5HT(1A) modulation was reduced in the presence of the specific N-type blocker ω-conotoxin GVIA (CgTx) and by the P-type channel blocker ω-agatoxin IVA (AgTx), but not by the L-type blocker nifedipine. 5HT did not modulate the slowed tail currents in the presence of the dihydropyridine agonist Bay K 8644. These data suggest that N- and P- type channels (but not L-type channels) were targeted by 5HT. 5. The modulation involved G proteins and utilized a membrane-delimited pathway. The modulation was rapid in onset (τ ~600 ms) and offset. About 50{\%} of the reduction in current by 5HT(1A) agonists was overcome by prepulses to 120 mV. 6. Slowing of current onset kinetics in response to 5HT(1A) agonists was seen rarely in neocortical pyramidal neurons (11{\%} of cases). The presence of slowing depended on agonist concentration, being evident only with high micromolar doses.",
author = "Robert Foehring",
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N2 - 1. The effects of serotonin (5HT) on neocortical pyramidal neurons were studied using whole cell and ON-cell patch-clamp recordings from acutely dissociated neurons. 2. 5HT decreased high voltage-activated calcium channel currents in a dose-dependent and reversible manner in acutely dissociated neocortical pyramidal neurons. The maximum block was 30% of the peak whole cell current (at -10 mV). 3. The 5HT modulation was mimicked by 5HT(1A) agonists and was reduced by 5HT(1A) antagonists. 5HT2 antagonists had no effect on the modulation. These data suggest that the 5HT effects were mediated by 5HT(1A) receptors. 4. The 5HT(1A) modulation was reduced in the presence of the specific N-type blocker ω-conotoxin GVIA (CgTx) and by the P-type channel blocker ω-agatoxin IVA (AgTx), but not by the L-type blocker nifedipine. 5HT did not modulate the slowed tail currents in the presence of the dihydropyridine agonist Bay K 8644. These data suggest that N- and P- type channels (but not L-type channels) were targeted by 5HT. 5. The modulation involved G proteins and utilized a membrane-delimited pathway. The modulation was rapid in onset (τ ~600 ms) and offset. About 50% of the reduction in current by 5HT(1A) agonists was overcome by prepulses to 120 mV. 6. Slowing of current onset kinetics in response to 5HT(1A) agonists was seen rarely in neocortical pyramidal neurons (11% of cases). The presence of slowing depended on agonist concentration, being evident only with high micromolar doses.

AB - 1. The effects of serotonin (5HT) on neocortical pyramidal neurons were studied using whole cell and ON-cell patch-clamp recordings from acutely dissociated neurons. 2. 5HT decreased high voltage-activated calcium channel currents in a dose-dependent and reversible manner in acutely dissociated neocortical pyramidal neurons. The maximum block was 30% of the peak whole cell current (at -10 mV). 3. The 5HT modulation was mimicked by 5HT(1A) agonists and was reduced by 5HT(1A) antagonists. 5HT2 antagonists had no effect on the modulation. These data suggest that the 5HT effects were mediated by 5HT(1A) receptors. 4. The 5HT(1A) modulation was reduced in the presence of the specific N-type blocker ω-conotoxin GVIA (CgTx) and by the P-type channel blocker ω-agatoxin IVA (AgTx), but not by the L-type blocker nifedipine. 5HT did not modulate the slowed tail currents in the presence of the dihydropyridine agonist Bay K 8644. These data suggest that N- and P- type channels (but not L-type channels) were targeted by 5HT. 5. The modulation involved G proteins and utilized a membrane-delimited pathway. The modulation was rapid in onset (τ ~600 ms) and offset. About 50% of the reduction in current by 5HT(1A) agonists was overcome by prepulses to 120 mV. 6. Slowing of current onset kinetics in response to 5HT(1A) agonists was seen rarely in neocortical pyramidal neurons (11% of cases). The presence of slowing depended on agonist concentration, being evident only with high micromolar doses.

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