Intracellular alkalinization potentiates slow inward current and prolonged bursting in a molluscan neuron

Research output: Contribution to journalArticle

Abstract

The bilaterally paired ventral white cells (VWCs) of the buccal ganglion of Pleurobranchaea drive the cyclic motor output of ingestive feeding behavior during prolonged and endogenously sustained burst episodes. The capacity to support burst episodes is specifically induced by appetitive (food) stimulation of chemosensory pathways. Cyclic 3',5'-adenosine monophosphate (cAMP) and its agonists also induce prolonged burst episodes through potentiation of a slow inward current. Intracellular alkalinzation of the VWC by externally applied ammonium ion and methylamine (5-20 mM) induces bursting and enhances slow inward current measured under voltage-clamp conditions. The enhancement of slow inward current is seen in the induction or augmentation of a negative slope resistance region in the current-voltage relation and in the enhancement of slowly decaying inward current tails recorded near the K+ equilibrium potential following depolarizing voltage commands. Intracellular injection of alkalinizing agents, bicarbonate ion and a strong buffer solution at pH 8.1, also enhance the inward current. In ammonium saline, enhancement of inward current is dependent on NH3 content, not NH+ 4; NH3 is the intracellular alkalinizing agent of ammonium saline. Therefore, the change in slow inward current is an effect specific to intracellular pH. The time courses of inward current enhancement and intracellular pH change in NH+ 4 saline are similar. The results of this study suggest that normal fluctuations in intracellular pH may be significant determinants of the excitability and consequent activity of these and perhaps other neurons. The potential interaction of intracellular pH and cyclic AMP metabolism is discussed.

Original languageEnglish (US)
Pages (from-to)509-515
Number of pages7
JournalJournal of neurophysiology
Volume49
Issue number2
DOIs
StatePublished - Jan 1 1983

Fingerprint

Neurons
Ammonium Compounds
Antacids
Cyclic AMP
Pleurobranchaea
Cheek
Feeding Behavior
Bicarbonates
Ganglia
Tail
Buffers
Ions
Food
Injections

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology

Cite this

Intracellular alkalinization potentiates slow inward current and prolonged bursting in a molluscan neuron. / Gillette, Rhanor.

In: Journal of neurophysiology, Vol. 49, No. 2, 01.01.1983, p. 509-515.

Research output: Contribution to journalArticle

@article{87113acd341b4192bb7ef0ea8978c7fb,
title = "Intracellular alkalinization potentiates slow inward current and prolonged bursting in a molluscan neuron",
abstract = "The bilaterally paired ventral white cells (VWCs) of the buccal ganglion of Pleurobranchaea drive the cyclic motor output of ingestive feeding behavior during prolonged and endogenously sustained burst episodes. The capacity to support burst episodes is specifically induced by appetitive (food) stimulation of chemosensory pathways. Cyclic 3',5'-adenosine monophosphate (cAMP) and its agonists also induce prolonged burst episodes through potentiation of a slow inward current. Intracellular alkalinzation of the VWC by externally applied ammonium ion and methylamine (5-20 mM) induces bursting and enhances slow inward current measured under voltage-clamp conditions. The enhancement of slow inward current is seen in the induction or augmentation of a negative slope resistance region in the current-voltage relation and in the enhancement of slowly decaying inward current tails recorded near the K+ equilibrium potential following depolarizing voltage commands. Intracellular injection of alkalinizing agents, bicarbonate ion and a strong buffer solution at pH 8.1, also enhance the inward current. In ammonium saline, enhancement of inward current is dependent on NH3 content, not NH+ 4; NH3 is the intracellular alkalinizing agent of ammonium saline. Therefore, the change in slow inward current is an effect specific to intracellular pH. The time courses of inward current enhancement and intracellular pH change in NH+ 4 saline are similar. The results of this study suggest that normal fluctuations in intracellular pH may be significant determinants of the excitability and consequent activity of these and perhaps other neurons. The potential interaction of intracellular pH and cyclic AMP metabolism is discussed.",
author = "Rhanor Gillette",
year = "1983",
month = "1",
day = "1",
doi = "10.1152/jn.1983.49.2.509",
language = "English (US)",
volume = "49",
pages = "509--515",
journal = "Journal of Neurophysiology",
issn = "0022-3077",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Intracellular alkalinization potentiates slow inward current and prolonged bursting in a molluscan neuron

AU - Gillette, Rhanor

PY - 1983/1/1

Y1 - 1983/1/1

N2 - The bilaterally paired ventral white cells (VWCs) of the buccal ganglion of Pleurobranchaea drive the cyclic motor output of ingestive feeding behavior during prolonged and endogenously sustained burst episodes. The capacity to support burst episodes is specifically induced by appetitive (food) stimulation of chemosensory pathways. Cyclic 3',5'-adenosine monophosphate (cAMP) and its agonists also induce prolonged burst episodes through potentiation of a slow inward current. Intracellular alkalinzation of the VWC by externally applied ammonium ion and methylamine (5-20 mM) induces bursting and enhances slow inward current measured under voltage-clamp conditions. The enhancement of slow inward current is seen in the induction or augmentation of a negative slope resistance region in the current-voltage relation and in the enhancement of slowly decaying inward current tails recorded near the K+ equilibrium potential following depolarizing voltage commands. Intracellular injection of alkalinizing agents, bicarbonate ion and a strong buffer solution at pH 8.1, also enhance the inward current. In ammonium saline, enhancement of inward current is dependent on NH3 content, not NH+ 4; NH3 is the intracellular alkalinizing agent of ammonium saline. Therefore, the change in slow inward current is an effect specific to intracellular pH. The time courses of inward current enhancement and intracellular pH change in NH+ 4 saline are similar. The results of this study suggest that normal fluctuations in intracellular pH may be significant determinants of the excitability and consequent activity of these and perhaps other neurons. The potential interaction of intracellular pH and cyclic AMP metabolism is discussed.

AB - The bilaterally paired ventral white cells (VWCs) of the buccal ganglion of Pleurobranchaea drive the cyclic motor output of ingestive feeding behavior during prolonged and endogenously sustained burst episodes. The capacity to support burst episodes is specifically induced by appetitive (food) stimulation of chemosensory pathways. Cyclic 3',5'-adenosine monophosphate (cAMP) and its agonists also induce prolonged burst episodes through potentiation of a slow inward current. Intracellular alkalinzation of the VWC by externally applied ammonium ion and methylamine (5-20 mM) induces bursting and enhances slow inward current measured under voltage-clamp conditions. The enhancement of slow inward current is seen in the induction or augmentation of a negative slope resistance region in the current-voltage relation and in the enhancement of slowly decaying inward current tails recorded near the K+ equilibrium potential following depolarizing voltage commands. Intracellular injection of alkalinizing agents, bicarbonate ion and a strong buffer solution at pH 8.1, also enhance the inward current. In ammonium saline, enhancement of inward current is dependent on NH3 content, not NH+ 4; NH3 is the intracellular alkalinizing agent of ammonium saline. Therefore, the change in slow inward current is an effect specific to intracellular pH. The time courses of inward current enhancement and intracellular pH change in NH+ 4 saline are similar. The results of this study suggest that normal fluctuations in intracellular pH may be significant determinants of the excitability and consequent activity of these and perhaps other neurons. The potential interaction of intracellular pH and cyclic AMP metabolism is discussed.

UR - http://www.scopus.com/inward/record.url?scp=0020683375&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020683375&partnerID=8YFLogxK

U2 - 10.1152/jn.1983.49.2.509

DO - 10.1152/jn.1983.49.2.509

M3 - Article

C2 - 6300347

AN - SCOPUS:0020683375

VL - 49

SP - 509

EP - 515

JO - Journal of Neurophysiology

JF - Journal of Neurophysiology

SN - 0022-3077

IS - 2

ER -