Presynaptic spike broadening reduces junctional potential amplitude

Nature ◽  
1989 ◽  
Vol 340 (6235) ◽  
pp. 636-638 ◽  
Author(s):  
Andrew N. Spencer ◽  
Jan Przysiezniak ◽  
Juan Acosta-Urquidi ◽  
Trent A. Basarsky
Keyword(s):  
Potential Amplitude ◽  
Junctional Potential ◽  
Presynaptic Spike

Neuromuscular Facilitation in Crayfish: Dependence on Potassium and Strophanthidin

1980 ◽  
Vol 86 (1) ◽  
pp. 39-47
Author(s):  
C. LEO ORTIZ ◽  
R. K. ORKAND
Keyword(s):  
Neuromuscular Junctions ◽  
Short Term ◽  
Presynaptic Terminals ◽  
Potential Amplitude ◽  
Junctional Potential ◽  
Long Term Facilitation

1. Long-term facilitation (LTF) and short-term facilitation (STF) at excitatory neuromuscular junctions were studied under conditions of varying [K+]0 and with the addition of strophanthidin. 2. The magnitude of LTF varied inversely with [K+]0, while STF was unaffected. 3. Strophanthidin concentrations greater than 10−5 M greatly increased LTF, but not STF. 4. Both LTF and STF were unaffected by large decreases in excitatory junctional potential amplitude produced by the addition of GABA or Mn+2. 5. The results support the hypothesis that LTF is a consequence of Na+ accumulation in presynaptic terminals and behaves independently of STF.

scholarly journals Kv1.1 channelopathy abolishes presynaptic spike width modulation by subthreshold somatic depolarization

2017 ◽  
Vol 114 (9) ◽  
pp. 2395-2400 ◽  
Author(s):  
Umesh Vivekananda ◽  
Pavel Novak ◽  
Oscar D. Bello ◽  
Yuri E. Korchev ◽  
Shyam S. Krishnakumar ◽  
...  
Keyword(s):  
Potassium Channels ◽  
Calcium Influx ◽  
Digital Transmission ◽  
Ion Conductance ◽  
Scanning Ion Conductance Microscopy ◽  
Spike Shape ◽  
Presynaptic Spike ◽  
Synaptic Boutons ◽  
Episodic Ataxia Type

Although action potentials propagate along axons in an all-or-none manner, subthreshold membrane potential fluctuations at the soma affect neurotransmitter release from synaptic boutons. An important mechanism underlying analog–digital modulation is depolarization-mediated inactivation of presynaptic Kv1-family potassium channels, leading to action potential broadening and increased calcium influx. Previous studies have relied heavily on recordings from blebs formed after axon transection, which may exaggerate the passive propagation of somatic depolarization. We recorded instead from small boutons supplied by intact axons identified with scanning ion conductance microscopy in primary hippocampal cultures and asked how distinct potassium channels interact in determining the basal spike width and its modulation by subthreshold somatic depolarization. Pharmacological or genetic deletion of Kv1.1 broadened presynaptic spikes without preventing further prolongation by brief depolarizing somatic prepulses. A heterozygous mouse model of episodic ataxia type 1 harboring a dominant Kv1.1 mutation had a similar broadening effect on basal spike shape as deletion of Kv1.1; however, spike modulation by somatic prepulses was abolished. These results argue that the Kv1.1 subunit is not necessary for subthreshold modulation of spike width. However, a disease-associated mutant subunit prevents the interplay of analog and digital transmission, possibly by disrupting the normal stoichiometry of presynaptic potassium channels.

P15 in tibial nerve SEPs as an example of the junctional potential

1992 ◽  
Vol 84 (6) ◽  
pp. 486-491 ◽  
Author(s):  
Masahiro Sonoo ◽  
Kieko Genba ◽  
Takeshi Iwatsubo ◽  
Toru Mannen
Keyword(s):  
Tibial Nerve ◽  
Junctional Potential

Neuromodulation of Dendritic Action Potentials

1999 ◽  
Vol 81 (1) ◽  
pp. 408-411 ◽  
Author(s):  
Dax A. Hoffman ◽  
Daniel Johnston
Keyword(s):  
Protein Kinase ◽  
Action Potential ◽  
Action Potentials ◽  
Acetylcholine Receptors ◽  
Muscarinic Acetylcholine Receptors ◽  
Action Potential Amplitude ◽  
Neurotransmitter System ◽  
Potential Amplitude ◽  
Hippocampal Ca1 ◽  
Dopaminergic Neurotransmitter

Hoffman, Dax A. and Daniel Johnston. Neuromodulation of dendritic action potentials. J. Neurophysiol. 81: 408–411, 1999. The extent to which regenerative action potentials invade hippocampal CA1 pyramidal dendrites is dependent on both recent activity and distance from the soma. Previously, we have shown that the amplitude of back-propagating dendritic action potentials can be increased by activating either protein kinase A (PKA) or protein kinase C (PKC) and a subsequent depolarizing shift in the activation curve for dendritic K+ channels. Physiologically, an increase in intracellular PKA and PKC would be expected upon activation of β-adrenergic and muscarinic acetylcholine receptors, respectively. Accordingly, we report here that activation of either of these neurotransmitter systems results in an increase in dendritic action-potential amplitude. Activation of the dopaminergic neurotransmitter system, which is also expected to raise intracellular adenosine 3′,5′-cyclic monophosphate (cAMP) and PKA levels, increased action-potential amplitude in only a subpopulation of neurons tested.

scholarly journals Modafinil Increases Arousal Determined by P13 Potential Amplitude: An Effect Blocked by Gap Junction Antagonists

SLEEP ◽  
2008 ◽  
Vol 31 (12) ◽  
pp. 1647-1654 ◽  
Author(s):  
Paige Beck ◽  
Angela Odle ◽  
Tiffany Wallace-Huitt ◽  
Robert D. Skinner ◽  
Edgar Garcia-Rill
Keyword(s):  
Gap Junction ◽  
Potential Amplitude
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