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
1980 ◽  
Vol 86 (1) ◽  
pp. 39-47
Author(s):  
C. LEO ORTIZ ◽  
R. K. ORKAND

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.


2017 ◽  
Vol 114 (9) ◽  
pp. 2395-2400 ◽  
Author(s):  
Umesh Vivekananda ◽  
Pavel Novak ◽  
Oscar D. Bello ◽  
Yuri E. Korchev ◽  
Shyam S. Krishnakumar ◽  
...  

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.


Author(s):  
Masahiro Sonoo ◽  
Kieko Genba ◽  
Takeshi Iwatsubo ◽  
Toru Mannen

1999 ◽  
Vol 81 (1) ◽  
pp. 408-411 ◽  
Author(s):  
Dax A. Hoffman ◽  
Daniel Johnston

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.


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

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