Electrophysiological Roles of L-Type Channels in Different Classes of Guinea Pig Sympathetic Neuron

1999 ◽  
Vol 82 (2) ◽  
pp. 818-828 ◽  
Author(s):  
Philip J. Davies ◽  
David R. Ireland ◽  
Juan Martinez-Pinna ◽  
Elspeth M. McLachlan
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Hippocampal Neurons ◽  
Sympathetic Ganglia ◽  
Bk Channels ◽  
Half Width ◽  
Sk Channels ◽  
Single Action ◽  
Ganglion Neurons

The electrophysiological consequences of blocking Ca2+ entry through L-type Ca2+ channels have been examined in phasic ( Ph), tonic ( T), and long-afterhyperpolarizing ( LAH) neurons of intact guinea pig sympathetic ganglia isolated in vitro. Block of Ca2+entry with Co2+ or Cd2+ depolarized T and LAH neurons, reduced action potential (AP) amplitude in Ph and LAHneurons, and increased AP half-width in Ph neurons. The afterhyperpolarization (AHP) and underlying Ca2+-dependent K+ conductances ( gKCa1 and gKCa2) were reduced markedly in all classes. Addition of 10 μM nifedipine increased input resistance in LAHneurons, raised AP threshold in Ph and LAH neurons, and caused a small increase in AP half-width in Ph neurons. AHP amplitude and the amplitude and decay time constant of gKCa1 were reduced by nifedipine in all classes; the slower conductance, gKCa2, which underlies the prolonged AHP in LAH neurons, was reduced by 40%. Surprisingly, AHP half-width was lengthened by nifedipine in a proportion of neurons in all classes; despite this, neuron excitability was increased during a maintained depolarization. Nifedipine’s effects on AHP half-width were not mimicked by 2 mM Cs+ or 2 mM anthracene-9-carboxylic acid, a blocker of Cl− channels, and it did not modify transient outward currents of the A or D types. The effects of 100 μM Ni2+ differed from those of nifedipine. Thus in Ph neurons, Ca2+ entry through L-type channels during a single action potential contributes to activation of K+ conductances involved in both the AP and AHP, whereas in T and LAH neurons, it acts only on gKCa1 and gKCa2. These results differ from the results in rat superior cervical ganglion neurons, in which L-type channels are selectively coupled to BK channels, and in hippocampal neurons, in which L-type channels are selectively coupled to SK channels. We conclude that the sources of Ca2+ for activating the various Ca2+-activated K+conductances are distinct in different types of neuron.

Role of cyclooxygenase activation and prostaglandins in antigen-induced excitability changes of bronchial parasympathetic ganglia neurons

2003 ◽  
Vol 284 (4) ◽  
pp. L581-L587 ◽  
Author(s):  
Radhika Kajekar ◽  
Bradley J. Undem ◽  
Allen C. Myers
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Synaptic Transmission ◽  
Cyclooxygenase Inhibitors ◽  
Antigen Challenge ◽  
Parasympathetic Nerve ◽  
Parasympathetic Ganglia ◽  
Parasympathetic Ganglion ◽  
Ganglion Neurons

In vitro antigen challenge has multiple effects on the excitability of guinea pig bronchial parasympathetic ganglion neurons, including depolarization, causing phasic neurons to fire with a repetitive action potential pattern and potentiating synaptic transmission. In the present study, guinea pigs were passively sensitized to the antigen ovalbumin. After sensitization, the bronchi were prepared for in vitro electrophysiological intracellular recording of parasympathetic ganglia neurons to investigate the contribution of cyclooxygenase activation and prostanoids on parasympathetic nerve activity. Cyclooxygenase inhibition with either indomethacin or piroxicam before in vitro antigen challenge blocked the change in accommodation. These cyclooxygenase inhibitors also blocked the release of prostaglandin D2 (PGD2) from bronchial tissue during antigen challenge. We also determined that PGE2 and PGD2 decreased the duration of the action potential after hyperpolarization, whereas PGF2α potentiated synaptic transmission. Thus prostaglandins released during antigen challenge have multiple effects on the excitability of guinea pig bronchial parasympathetic ganglia neurons, which may consequently affect the output from these neurons and thereby alter parasympathetic tone in the lower airways.

Guinea pig visceral C-fiber neurons are diverse with respect to the K+ currents involved in action-potential repolarization

1994 ◽  
Vol 71 (2) ◽  
pp. 561-574 ◽  
Author(s):  
E. P. Christian ◽  
J. Togo ◽  
K. E. Naper
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Outward Current ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Whole Cell ◽  
C Fiber ◽  
K Current ◽  
Action Potential Repolarization

1. Intracellular recordings were made from C-fiber neurons identified by antidromic conduction velocity in intact guinea pig nodose ganglia maintained in vitro, and whole-cell patch clamp recordings were made from dissociated guinea pig nodose neurons to investigate the contribution of various K+ conductances to action-potential repolarization. 2. The repolarizing phase of the intracellularly recorded action potential was prolonged in a concentration-dependent manner by charybdotoxin (Chtx; EC50 = 39 nM) or iberiatoxin (Ibtx; EC50 = 48 nM) in a subpopulation of 16/36 C-fiber neurons. In a subset of these experiments, removal of extracellular Ca2+ reversibly prolonged action-potential duration (APD) in the same 4/9 intracellularly recorded C-fiber neurons affected by Chtx (> or = 100 nM). These convergent results support that a Ca(2+)-activated K+ current (IC) contributes to action-potential repolarization in a restricted subpopulation of C-fiber neurons. 3. Tetraethylammonium (TEA; 1-10 mM) increased APD considerably further in the presence of 100-250 nM Chtx or Ibtx, or in nominally Ca(2+)-free superfusate in 14/14 intracellularly recorded C-fiber neurons. TEA affected APD similarly in subpopulations of neurons with and without IC, suggesting that a voltage-dependent K+ current (IK) contributes significantly to action-potential repolarization in most nodose C-fiber neurons. 4. Substitution of Mn2+ for Ca2+ reduced outward whole-cell currents elicited by voltage command steps positive to -30 mV (2-25 ms) in a subpopulation of 21/36 dissociated nodose neurons, supporting the heterogeneous expression of IC. The kinetics of outward tail current relaxations (tau s of 1.5-2 ms) measured at the return of 2-3 ms depolarizing steps to -40 mV were indistinguishable in neurons with and without IC, precluding a separation of the nodose IC and IK by a difference in deactivation rates. 5. Chtx (10-250 nM) reduced in a subpopulation of 3/8 C-fiber neurons the total outward current elicited by voltage steps depolarized to -30 mV in single microelectrode voltage-clamp recordings. TEA (5-10 mM) further reduced outward current in the presence of 100-250 nM Chtx in all eight experiments. The Chtx-sensitive current was taken to represent IC, and the TEA-sensitive current, the IK component contributing to action-potential repolarization. 6. Rapidly inactivating current (IA) was implicated in action-potential repolarization in a subpopulation of intracellularly recorded C-fiber neurons. In 4/7 neurons, incremented hyperpolarizing prepulses negative to -50 mV progressively shortened APD.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Polarized localization of voltage-gated Na+ channels is regulated by concerted FGF13 and FGF14 action

2016 ◽  
Vol 113 (19) ◽  
pp. E2665-E2674 ◽  
Author(s):  
Juan Lorenzo Pablo ◽  
Chaojian Wang ◽  
Matthew M. Presby ◽  
Geoffrey S. Pitt
Keyword(s):  
Action Potential ◽  
Hippocampal Neurons ◽  
Single Point ◽  
Point Mutations ◽  
Surface Expression ◽  
Voltage Gated ◽  
Voltage Gated Sodium Channels ◽  
Action Potential Initiation ◽  
Potential Initiation

Clustering of voltage-gated sodium channels (VGSCs) within the neuronal axon initial segment (AIS) is critical for efficient action potential initiation. Although initially inserted into both somatodendritic and axonal membranes, VGSCs are concentrated within the axon through mechanisms that include preferential axonal targeting and selective somatodendritic endocytosis. How the endocytic machinery specifically targets somatic VGSCs is unknown. Here, using knockdown strategies, we show that noncanonical FGF13 binds directly to VGSCs in hippocampal neurons to limit their somatodendritic surface expression, although exerting little effect on VGSCs within the AIS. In contrast, homologous FGF14, which is highly concentrated in the proximal axon, binds directly to VGSCs to promote their axonal localization. Single-point mutations in FGF13 or FGF14 abrogating VGSC interaction in vitro cannot support these specific functions in neurons. Thus, our data show how the concerted actions of FGF13 and FGF14 regulate the polarized localization of VGSCs that supports efficient action potential initiation.

scholarly journals Nicotine suppresses hyperexcitability of colonic sensory neurons and visceral hypersensivity in mouse model of colonic inflammation

2012 ◽  
Vol 302 (7) ◽  
pp. G740-G747 ◽  
Author(s):  
Galya R. Abdrakhmanova ◽  
Minho Kang ◽  
M. Imad Damaj ◽  
Hamid I. Akbarali
Keyword(s):  
Mouse Model ◽  
Action Potential ◽  
Action Potentials ◽  
Drg Neurons ◽  
Action Potential Firing ◽  
Colonic Inflammation ◽  
Single Action ◽  
Nicotine Administration ◽  
Potential Firing

Recently, we reported that nicotine in vitro at a low 1-μM concentration suppresses hyperexcitability of colonic dorsal root ganglia (DRG; L1-L2) neurons in the dextran sodium sulfate (DSS)-induced mouse model of acute colonic inflammation ( 1 ). Here we show that multiple action potential firing in colonic DRG neurons persisted at least for 3 wk post-DSS administration while the inflammatory signs were diminished. Similar to that in DSS-induced acute colitis, bath-applied nicotine (1 μM) gradually reduced regenerative multiple-spike action potentials in colonic DRG neurons to a single action potential in 3 wk post-DSS neurons. Nicotine (1 μM) shifted the activation curve for tetrodotoxin (TTX)-resistant sodium currents in inflamed colonic DRG neurons (voltage of half-activation changed from −37 to −32 mV) but did not affect TTX-sensitive currents in control colonic DRG neurons. Further, subcutaneous nicotine administration (2 mg/kg b.i.d.) in DSS-treated C57Bl/J6 male mice resulted in suppression of hyperexcitability of colonic DRG (L1-L2) neurons and the number of abdominal constrictions in response to intraperitoneal injection of 0.6% acetic acid. Collectively, the data suggest that neuronal nicotinic acetylcholine receptor-mediated suppression of hyperexcitability of colonic DRG neurons attenuates reduction of visceral hypersensitivity in DSS mouse model of colonic inflammation.

scholarly journals Calcium stores regulate excitability in cultured rat hippocampal neurons

2018 ◽  
Vol 120 (5) ◽  
pp. 2694-2705 ◽  
Author(s):  
Menahem Segal
Keyword(s):  
Action Potential ◽  
Hippocampal Neurons ◽  
Extracellular Calcium ◽  
Calcium Stores ◽  
Sk Channels ◽  
Central Neurons ◽  
Action Potential Threshold ◽  
Potential Threshold ◽  
Small Conductance ◽  
Cultured Hippocampal Neurons

Extracellular calcium ions support synaptic activity but also reduce excitability of central neurons. In the present study, the effect of calcium on excitability was explored in cultured hippocampal neurons. CaCl2 injected by pressure in the vicinity of a neuron that is bathed only in MgCl2 as the main divalent cation caused a depolarizing shift in action potential threshold and a reduction in excitability. This effect was not seen if the intracellular milieu consisted of Cs+ instead of K-gluconate as the main cation or when it contained ruthenium red, which blocks release of calcium from stores. The suppression of excitability by calcium was mimicked by caffeine, and calcium store antagonists cyclopiazonic acid or thapsigargin blocked this action. Neurons taken from synaptopodin-knockout mice show significantly reduced efficacy of calcium modulation of action potential threshold. Likewise, in Orai1 knockdown cells, calcium is less effective in modulating excitability of neurons. Activation of small-conductance K (SK) channels increased action potential threshold akin to that produced by calcium ions, whereas blockade of SK channels but not big K channels reduced the threshold for action potential discharge. These results indicate that calcium released from stores may suppress excitability of central neurons. NEW & NOTEWORTHY Extracellular calcium reduces excitability of cultured hippocampal neurons. This effect is mediated by calcium-gated potassium currents, possibly small-conductance K channels. Release of calcium from internal stores mimics the effect of extracellular calcium. It is proposed that calcium stores modulate excitability of central neurons.

scholarly journals BK current contributions to action potentials across the first postnatal week reflect age dependent changes in BK current kinetics in rat hippocampal neurons

2019 ◽  
Author(s):  
Michael Hunsberger ◽  
Michelle Mynlieff
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Hippocampal Neurons ◽  
Expression Patterns ◽  
Bk Channels ◽  
Bk Channel ◽  
Action Potential Firing ◽  
Developmental Trends ◽  
Channel Expression ◽  
Old Rats

AbstractThe large conductance calcium-activated potassium (BK) channel is a critical regulator of neuronal action potential firing and follows two distinct trends in early postnatal development: an increase in total expression and a shift from the faster activating STREX isoform to the slower ZERO isoform. We analyzed the functional consequences of developmental trends in BK channel expression in hippocampal neurons isolated from neonatal rats aged one to seven days. Following overnight cultures, action potentials were recorded using whole-cell patch clamp electrophysiology. This population of neurons undergoes a steady increase in excitability during this time and the effect of blockade of BK channel activity with 100 nM iberiotoxin, changes as the neurons mature. BK currents contribute significantly more to single action potentials in neurons of one-day old rats (with BK blockade extending action potential duration by 0.46±0.12 ms) than in those of seven-day old rats (with BK blockade extending action potential duration by 0.17±0.05 ms). BK currents also contribute consistently to maintain firing rates in neurons of one-day old rats throughout extended action potential firing; BK blockade evenly depresses action potentials frequency across action potential trains. In neurons from seven-day old rats, BK blockade initially increases firing frequency and then progressively decreases frequency as firing continues, ultimately depressing neuronal firing rates to a greater extent than in the neurons from one day old animals. These results are consistent with a transition from low expression of a fast activating BK isoform (STREX) to high expression of a slower activating isoform (ZERO).New and NoteworthyThis work describes the early developmental trends of BK channel activity. Early developmental trends in expression of BK channels, both total expression and relative isoform expression, have been previously reported, but little work describes the effect of these changes in expression patterns on excitability. Here, we show that early changes in BK channel expression patterns lead to changes in the role of BK channels in determining the action potential waveform and neuronal excitability.

Biophysical Properties and Responses to Neurotransmitters of Petrosal and Geniculate Ganglion Neurons Innervating the Tongue

2000 ◽  
Vol 84 (3) ◽  
pp. 1404-1413 ◽  
Author(s):  
Tomoshige Koga ◽  
Robert M. Bradley
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Membrane Properties ◽  
Patch Clamp Recording ◽  
Potential Decay ◽  
Ganglion Neurons ◽  
Fast Rise ◽  
Posterior Tongue ◽  
Passive Membrane Properties

The properties of afferent sensory neurons supplying taste receptors on the tongue were examined in vitro. Neurons in the geniculate (GG) and petrosal ganglia (PG) supplying the tongue were fluorescently labeled, acutely dissociated, and then analyzed using patch-clamp recording. Measurement of the dissociated neurons revealed that PG neurons were significantly larger than GG neurons. The active and passive membrane properties of these ganglion neurons were examined and compared with each other. There were significant differences between the properties of neurons in the PG and GG ganglia. The mean membrane time constant, spike threshold, action potential half-width, and action potential decay time of GG neurons was significantly less than those of PG neurons. Neurons in the PG had action potentials that had a fast rise and fall time (sharp action potentials) as well as action potentials with a deflection or hump on the falling phase (humped action potentials), whereas action potentials of GG neurons were all sharp. There were also significant differences in the response of PG and GG neurons to the application of acetylcholine (ACh), serotonin (5HT), substance P (SP), and GABA. Whereas PG neurons responded to ACh, 5HT, SP, and GABA, GG neurons only responded to SP and GABA. In addition, the properties of GG neurons were more homogeneous than those of the PG because all the GG neurons had sharp spikes and when responses to neurotransmitters occurred, either all or most of the neurons responded. These differences between neurons of the GG and PG may relate to the type of receptor innervated. PG ganglion neurons innervate a number of receptor types on the posterior tongue and have more heterogeneous properties, while GG neurons predominantly innervate taste buds and have more homogeneous properties.

Foreign connections are formed in vitro by Aplysia californica interneuron L10 and its in vivo followers and non-followers

1990 ◽  
Vol 154 (1) ◽  
pp. 237-255
Author(s):  
D. Kleinfeld ◽  
T. D. Parsons ◽  
F. Raccuia-Behling ◽  
B. M. Salzberg ◽  
A. L. Obaid
Keyword(s):  
Action Potential ◽  
Synapse Formation ◽  
Aplysia Californica ◽  
Inhibitory Connection ◽  
Single Action ◽  
Inhibitory Postsynaptic Potentials ◽  
Neuronal Processes ◽  
Dual Action

Aplysia californica interneurone L10 forms a set of presynaptic connections with many postsynaptic ‘follower’ cells in the abdominal ganglion. These followers do not connect back to L10. The present study tests whether the direction and sign of these connections are obligatory and are reconstructed when neuronal processes regenerate in vitro. L10 was co-cultured with one of six different followers and two non-followers. 1. In vitro connections that preserve the sign of those formed in vivo were made by L10 onto neurones L11, L12 and L13. The connections consisted of inhibitory postsynaptic potentials (IPSPs) with characteristic fast and slow components. 2. In vitro connections that did not preserve the sign of connections found in vivo were made by L10 onto R15, R16 and L7. Neurones R15 and R16 receive excitatory inputs from L10 in vivo and L7 receives a dual-action input in vivo, with inhibition followed by excitation. A purely inhibitory connection from L10 was formed in vitro onto all these cells. 3. Connections that have never been observed in vivo in terms of both direction and sign were formed in vitro. Followers L7, L11, L12, L13 and R16 and non-follower L14A formed novel connections onto L10. All these connections were inhibitory and some were strong. For example, IPSPs with a magnitude of 20 mV were observed in L10 following a single action potential in L13. Our results show that identified Aplysia neurones can form stereotyped specific connections in vitro. The specificity is different from that in the intact ganglion. The ubiquity of novel connections suggests that restrictions imposed on synaptogenesis in the animal are distinct from those regulating synapse formation in culture.

scholarly journals Small-conductance Ca2+-activated K+ channels modulate action potential-induced Ca2+ transients in hippocampal neurons

2013 ◽  
Vol 109 (6) ◽  
pp. 1514-1524 ◽  
Author(s):  
Raffaella Tonini ◽  
Teresa Ferraro ◽  
Marisol Sampedro-Castañeda ◽  
Anna Cavaccini ◽  
Martin Stocker ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Apical Dendrite ◽  
Channel Blockers ◽  
Sk Channels ◽  
Hippocampal Pyramidal Neurons ◽  
Voltage Gated ◽  
Small Conductance

In hippocampal pyramidal neurons, voltage-gated Ca2+ channels open in response to action potentials. This results in elevations in the intracellular concentration of Ca2+ that are maximal in the proximal apical dendrites and decrease rapidly with distance from the soma. The control of these action potential-evoked Ca2+ elevations is critical for the regulation of hippocampal neuronal activity. As part of Ca2+ signaling microdomains, small-conductance Ca2+-activated K+ (SK) channels have been shown to modulate the amplitude and duration of intracellular Ca2+ signals by feedback regulation of synaptically activated Ca2+ sources in small distal dendrites and dendritic spines, thus affecting synaptic plasticity in the hippocampus. In this study, we investigated the effect of the activation of SK channels on Ca2+ transients specifically induced by action potentials in the proximal processes of hippocampal pyramidal neurons. Our results, obtained by using selective SK channel blockers and enhancers, show that SK channels act in a feedback loop, in which their activation by Ca2+ entering mainly through L-type voltage-gated Ca2+ channels leads to a reduction in the subsequent dendritic influx of Ca2+. This underscores a new role of SK channels in the proximal apical dendrite of hippocampal pyramidal neurons.

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