Effects of muscarine on K+-channel currents in the C-cells of bullfrog sympathetic ganglion

Kurenny, Dmitry E.; Chen, Hsinyo; Smith, Peter A.

doi:10.1016/s0006-8993(09)90031-2

Cited by 11 publications

(9 citation statements)

References 49 publications

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“…Neurons in the VIIIth to Xth paravertebral sympathetic ganglia of male or female Rana catesbeiana were dissociated using trypsin and collagenase as previously described (Selyanko et al ., 1990a; Kurenny et al ., 1994). Animals were killed by ‘pithing’.…”

Section: Tissue Culture and Electrophysiologymentioning

confidence: 99%

Possible role of phosphatidylinositol 4,5, bisphosphate in luteinizing hormone releasing hormone‐mediated M‐current inhibition in bullfrog sympathetic neurons

Ford

Stemkowski

Smith

2004

Eur J of Neuroscience

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Luteinizing hormone releasing hormone (LHRH) is a physiological modulator of neuronal excitability in bullfrog sympathetic ganglia (BFSG). Actions of LHRH involve suppression of the noninactivating, voltage-dependent M-type K+ channel conductance (gM). We found, using whole-cell recordings from these neurons, that LHRH-induced suppression of gM was attenuated by the phospholipase C (PLC) inhibitor U73122 (10 microM) but not by the inactive isomer U73343 (10 microM). Buffering internal Ca2+ to 117 nM with intracellular 20 mM BAPTA + 8 mM Ca2+ or to < 10 nM with intracellular 20 mM BAPTA + 0.4 mM Ca2+ did not attenuate LHRH-induced gM suppression. Suppression of gM by LHRH was not antagonized by the inositol 1,4,5 trisphosphate (InsP3) receptor antagonist heparin (approximately 300 microM). Preventing phosphatidylinositol-4,5-bisphosphate (PIP2) synthesis by blocking phosphatidylinositol-4-kinase with wortmannin (10 microM) or with the nonhydrolysable ATP analogue AMP-PNP (3 mM) prolonged recovery of LHRH-induced gM suppression. This effect was not produced by blocking phosphatidyl inositol-3-kinase with LY294002 (10 microM). Rundown of gM was attenuated when cells were dialysed with 240 microM di-octanoyl PIP2 or 240 microM di-octanoyl phosphatidylinositol-3,4,5-trisphosphate (PIP3) but not with 240 microM di-octanoyl phosphatidylcholine. LHRH-induced gM suppression was competitively antagonized by dialysis with 240 microM di-octanoyl PIP2, but not with di-octanoyl phosphatidylcholine. These results would be expected if LHRH-induced gM suppression reflects a PLC-mediated decrease in plasma membrane PIP2 levels.

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Section: Tissue Culture and Electrophysiologymentioning

confidence: 99%

Possible role of phosphatidylinositol 4,5, bisphosphate in luteinizing hormone releasing hormone‐mediated M‐current inhibition in bullfrog sympathetic neurons

Ford

Stemkowski

Smith

2004

Eur J of Neuroscience

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“…Only recordings with access resistances <10 MΩ and resting potentials of at least −45 mV were accepted for analysis. B and C neurons were identified by their different muscarinic responses, which were assessed by measuring I–V relations under voltage clamp with slow voltage ramps (Kurenny et al 1994). B neurons responded to oxotremorine M (oxo‐M) with an inhibition of M‐current, while C neurons responded with activation of a small inwardly rectifying K + current.…”

Section: Methodsmentioning

confidence: 99%

“…To understand how muscarinic excitation modulates the integration of fast nicotinic EPSPs in sympathetic ganglia, we have stimulated fully differentiated adult bullfrog sympathetic neurons in primary cell culture with complex patterns of virtual synaptic activity using the dynamic clamp method (Kullmann et al 2004; Wheeler et al 2004). With this approach one can functionally identify secretomotor B neurons and vasomotor C neurons by their different responses to muscarinic agonists (Kurenny et al 1994) and then study their responses to stimulus patterns that reproduce synaptic activity observed in vivo (Ivanoff & Smith, 1995; McLachlan et al 1997; McLachlan et al 1998). Results from such experiments support the hypothesis that sympathetic ganglia act as amplifiers of presynaptic activity (Karila & Horn, 2000; Wheeler et al 2004) and the prediction that postsynaptic muscarinic suppression of g K M can enhance synaptic gain (Schobesberger et al 2000; Kullmann & Horn, 2006).…”

Section: Introductionmentioning

confidence: 99%

Homeostatic regulation of M-current modulates synaptic integration in secretomotor, but not vasomotor, sympathetic neurons in the bullfrog

Kullmann

Horn

2010

The Journal of Physiology

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We compared how vasomotor C neurons and secretomotor B neurons integrated identical patterns of virtual synaptic activity using dynamic clamp, perforated-patch recordings from dissociated bullfrog sympathetic ganglion cells. The synaptic template modelled one strong nicotinic synapse and nine weak synapses, each firing randomly at 5 Hz, with strength normalized to each cell. B neurons initially fired at 12 Hz, but this declined within seconds, decreasing 27% after 40 s and recovering slowly as evidenced by the threshold synaptic conductance for firing (τ recovery = 136 ± 23 s). C neurons gave an identical initial response that remained steady, declining only 6% after 40 s. The difference resulted from an activity-dependent 379 ± 65% increase in M-current (I M ) in B cells (τ recovery = 153 ± 22 s), which was absent in C cells. In addition, action potential afterhyperpolarizations were 2-fold longer in B cells, but this did not produce the differential response to synaptic stimulation. Activity-dependent increases in I M were sensitive to 100 μm Cd 2+ and 2.5 μm oxotremorine M (oxo-M), a muscarinic agonist, and fully blocked by zero Ca 2+ , 10 μm oxo-M and 2.5 μm oxo-M plus 50 μm wortmannin, a PIP 2 synthesis inhibitor. A leftward shift in voltage-dependent activation could not fully account for the I M increase. Firing at 0.5 Hz was sufficient to modulate I M . Opposing influences of activity and muscarinic excitation thus produce homeostatic I M regulation, to stabilize excitability and postsynaptic output in secretomotor sympathetic neurons. Absence of this regulation in vasomotor neurons suggests a different integrative function, where synaptic gain increases in proportion to presynaptic activity.

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“…Secretomotor B cells and vasomotor C cells were identified by their different responses to bath-applied muscarinic agonists (1–10 μM oxotremorine-M or 1–10 μM ±-muscarine chloride) using slow voltage-ramps in a voltage-clamp protocol (Kurenny et al, 1994). Muscarinic stimulation inhibited M-current in B cells and activated an inwardly rectifying potassium current in C cells.…”

Section: Methodsmentioning

confidence: 99%

Vasomotor sympathetic neurons are more excitable than secretomotor sympathetic neurons in bullfrog paravertebral ganglia

Kullmann

Horn

2010

Autonomic Neuroscience

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We compared the excitability of secretomotor B and vasomotor C neurons using virtual nicotinic synapses implemented with the dynamic clamp technique. In response to fast synaptic conductance (g syn ) waveforms modeled after B cell synaptic currents, it took 17.1 ± 1.2 nS to elicit spikes in 104 B cells and 3.3 ± 0.3 nS in 35 C cells. After normalizing for whole cell capacitance, C cells were still more excitable than B cells (76 ± 5 pS/pF vs. 169 ± 8 pS/pF). Stimulating C cells with slower g syn waveforms, identical to synaptic currents in C cells, further accentuated the difference between cell types. The phentoypic excitability difference did not correlate with time in culture (1-12 days) and could not be explained by resting potential (B cells: −65.6 ± 0.9 mV, C cells: −63.1 ± 1.6 mV) or input conductance density, which was greater in C cells (24.4 ± 4.3 pS/pF) than B cells (14.5 ± 1.5 pS/pF). Action potentials elicited by virtual EPSPs had a threshold voltage for firing that was −28.4 ± 0.7 mV in C cells and −19.7 ± 0.4 mV B cells, and an upstroke velocity and peak spike potential that were greater in B cells. The repetitive firing properties of B and C cells were similar; 69-78 % phasic, 11-16 % adapting and 11-15 % tonic. We propose that B and C neurons express different types of Na + channels that shape how they integrate nicotinic synaptic potentials.

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Effects of muscarine on K+-channel currents in the C-cells of bullfrog sympathetic ganglion

Cited by 11 publications

References 49 publications

Possible role of phosphatidylinositol 4,5, bisphosphate in luteinizing hormone releasing hormone‐mediated M‐current inhibition in bullfrog sympathetic neurons

Possible role of phosphatidylinositol 4,5, bisphosphate in luteinizing hormone releasing hormone‐mediated M‐current inhibition in bullfrog sympathetic neurons

Homeostatic regulation of M-current modulates synaptic integration in secretomotor, but not vasomotor, sympathetic neurons in the bullfrog

Vasomotor sympathetic neurons are more excitable than secretomotor sympathetic neurons in bullfrog paravertebral ganglia

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