Continuous repetitive stimuli are more effective than bursts for evoking LHRH release in bullfrog sympathetic ganglia

Peng, Yan-Yi; Horn, John P.

doi:10.1523/jneurosci.11-01-00085.1991

Cited by 63 publications

(49 citation statements)

References 39 publications

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“…Preparation of isolated bullfrog sympathetic ganglia, electrical stimulation to presynaptic nerve, selective filling of preganglionic nerve terminals with membrane-impermeant fura-2 pentapotassium salt, and fura-2 fluorimetric measurements of [Ca 2ϩ ] i in these terminals were carried out as described previously (Dodd and Horn, 1983;Peng and Horn, 1991;Zucker, 1991, 1993). Briefly, preparations containing paravertebral ganglia 8 -10 were isolated from 12-18 cm bullfrogs (Rana catesbiana).…”

Section: Methodsmentioning

confidence: 99%

“…Intraterminal [Ca 2ϩ ] i , measured by fura-2 fluorimetry, was elevated by trains of electrical shocks to the cut end of presynaptic nerves. The stimuli were delivered at 20 Hz because it is the favorable stimulation for LHRH release (Peng and Horn, 1991). Intraterminal [Ca 2ϩ ] i was studied in a group of boutons contacting a cell (i.e., a unit) instead of individual boutons for three reasons.…”

Section: Effects Of Ryanodine On Intraterminal [Ca 2؉ ] Transients Evmentioning

confidence: 99%

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Ryanodine-Sensitive Component of Calcium Transients Evoked by Nerve Firing at Presynaptic Nerve Terminals

Peng

1996

J. Neurosci.

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Whether Ca 2ϩ released from stores within the presynaptic nerve terminals also contributes to the Ca 2ϩ elevation evoked by action potentials was tested in intact bullfrog sympathetic ganglia. Intraterminal Ca 2ϩ transients (⌬[Ca 2ϩ ] i ) were evoked by electrical shocks to the presynaptic nerves at 20 Hz and were monitored by fura-2 fluorimetry. Ca 2ϩ released through intraterminal ryanodine-sensitive channels accounted for 46% of the peak Ca 2ϩ elevation. Moreover, in half of the terminals when intraterminal release was blocked by ryanodine, ⌬[Ca 2ϩ ] i reached a plateau at 200 Ϯ 24 nM. Because 20 Hz is a frequency favorable for the release of a neuropeptide, luteinizing hormone releasing hormone (LHRH) from these presynaptic nerve terminals, and because the threshold level for LHRH release is 186 nM, intraterminal Ca 2ϩ release during nerve firing is likely to play a major role in regulating LHRH release. The intraterminal ryanodine channels were facilitated by caffeine as in other tissue. The releasable ryanodine-sensitive store could elevate the intraterminal [Ca 2ϩ ] by an amount as high as 1.6 M at a rate as fast as 250 nM/sec. The store could be refilled within 100 sec after a maximal discharge of its content by 20 Hz firing. Oscillation of [Ca 2ϩ ] i evoked by 20 Hz nerve firing occurred in normal Ringer solution, in ryanodine, and in caffeine with a periodicity of ϳ10 sec. Besides the facilitatory effects on the ryanodine-sensitive channels, caffeine also had inhibitory effects on ⌬[Ca 2ϩ ] i via its action on a different process.

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Section: Methodsmentioning

confidence: 99%

Section: Effects Of Ryanodine On Intraterminal [Ca 2؉ ] Transients Evmentioning

confidence: 99%

Ryanodine-Sensitive Component of Calcium Transients Evoked by Nerve Firing at Presynaptic Nerve Terminals

Peng

1996

J. Neurosci.

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“…Preparations of paravertebrate sympathetic ganglia 7-10 were isolated from 5-to 10-cm bullfrogs and were set up for intracellular electrophysiological recording as described (14,15). Impaled cells were classified as B or C neurons according to the conduction velocity of their axons (14).…”

Section: Methodsmentioning

confidence: 99%

Activation of nicotinic receptor-induced postsynaptic responses to luteinizing hormone-releasing hormone in bullfrog sympathetic ganglia via a Na ⁺ -dependent mechanism

Cao¹,

Peng²

1998

Proc. Natl. Acad. Sci. U.S.A.

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Nicotine at very low doses (5-30 nM) induced large amounts of luteinizing hormone-releasing hormone (LHRH) release, which was monitored as slow membrane depolarizations in the ganglionic neurons of bullfrog sympathetic ganglia. A nicotinic antagonist, d-tubocurarine chloride, completely and reversibly blocked the nicotine-induced LHRH release, but it did not block the nerve-firing-evoked LHRH release. Thus, nicotine activated nicotinic acetylcholine receptors and produced LHRH release via a mechanism that is different from the mechanism for evoked release. Moreover, this release was not caused by Ca 2؉ inf lux through either the nicotinic receptors or the voltage-gated Ca 2؉ channels because the release was increased moderately when the extracellular solution was changed into a Ca 2؉ -free solution that also contained Mg 2؉ (4 mM) and Cd 2؉ (200 M). The release did not depend on Ca 2؉ release from the intraterminal Ca 2؉ stores either because fura-2 f luorimetry showed extremely low Ca 2؉ elevation (Ϸ30 nM) in response to nicotine (30 nM). Moreover, nicotine evoked LHRH release when [Ca 2؉ ] elevation in the terminals was prevented by loading the terminals with 1,2-bis(2-aminophenoxy)ethane-N,N,N,Ntetraacetic acid and fura-2. Instead, the nicotine-induced release required extracellular Na ؉ because substitution of extracellular NaCl with N-methyl-D-glucamine chloride completely blocked the release. The Na ؉ -dependent mechanism was not via Na ؉ inf lux through the voltage-gated Na ؉ channels because the release was not affected by tetrodotoxin (1-50 M) plus Cd 2؉ (200 M). Thus, nicotine at very low concentrations induced LHRH release via a Na ؉ -dependent, Ca 2؉ -independent mechanism.

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“…This may relate to the transient effect of LHRH compared with the sustained effect of NGF on ERK1/2 phosphorylation. Since neuropeptide release is favored by intense neuronal activity (Peng and Horn 1991), regulation of Ca 2ϩ channels by LHRH may couple preganglionic activity to alterations in the electrical properties of postganglionic cells. The release of neuropeptides from preganglionic fibers also causes long-term increases in tyrosine hydroxylase activity and noradrenaline synthesis (McKeon and Zigmond 1993).…”

Section: Lack Of Effect Of Lhrh On Na ϩ Currentsmentioning

confidence: 99%

Differential Neurotrophic Regulation of Sodium and Calcium Channels in an Adult Sympathetic Neuron

Ford

Wong

et al. 2008

Journal of Neurophysiology

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Ford CP, Wong KV, Lu VB, Posse de Chaves E, Smith PA. Differential neurotrophic regulation of sodium and calcium channels in an adult sympathetic neuron. J Neurophysiol 99: 1319 -1332, 2008. First published January 23, 2008 doi:10.1152/jn.00966.2007. Adult neuronal phenotype is maintained, at least in part, by the sensitivity of individual neurons to a specific selection of neurotrophic factors and the availability of such factors in the neurons' environment. Nerve growth factor (NGF) increases the functional expression of Na ϩ channel currents (I Na ) and both N-and L-type Ca 2ϩ currents (I Ca,N and I Ca,L ) in adult bullfrog sympathetic ganglion (BFSG) B-neurons. The effects of NGF on I Ca involve the mitogen-activated protein kinase (MAPK) pathway. Prolonged exposure to the ganglionic neurotransmitter luteinizing hormone releasing hormone (LHRH) also increases I Ca,N but the transduction mechanism remains to be elucidated as does the transduction mechanism for NGF regulation of Na ϩ channels. We therefore exposed cultured BFSG B-neurons to chicken II LHRH (0.45 M; 6 -9 days) or to NGF (200 ng/ml; 9 -10 days) and used whole cell recording, immunoblot analysis, and ras or rap-1 pulldown assays to study effects of various inhibitors and activators of transduction pathways. We found that 1) LHRH signals via ras-MAPK to increase I Ca,N , 2) this effect is mediated via protein kinase C-␤ (PKC-␤-⌱⌱), 3) protein kinase A (PKA) is necessary but not sufficient to effect transduction, 4) NGF signals via phosphatidylinositol 3-kinase (PI3K) to increase I Na , and 5) long-term exposure to LHRH fails to affect I Na . Thus downstream signaling from LHRH has access to the ras-MAPK pathway but not to the PI3K pathway. This allows for differential retrograde and anterograde neurotrophic regulation of sodium and calcium channels in an adult sympathetic neuron.

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Continuous repetitive stimuli are more effective than bursts for evoking LHRH release in bullfrog sympathetic ganglia

Cited by 63 publications

References 39 publications

Ryanodine-Sensitive Component of Calcium Transients Evoked by Nerve Firing at Presynaptic Nerve Terminals

Ryanodine-Sensitive Component of Calcium Transients Evoked by Nerve Firing at Presynaptic Nerve Terminals

Activation of nicotinic receptor-induced postsynaptic responses to luteinizing hormone-releasing hormone in bullfrog sympathetic ganglia via a Na ⁺ -dependent mechanism

Differential Neurotrophic Regulation of Sodium and Calcium Channels in an Adult Sympathetic Neuron

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Continuous repetitive stimuli are more effective than bursts for evoking LHRH release in bullfrog sympathetic ganglia

Cited by 63 publications

References 39 publications

Ryanodine-Sensitive Component of Calcium Transients Evoked by Nerve Firing at Presynaptic Nerve Terminals

Ryanodine-Sensitive Component of Calcium Transients Evoked by Nerve Firing at Presynaptic Nerve Terminals

Activation of nicotinic receptor-induced postsynaptic responses to luteinizing hormone-releasing hormone in bullfrog sympathetic ganglia via a Na + -dependent mechanism

Differential Neurotrophic Regulation of Sodium and Calcium Channels in an Adult Sympathetic Neuron

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Activation of nicotinic receptor-induced postsynaptic responses to luteinizing hormone-releasing hormone in bullfrog sympathetic ganglia via a Na ⁺ -dependent mechanism