Presynaptic muscarinic inhibition in bullfrog sympathetic ganglia.

Shen, Wei; Horn, John P.

doi:10.1113/jphysiol.1996.sp021225

Cited by 20 publications

(15 citation statements)

References 39 publications

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“…Consistent with a decrease in presynaptic transmitter release (e.g., Choi and Lovinger 1997;Shen and Horn 1996), the CV 2 of pharmacologically isolated AMPAR-EPSCs was significantly increased after TBS of MFs (n ϭ 8, P ϭ 0.0039 Wilcoxon signed-rank test); a similar increase was observed for the CV 2 of pharmacologically isolated NMDAR-EPSCs after MF TBS (n ϭ 14, P Ͻ 0.0001 Wilcoxon signed-rank test). Also consistent with a presynaptic change (Faber and Korn 1991;Shen and Horn 1996), the plot of the fractional change in CV 2 (r) versus the synaptic gain factor (f) showed a significant correlation with all points to the right of the diagonal (r ϭ f; AMPAR-EPSCs linear regression slope ϭ 0.40, significantly different from unity P ϭ 0.0246, n ϭ 8; NMDAREPSCs linear regression slope ϭ 0.35, significantly different from unity P ϭ 0.0012, n ϭ 14; Fig. 4D).…”

Section: Tbs Of Mfs Causes a Bdnf-dependent Depression Of Excitatory supporting

confidence: 71%

“…Indeed, both AMPAR-and NMDAR-mediated EPSCs were significantly depressed after TBS of MFs, an effect prevented by the BDNF scavenger TrkBIgG and the tyrosine kinase inhibitor k-252b. Because this depression was associated with changes in CV 2 but not in the NMDAR/ AMPAR ratio, its expression mechanism appears to be a reduction in presynaptic neurotransmitter release (Faber and Korn 1991;Shen and Horn 1996), an unexpected result considering the well-documented enhancement of presynaptic transmitter release by BDNF (Carvalho et al 2008;Tyler et al 2002). Regarding the LTP induced in CA3 pyramidal neurons by TBS of MFs reported by Nicholls et al (2006), we should note that differences in the duration of TBS conditioning stimuli likely account for the different outcomes in that study and in the present communication.…”

Section: Discussionmentioning

confidence: 99%

“…The fractional change in CV 2 (r ϭ CV 2 before TBS /CV 2 after TBS ) was plotted against a synaptic gain factor (f ϭ EPSC amplitude after TBS /EPSC amplitude before TBS ), as described (Faber and Korn 1991;Shen and Horn 1996).…”

Section: Coefficient Of Variation Analysismentioning

confidence: 99%

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Activity-Dependent Release of Endogenous BDNF From Mossy Fibers Evokes a TRPC3 Current and Ca²⁺Elevations in CA3 Pyramidal Neurons

Calfa

Inoue

et al. 2010

Journal of Neurophysiology

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Multiple studies have demonstrated that brain-derived neurotrophic factor (BDNF) is a potent modulator of neuronal structure and function in the hippocampus. However, the majority of studies to date have relied on the application of recombinant BDNF. We herein report that endogenous BDNF, released via theta burst stimulation of mossy fibers (MF), elicits a slowly developing cationic current and intracellular Ca 2ϩ elevations in CA3 pyramidal neurons with the same pharmacological profile of the transient receptor potential canonical 3 (TRPC3)-mediated I BDNF activated in CA1 neurons by brief localized applications of recombinant BDNF. Indeed, sensitivity to both the extracellular BDNF scavenger tropomyosin-related kinase B (TrkB)-IgG and small hairpin interference RNA-mediated TRPC3 channel knockdown confirms the identity of this conductance as such, henceforth-denoted MF-I BDNF . Consistent with such activity-dependent release of BDNF, these MF-I BDNF responses were insensitive to manipulations of extracellular Zn 2ϩ concentration. Brief theta burst stimulation of MFs induced a long-lasting depression in the amplitude of excitatory postsynaptic currents (EPSCs) mediated by both AMPA and N-methyl-D-aspartate (NMDA) receptors without changes in the NMDA receptor/AMPA receptor ratio, suggesting a reduction in neurotransmitter release. This depression of NMDAR-mediated EPSCs required activitydependent release of endogenous BDNF from MFs and activation of Trk receptors, as it was sensitive to the extracellular BDNF scavenger TrkB-IgG and the tyrosine kinase inhibitor k-252b. These results uncovered the most immediate response to endogenously releasednative-BDNF in hippocampal neurons and lend further credence to the relevance of BDNF signaling for synaptic function in the hippocampus.

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Section: Tbs Of Mfs Causes a Bdnf-dependent Depression Of Excitatory supporting

confidence: 71%

Section: Discussionmentioning

confidence: 99%

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Activity-Dependent Release of Endogenous BDNF From Mossy Fibers Evokes a TRPC3 Current and Ca²⁺Elevations in CA3 Pyramidal Neurons

Calfa

Inoue

et al. 2010

Journal of Neurophysiology

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“…The subsequent activation of G proteins can lead to inhibition of presynaptic Ca 2ϩ current and depression of transmitter release (Chen and van den Pol 1998;Shen and Horn 1996;Shen and Johnson 1997;Wu and Saggau 1997). Here we investigate the effects of different G␤-Ca v ␤ subunit combinations on synaptic depression induced by autoinhibition.…”

Section: Synaptic Depression Through Autoinhibitionmentioning

confidence: 99%

A Minimal Model for G Protein–Mediated Synaptic Facilitation and Depression

Bertram

Swanson

Yousef

et al. 2003

Journal of Neurophysiology

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hormones or neurotransmitters splits the G protein heterotrimer into G␣ and G␤␥ subunits. It is now clear that G␤␥ directly inhibits Ca 2ϩ channels, putting them into a reluctant state. The effects of G␤␥ depend on the specific ␤ and ␥ subunits present, as well as the ␤ subunit isoform of the N-type Ca 2ϩ channel. We describe a minimal mathematical model for the effects of G protein action on the dynamics of synaptic transmission. The model is calibrated by data obtained by transfecting G protein and Ca 2ϩ channel subunits into tsA-201 cells. We demonstrate with numerical simulations that G protein action can provide a mechanism for either short-term synaptic facilitation or depression, depending on the manner in which G protein-coupled receptors are activated. The G protein action performs high-pass filtering of the presynaptic signal, with a filter cutoff that depends on the combination of G protein and Ca 2ϩ channel subunits present. At stimulus frequencies above the cutoff, trains of single spikes are transmitted, while only doublets are transmitted at frequencies below the cutoff. Finally, we demonstrate that relief of G protein inhibition can contribute to pairedpulse facilitation.

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“…Paravertebral sympathetic ganglia 9 and 10 in the bullfrog contain two parallel systems, the B pathway and the C pathway (Libet, Chichibu & Tosaka, 1968;Dodd & Horn, 1983). Ganglionic B and C neurones all have nicotinic synapses but differ in their expression of muscarinic and peptidergic mechanisms of cotransmission (Kuffler, 1980;Horn, 1992;Smith, 1994;Shen & Horn, 1996). In addition, the two cell types control different targets.…”

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confidence: 99%

In vitro relation between preganglionic sympathetic stimulation and activity of cutaneous glands in the bullfrog.

Jobling

Horn

1996

The Journal of Physiology

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Repetitive preganglionic stimulation of the C pathway (> 100 at 20 Hz) evoked little change in TEP and did not modulate depolarizations evoked through the B pathway. In nicotine, peptidergic cotransmission was enhanced in the ganglia, and repetitive C pathway stimulation evoked cutaneous depolarizations whose time course mirrored that of the postganglionic peptidergic after-discharge. The after-discharge and associated cutaneous depolarization were blocked by a luteinizing hormone-releasing hormone antagonist. 5. The results show cutaneous glands are selectively innervated by B neurones and respond to low levels of neural activity. Asynchronous postganglionic firing mediated by peptidergic cotransmission can provide a basis for heterosynaptic interactions between the B and C pathways.

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Presynaptic muscarinic inhibition in bullfrog sympathetic ganglia.

Cited by 20 publications

References 39 publications

Activity-Dependent Release of Endogenous BDNF From Mossy Fibers Evokes a TRPC3 Current and Ca²⁺Elevations in CA3 Pyramidal Neurons

Activity-Dependent Release of Endogenous BDNF From Mossy Fibers Evokes a TRPC3 Current and Ca²⁺Elevations in CA3 Pyramidal Neurons

A Minimal Model for G Protein–Mediated Synaptic Facilitation and Depression

In vitro relation between preganglionic sympathetic stimulation and activity of cutaneous glands in the bullfrog.

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Presynaptic muscarinic inhibition in bullfrog sympathetic ganglia.

Cited by 20 publications

References 39 publications

Activity-Dependent Release of Endogenous BDNF From Mossy Fibers Evokes a TRPC3 Current and Ca2+Elevations in CA3 Pyramidal Neurons

Activity-Dependent Release of Endogenous BDNF From Mossy Fibers Evokes a TRPC3 Current and Ca2+Elevations in CA3 Pyramidal Neurons

A Minimal Model for G Protein–Mediated Synaptic Facilitation and Depression

In vitro relation between preganglionic sympathetic stimulation and activity of cutaneous glands in the bullfrog.

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Product

Resources

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Activity-Dependent Release of Endogenous BDNF From Mossy Fibers Evokes a TRPC3 Current and Ca²⁺Elevations in CA3 Pyramidal Neurons

Activity-Dependent Release of Endogenous BDNF From Mossy Fibers Evokes a TRPC3 Current and Ca²⁺Elevations in CA3 Pyramidal Neurons