The Interaction between Tropomyosin-Related Kinase B Receptors and Presynaptic Muscarinic Receptors Modulates Transmitter Release in Adult Rodent Motor Nerve Terminals

García, Neus; Tomàs, Marta; Santafé, Manel M.; Besalduch, Núria; Lanuza, María A.; Tomàs, Josep

doi:10.1523/jneurosci.2676-10.2010

Cited by 54 publications

(78 citation statements)

References 44 publications

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“…BDNF interaction with tropomyosin-related kinase B receptors and presynaptic muscarinic receptors modulates transmitter release in adult rodent motor nerve terminal, which can improve stroke motor function recovery [51]. Previous studies reported that catalpol increased the hippocampal neuroplasticity in the aged rats [52] and attenuated MPTP-induced neuronal degeneration of nigral-striatal dopaminergic pathway in mice [53] partly attributed to BDNF upregulation.…”

Section: Discussionmentioning

confidence: 99%

Catalpol Induces Neuroprotection and Prevents Memory Dysfunction through the Cholinergic System and BDNF

Wan

Xue²,

Zhu

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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To investigate the role and mechanism of catalpol on neuroprotective effects and memory enhancing effects simultaneously, neuroprotective effects of catalpol were assessed by neurological deficits score, TTC staining, and cerebral blood flow detecting. Morris water maze was employed to investigate its effects on learning and memory and then clarify its possible mechanisms relating the central cholinergic system and BDNF. Edaravone and oxiracetam were used for positive control drugs based on its different action. Results showed that catalpol and edaravone significantly facilitated neurological function recovery, reduced infarction volume, and increased cerebral blood flow in stroke mice. Catalpol and oxiracetam decreased the escape latency significantly and increased the numbers of crossing platform obviously. The levels of ACh, ChAT, and BDNF in catalpol group were increased in a dose-dependent manner, and AChE declined with a U-shaped dose-response curve. Moreover, the levels of muscarinic AChR subtypes M1 and M2 in hippocampus were considerably raised by catalpol. These results demonstrated that catalpol may be useful for neuroprotection and memory enhancement, and the mechanism may be related to the central cholinergic system.

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Section: Discussionmentioning

confidence: 99%

Catalpol Induces Neuroprotection and Prevents Memory Dysfunction through the Cholinergic System and BDNF

Wan

Xue²,

Zhu

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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“…No differences were found between the muscles injected with PBS and those that were not, which suggests that the injection procedure did not in itself induce changes in the overall morphology of the motor end plate and nerve terminals. The solutions were administered at a concentration in accordance with the previously reported biological action of the substance [15,22,23] . The final concentration of dimethyl sulfoxide (DMSO) in control and drugtreated preparations was 0.1% (v/v).…”

Section: Injection Proceduresmentioning

confidence: 99%

“…The influx of external Ca 2+ required for Ca 2+ -triggered exocytosis and the fast mode of endocytosis seems to be promoted with the involvement of the presynaptic mAChR [34] , and interaction with the AR [44] but also with the BDNF-TrkB receptor pathway [23,43] . The mAChR and AR pathways (M 1 and A 1 receptors) share a link mediated by the set phospholipase C-phosphatidylinositol 4,5-bisphosphate (PIP2)-diacylglycerol (DAG)-PKC, which modulates P/Q-type voltage-dependent calcium channels [34,43] .…”

Section: Relation Between Machrs and Arsmentioning

confidence: 99%

Synergistic Action of Presynaptic Muscarinic Acetylcholine Receptors and Adenosine Receptors in Developmental Axonal Competition at the Neuromuscular Junction

Nadal

García²,

Hurtado³

et al. 2016

Dev Neurosci

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The development of the nervous system involves the initial overproduction of synapses, which promotes connectivity. Hebbian competition between axons with different activities leads to the loss of roughly half of the overproduced elements and this refines connectivity. We used quantitative immunohistochemistry to investigate, in the postnatal day 7 (P7) to P9 neuromuscular junctions, the involvement of muscarinic receptors (muscarinic acetylcholine autoreceptors and the M₁, M₂, and M₄ subtypes) and adenosine receptors (A₁ and A_2A subtypes) in the control of axonal elimination after the mouse levator auris longus muscle had been exposed to selective antagonists in vivo. In a previous study we analyzed the role of each of the individual receptors. Here we investigate the additive or occlusive effects of their inhibitors and thus the existence of synergistic activity between the receptors. The main results show that the A_2A, M₁, M₄, and A₁ receptors (in this order of ability) delayed axonal elimination at P7. M₄ produces some occlusion of the M₁ pathway and some addition to the A₁ pathway, which suggests that they cooperate. M₂ receptors may modulate (by allowing a permissive action) the other receptors, mainly M₄ and A₁. The continued action of these receptors (now including M₂ but not M₄) finally promotes axonal loss at P9. All 4 receptors (M₂, M₁, A₁, and A_2A, in this order of ability) are necessary. The M₄ receptor (which in itself does not affect axon loss) seems to modulate the other receptors. We found a synergistic action between the M₁, A₁, and A_2A receptors, which show an additive effect, whereas the potent M₂ effect is largely independent of the other receptors (though can be modulated by M₄). At P9, there is a full mutual dependence between the A₁ and A_2A receptors in regulating axon loss. In summary, postnatal axonal elimination is a regulated multireceptor mechanism that involves the cooperation of several muscarinic and adenosine receptor subtypes.

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“…We further provided evidence that p75NTR is important for BDNF-induced postsynaptic Ca 2+ elevation and synaptic potentiation at the developing NMJ. A recent study demonstrated that inhibition of either the TrkB receptor or p75NTR could inhibit synaptic potentiation at the rodent NMJ, although it was not determined whether the receptors were required pre- or postsynaptically (Garcia et al, 2010). In addition, a postsynaptic role of p75NTR has been implicated in regulation of dendritic spine density and dendritic complexity (Zagrebelsky et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…It has been well documented that blockade of TrkB function restricts BDNF-induced potentiation at the NMJ and at CNS synapses (Lohof et al, 1993; Kang and Schuman, 1995). Recently, p75NTR has been shown to be present at both presynaptic and postsynaptic sites in the adult mouse NMJ (Garcia et al, 2010). However, a functional role of p75NTR in neurotrophin-induced synaptic enhancement at NMJ has not been clearly established.…”

Section: Introductionmentioning

confidence: 99%

Postsynaptic TRPC1 Function Contributes to BDNF-Induced Synaptic Potentiation at the Developing Neuromuscular Junction

McGurk¹,

Shim²,

Kim³

et al. 2011

J. Neurosci.

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Brain-derived neurotrophic factor (BDNF) induces synaptic potentiation at both neuromuscular junctions (NMJs) and synapses of the central nervous system through a Ca2+-dependent pathway. The molecular mechanism underlying BDNF-induced synaptic potentiation, especially the regulation of Ca2+ dynamics, is not well understood. Using the Xenopus NMJ in culture as a model system, we show that pharmacological inhibition or morpholino-mediated knockdown of Xenopus TRPC1 (XTRPC1) significantly attenuated the BDNF-induced potentiation of the frequency of spontaneous synaptic responses at the NMJ. Functionally, XTRPC1 was required specifically in postsynaptic myocytes for BDNF-induced Ca2+ elevation and full synaptic potentiation at the NMJ, suggesting a previously under-appreciated postsynaptic function of Ca2+ signaling in neurotrophin-induced synaptic plasticity, in addition to its well-established role at presynaptic sites. Mechanistically, blockade of the p75 neurotrophin receptor abolished BDNF-induced postsynaptic Ca2+ elevation and restricted BDNF-induced synaptic potentiation, while knockdown of the TrkB receptor in postsynaptic myocytes had no effect. Our study suggests that BDNF-induced synaptic potentiation involves coordinated presynaptic and postsynaptic responses and identifies TRPC1 as a molecular mediator for postsynaptic Ca2+ elevation required for BDNF-induced synaptic plasticity.

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The Interaction between Tropomyosin-Related Kinase B Receptors and Presynaptic Muscarinic Receptors Modulates Transmitter Release in Adult Rodent Motor Nerve Terminals

Cited by 54 publications

References 44 publications

Catalpol Induces Neuroprotection and Prevents Memory Dysfunction through the Cholinergic System and BDNF

Catalpol Induces Neuroprotection and Prevents Memory Dysfunction through the Cholinergic System and BDNF

Synergistic Action of Presynaptic Muscarinic Acetylcholine Receptors and Adenosine Receptors in Developmental Axonal Competition at the Neuromuscular Junction

Postsynaptic TRPC1 Function Contributes to BDNF-Induced Synaptic Potentiation at the Developing Neuromuscular Junction

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