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Neuromuscular synapses inAplysia have been used as model systems to study peptidergic cotransmission. Here we describe neuromuscular preparations in which
it has been possible to investigate the physiological consequences of peptide transmitter release in detail. In the first
preparation, the release of peptide cotransmitters from identified motor neuron B15 has been shown to be sensitive to the
pattern of stimulation. High frequencies and long burst durations evoke peptide release that modulates muscle contractions
in a manner similar to that produced by exogenous cotransmitter. By contrast, the release of the same peptide transmitters
from motor neuron B1 show little dependence on pattern. We conclude that there are no stimulation patterns that are prerequisites
for peptide release. Peptide cotransmitter release from motor neuron B47 has also been studied. B47, depending on the stimulation
pattern, uses either ACh, which acts as a conventional inhibitory transmitter, or Ach plus neuropeptides, which act as excitatory
modulatory cotransmitters. Thus, neuropeptide cotransmitters have the capability to greatly increase synaptic plasticity at
neuromuscular synapses. 相似文献
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Maddison R. Johnstone Rhys D. Brady Jarrod E. Church David Orr Stuart J. McDonald Brian L. Grills 《Journal of musculoskeletal & neuronal interactions》2021,21(2):263
Objectives:To study the effects of the selective TrkB agonist, 7,8-dihydroxyflavone (7,8-DHF), on fracture healing in mice and on an osteoprogenitor cell line, Kusa4b10, in vitro.Methods:Mice received unilateral closed mid-shaft tibial fractures and treated for two weeks with vehicle or 5 mg/kg/day DHF and euthanised at 28 days post-fracture. Calluses were analysed by micro-computed tomography (µCT) and three-point bending biomechanical test. Kusa4b10 cells were cultured with 50nM of 7,8-DHF or vehicle for 3-, 7-, 14-days for RT-PCR, and 21 days for mineralization.Results:µCT found 7,8-DHF calluses had decreased tissue volume (p=0.042), mean polar moment of inertia (p = 0.004), and mean cross-sectional area (p=0.042) compared to controls. At 28 days biomechanical analyses showed 7,8-DHF treatment decreased peak force (p=0.011) and stiffness per unit area (p=0.012). 7,8-DHF treatment did not change Kusa4b10 gene expression of Runx2 and alkaline phosphatase at all time points, nor mineralization.Conclusions:7,8-DHF treatment had a negative impact on fracture healing at 28 days post-fracture via an unknown mechanism. 7,8-DHF may have had a central role in impairing fracture healing. 相似文献
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