Glutamate and acetylcholine release from cholinergic nerve terminals, a calcium control of the specificity of the release mechanism

Israël, Maurice; Lesbats, B.; Bruner, J.

doi:10.1016/0197-0186(93)90068-g

Cited by 41 publications

(25 citation statements)

References 12 publications

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“…The authors have shown the corelease of these two mediators in Ca 2+ -dependent manner under the action of depolarizing agents [78]. This fact of a simultaneous release ACh and amino acid was confirmed later by other authors [79]. Electrophysiological data showing action potential induced corelease of glutamate and ACh from of mammals motor neurons was obtained recently [80,81].…”

Section: Glutamatergic Signalingsupporting

confidence: 60%

Non-Cholinergic Signaling Pathways at Vertebrate Neuromuscular Junctions

Malomouzh¹

2012

Skeletal Muscle - From Myogenesis to Clinical Relations

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Section: Glutamatergic Signalingsupporting

confidence: 60%

Non-Cholinergic Signaling Pathways at Vertebrate Neuromuscular Junctions

Malomouzh¹

2012

Skeletal Muscle - From Myogenesis to Clinical Relations

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“…Corelease of ACh and glutamate has been described previously in Torpedo electric organ synaptosomes (Israel et al, 1993) and from amphibian neurons (Li et al, 2004), and very recently, a component of the synaptic current at the classical nicotinic motoneuron-Renshaw cell synapse in the spinal cord has been attributed to the release of glutamate (Mentis et al, 2005;Nishimura et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Simultaneous Release of Glutamate and Acetylcholine from Single Magnocellular “Cholinergic” Basal Forebrain Neurons

2006

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Basal forebrain (BF) neurons provide the principal cholinergic drive to the hippocampus and cortex. Their degeneration is associated with the cognitive defects of Alzheimer's disease. Immunohistochemical studies suggest that some of these neurons contain glutamate, so might also release it. To test this, we made microisland cultures of single BF neurons from 12-to 14-d-old rats. Over 1-8 weeks in culture, neuronal processes made autaptic connections onto the neuron. In 34 of 36 cells tested, a somatically generated action potential was followed by a short-latency EPSC that was blocked by 1 mM kynurenic acid, showing that they released glutamate. To test whether the same neuron also released acetylcholine, we placed a voltage-clamped rat myoball expressing nicotinic receptors in contact with a neurite. In six of six neurons tested, the glutamatergic EPSC was accompanied by a nicotinic (hexamethonium-sensitive) myoball current. Stimulation of the M 2 -muscarinic presynaptic receptors (characterized using tripitramine and pirenzepine) produced a parallel inhibition of autaptic glutamatergic and myoball nicotinic responses; metabotropic glutamate receptor stimulation produced similar but less consistent and weaker effects. Atropine enhanced the glutamatergic EPSCs during repetitive stimulation by 25 Ϯ 6%; the anti-cholinesterase neostigmine reduced the train EPSCs by 37 Ϯ 6%. Hence, synaptically released acetylcholine exerted a negative-feedback inhibition of coreleased glutamate. We conclude that most cholinergic basal forebrain neurons are capable of releasing glutamate as a cotransmitter and that the release of both transmitters is subject to simultaneous feedback inhibition by synaptically released acetylcholine. This has implications for BF neuron function and for the use of cholinesterase inhibitors in Alzheimer's disease.

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“…If glutamate and acetylcholine are stored in separate vesicles, the two transmitters could be released concurrently or differentially. In the Torpedo electric organ synaptosomal preparation, acetylcholine and glutamate release occur differentially as a function of calcium concentrations (Israel et al, 1993). In this preparation, the release of acetylcholine requires lower calcium concentrations than glutamate.…”

Section: Functional Implications Of Vglut3 In Cholinergic Axon Terminalsmentioning

confidence: 99%

Vesicular glutamate transporter 3 immunoreactivity is present in cholinergic basal forebrain neurons projecting to the basolateral amygdala in rat

Poulin

Guerci

Mestikawy

et al. 2006

J of Comparative Neurology

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The basal forebrain (BF) plays a role in behavioral and cortical arousal, attention, learning, and memory. It has been suggested that cholinergic BF neurons co-release glutamate, and some cholinergic BF neurons have been reported to contain vesicular glutamate transporter 3 (VGLUT3). We examined the distribution and projections of BF cholinergic neurons containing VGLUT3, by using dual-label immunofluorescence for choline acetyltransferase (ChAT) and VGLUT3, in situ hybridization, and retrograde tracing. Neurons immunoreactive (+) or containing mRNAs for both ChAT and VGLUT3 were mainly localized to the ventral pallidum and more caudal BF regions; the co-immunoreactive neurons represented 31% of cholinergic neurons in the ventral pallidum and 5-9% more caudally. Examination of cholinergic axon terminals in known target areas of BF projections indicated that the basolateral amygdaloid nucleus contained numerous terminals co-immunoreactive for ChAT and VGLUT3, whereas sampled areas of the olfactory bulb, neocortex, hippocampus, reticular thalamic nucleus, and interpeduncular nucleus were devoid of double-labeled terminals. The basolateral amygdala is innervated by cholinergic BF neurons lacking low-affinity p75 nerve growth factor receptors; many ChAT+VGLUT3+ BF neurons were immunonegative to this receptor. Twenty-five to 79% of ChAT+VGLUT3+ neurons in different BF regions were retrogradely labeled from the basolateral amygdala, up to 52% (ventral pallidum) of the retrogradely labeled ChAT+ neurons were VGLUT3+, and the largest number of amygdala-projecting ChAT+VGluT3+ neurons was found in the ventral pallidum. These findings indicate that BF cholinergic neurons containing VGLUT3 project to the basolateral amygdala and suggest that these neurons might have the capacity to release both acetylcholine and glutamate.

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Glutamate and acetylcholine release from cholinergic nerve terminals, a calcium control of the specificity of the release mechanism

Cited by 41 publications

References 12 publications

Non-Cholinergic Signaling Pathways at Vertebrate Neuromuscular Junctions

Non-Cholinergic Signaling Pathways at Vertebrate Neuromuscular Junctions

Simultaneous Release of Glutamate and Acetylcholine from Single Magnocellular “Cholinergic” Basal Forebrain Neurons

Vesicular glutamate transporter 3 immunoreactivity is present in cholinergic basal forebrain neurons projecting to the basolateral amygdala in rat

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