State-Dependent Mechanisms of LTP Expression Revealed by Optical Quantal Analysis

Ward, Bonnie C; McGuinness, Lindsay; Akerman, Colin J.; Fine, Alan; Bliss, T. V. P.; Emptage, Nigel J.

doi:10.1016/j.neuron.2006.10.007

Cited by 56 publications

(70 citation statements)

References 77 publications

(126 reference statements)

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“…Nevertheless, they provide evidence that this indirect assay is capable of approximating the probability of presynaptic neurotransmitter release (P r ) by measuring the probability of eliciting an EPSCaT (P Ca ) from electrical stimulation. They find that LTP induction caused P Ca to increase, leading to the conclusion that P r has also increased [16,18], except in silent synapses, where LTP expression is mediated entirely by AMPAR insertion [17], i.e. a purely postsynaptic modification.…”

Section: Multiple Forms Of Long-term Potentiationmentioning

confidence: 99%

Expression mechanisms underlying long-term potentiation: a postsynaptic view, 10 years on

Granger

2014

Phil. Trans. R. Soc. B

101

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This review focuses on the research that has occurred over the past decade which has solidified a postsynaptic expression mechanism for long-term potentiation (LTP). However, experiments that have suggested a presynaptic component are also summarized. It is argued that the pairing of glutamate uncaging onto single spines with postsynaptic depolarization provides the final and most elegant demonstration of a postsynaptic expression mechanism for NMDA receptor-dependent LTP. The fact that the magnitude of this LTP is similar to that evoked by pairing synaptic stimulation and depolarization leaves little room for a substantial presynaptic component. Finally, recent data also require a revision in our thinking about the way AMPA receptors (AMPARs) are recruited to the postsynaptic density during LTP. This recruitment is independent of subunit type, but does require an adequate reserve pool of extrasynaptic receptors.

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Section: Multiple Forms Of Long-term Potentiationmentioning

confidence: 99%

Expression mechanisms underlying long-term potentiation: a postsynaptic view, 10 years on

Granger

2014

Phil. Trans. R. Soc. B

101

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“…Regardless of the mechanisms, the same background DA tone may set D1-, D2-, and the putative D1/D2-containing spines at distinct biochemical, physiological, and activity states. Different basal states could determine how individual synapses undergo different experience-dependent changes [89].…”

Section: Diadsmentioning

confidence: 99%

Dopaminergic signaling in dendritic spines

Yao

Spealman

Zhang

2008

Biochemical Pharmacology

108

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Dopamine regulates movement, motivation, reward, and learning and is implicated in numerous neuropsychiatric and neurological disorders. The action of dopamine is mediated by a family of seven-transmembrane G protein-coupled receptors encoded by at least five dopamine receptor genes (D1, D2, D3, D4, and D5), some of which are major molecular targets for diverse neuropsychiatric medications. Dopamine receptors are present throughout the soma and dendrites of the neuron, but accumulating ultrastructural and biochemical evidence indicates that they are concentrated in dendritic spines, where most of the glutamatergic synapses are established. By modulating local channels, receptors, and signaling modules in spines, this unique population of postsynaptic receptors is strategically positioned to control the excitability and synaptic properties of spines and mediate both the tonic and phasic aspects of dopaminergic signaling with remarkable precision and versatility. The molecular mechanisms that underlie the trafficking, targeting, anchorage, and signaling of dopamine receptors in spines are, however, largely unknown. The present commentary focuses on this important subpopulation of postsynaptic dopamine receptors with emphases on recent molecular, biochemical, pharmacological, ultrastructural, and physiological studies that provide new insights about their regulatory mechanisms and unique roles in dopamine signaling. The Central Dopaminergic Systems: An OverviewDopamine (DA) is a prototypical slow neurotransmitter that plays pivotal roles in a variety of cognitive, motivational, neuroendocrine, and motor functions [1][2]. Two major groups of DAcontaining neurons in the mammalian brain reside in the substantia nigra pars compacta (SN) and the ventral tegmental area (VTA) [3]. SN neurons form the nigrostriatal pathway, which projects mainly to the dorsal part of striatum where they control postural reflexes and initiation of movements. VTA neurons give rise to two pathways: the mesolimbic pathway, which projects to the subcortical and limbic nuclei, and the mesocortical pathway, which projects mainly to the cingulate, entorhinal and medial prefrontal cortices. Dysfunction of dopaminergic transmission in these major pathways has been implicated in an array of neurological and neuropsychiatric disorders, including Parkinson's disease, Huntington's diseases, schizophrenia, attention-deficit hyperactivity disorder (ADHD), and drug addiction [1][2]. Drugs targeting dopaminergic mechanisms are widely used to manage these and other conditions.The action of DA is mediated by a family of seven-transmembrane G protein-coupled receptors (GPCRs) encoded by at least five DA receptor genes (D1, D2, D3, D4, and D5) in the mammalian brain [4]. These receptors are classified into two subfamilies, the D1-class and Corresponding author: Wei-Dong Yao, Ph.D., Department of Psychiatry, Harvard Medical School, Beth Israel Deaconess Medical Center, New England Primate Research Center, One Pine Hill Drive, P.O. Box 9102, Southborough,...

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“…However, presynaptic mechanisms may also play a role, particularly given that the silent synapses were observed at room temperature, conditions under which spillover is enhanced (Asztely et al, 1997). Interestingly, to achieve maximal potentiation, it has been suggested that synapses draw on both presynaptic and postsynaptic resources, with presynaptic potentiation emerging once silent synapses are unsilenced by postsynaptic mechanisms (Ward et al, 2006;Kerchner and Nicoll, 2008). Therefore, the emergence of novel A␦-fiber inputs after CFA inflammation may well result from a combination of both postsynaptic and presynaptic mechanisms.…”

mentioning

confidence: 99%

Inflammatory Pain Unmasks Heterosynaptic Facilitation in Lamina I Neurokinin 1 Receptor-Expressing Neurons in Rat Spinal Cord

Torsney¹

2011

J. Neurosci.

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Central sensitization in inflammatory pain conditions results in behavioral mechanical hypersensitivity. Specifically, C-fiber-driven spinal hyperexcitability enables A fibers to gain access to specific spinal circuitry, via heterosynaptic facilitatory mechanisms, to mediate mechanical hypersensitivity. However, the precise circuitry engaged is not known. Lamina I neurokinin 1 (NK1) receptor expressing (NK1R Control neurons predominantly received monosynaptic C-fiber input (69%) with a smaller proportion receiving monosynaptic A␦-fiber input (28%). In contrast, CFA inflammation significantly increased the incidence (by twofold) and magnitude (by 75% in a subset) of monosynaptic A␦-fiber but not monosynaptic C-fiber-evoked responses. A␤-fiber input to lamina I NK1Rϩ neurons was minimal, polysynaptic in nature, and unaltered by CFA inflammation. Additional examination of control neurons revealed that a proportion received silent monosynaptic A␦-fiber input, suggesting that these may provide the substrate for the novel A␦ inputs observed in CFA inflammation. This inflammation induced unmasking and strengthening of monosynaptic A␦ drive to lamina I NK1R ϩ neurons may contribute to the heterosynaptic facilitatory mechanisms underlying mechanical hyperalgesia in inflammatory pain.

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State-Dependent Mechanisms of LTP Expression Revealed by Optical Quantal Analysis

Cited by 56 publications

References 77 publications

Expression mechanisms underlying long-term potentiation: a postsynaptic view, 10 years on

Expression mechanisms underlying long-term potentiation: a postsynaptic view, 10 years on

Dopaminergic signaling in dendritic spines

Inflammatory Pain Unmasks Heterosynaptic Facilitation in Lamina I Neurokinin 1 Receptor-Expressing Neurons in Rat Spinal Cord

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