Cell Type-Specific, Presynaptic LTP of Inhibitory Synapses on Fast-Spiking GABAergic Neurons in the Mouse Visual Cortex

Sarihi, Abdolrahman; Mirnajafi‐Zadeh, Javad; Jiang, Bin; Sohya, Kazuhiro; Safari, Mir-Shahram; Kourosh-Arami, Masoumeh; Yanagawa, Yuchio; Tsumoto, Tadaharu

doi:10.1523/jneurosci.1386-12.2012

Cited by 25 publications

(25 citation statements)

References 71 publications

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“…FSI dysfunction is implicated in diseases such as schizophrenia and Dravet Syndrome (Yamakawa, 2011; Nakazawa et al, 2012). A presynaptic form of LTP has recently been described in FSIs at layer II/III of the mouse visual cortex (Sarihi et al, 2012). Tetanic stimulation of the presynaptic FSI in a paired whole-cell recording configuration demonstrated potentiation of unitary IPSCs in FSI → FSI pairs, but not non-FSI → FSI pairs.…”

Section: Forms Of Presynaptic Long-term Plasticitymentioning

confidence: 98%

“…Since its introduction, quantal analysis and its derivatives, such as coefficient of variation ( CV ) and minimal stimulation, have been used widely to investigate whether a change in neurotransmitter release accompanies long-term changes in synaptic strength. These methods were used in the first studies that proposed a presynaptic expression locus of LTP (at hippocampal mossy fiber-CA3 synapses) (Malinow and Tsien, 1990; Hirata et al, 1991), and have been subsequently employed to support a presynaptic expression locus during long-term plasticity in diverse brain regions which include hippocampal mossy fiber-interneuron synapses (Pelkey et al, 2005), hippocampal GABAergic synapses (Laezza et al, 1999), the amygdala (Tsvetkov et al, 2002; Fourcaudot et al, 2008), the neocortex (Torii et al, 1997; Sjöström et al, 2003, 2004; Huang et al, 2008a; Sarihi et al, 2012), striatum (Choi and Lovinger, 1997a), ventral tegmental area (VTA) (Pan et al, 2008) and cerebellum (Maejima et al, 2001). …”

Section: Physiological Characteristics Supporting a Presynaptic Locusmentioning

confidence: 99%

“…The mechanism for this change has been attributed to effects of presynaptic calcium dynamics and depletion of “release-ready” vesicles (Zucker, 1989; Debanne et al, 1996; Inchauspe et al, 2004; Catterall and Few, 2008). A decrease in PPR accompanies LTP at mossy fiber-CA3 pyramidal synapses (Zalutsky and Nicoll, 1990), corticothalamic synapses (Castro-Alamancos and Calcagnotto, 1999), cortical and thalamic synapses with lateral amygdala (Tsvetkov et al, 2002; Samson and Paré, 2005) and in other brain regions (Li et al, 2000; Lauri et al, 2007; Sarihi et al, 2012). Conversely, an increase in PPR accompanies LTD from electric stimulation or drug applications in various brain regions (Huang et al, 2001; Gerdeman et al, 2002; Chevaleyre and Castillo, 2003; Nosyreva and Huber, 2005).…”

Section: Physiological Characteristics Supporting a Presynaptic Locusmentioning

confidence: 99%

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Presynaptic long-term plasticity

Yang

Calakos

2013

Front. Synaptic Neurosci.

118

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Long-term synaptic plasticity is a major cellular substrate for learning, memory, and behavioral adaptation. Although early examples of long-term synaptic plasticity described a mechanism by which postsynaptic signal transduction was potentiated, it is now apparent that there is a vast array of mechanisms for long-term synaptic plasticity that involve modifications to either or both the presynaptic terminal and postsynaptic site. In this article, we discuss current and evolving approaches to identify presynaptic mechanisms as well as discuss their limitations. We next provide examples of the diverse circuits in which presynaptic forms of long-term synaptic plasticity have been described and discuss the potential contribution this form of plasticity might add to circuit function. Finally, we examine the present evidence for the molecular pathways and cellular events underlying presynaptic long-term synaptic plasticity.

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Section: Forms Of Presynaptic Long-term Plasticitymentioning

confidence: 98%

Section: Physiological Characteristics Supporting a Presynaptic Locusmentioning

confidence: 99%

Section: Physiological Characteristics Supporting a Presynaptic Locusmentioning

confidence: 99%

See 1 more Smart Citation

Presynaptic long-term plasticity

Yang

Calakos

2013

Front. Synaptic Neurosci.

118

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“…For instance, mefloquine does not appear to interact with glutamate receptors (Caridha et al, (2008), but the psychotropic effects of lysergic acid diethylamide (LSD) may include indirect changes in the regulation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors (Marona-Lewicka et al, 2011), and the psychotomimetic, phencyclidine, is an NMDA receptor antagonist (Thomson et al, 1985). In addition, there is literally no evidence concerning the interactions of LSD and other psychotomimetics with gap junction elements, but mefloquine (25 μM) blocks a number of connexins (Cruikshank et al, 2004; Iglesias et al, 2008; Wang et al, 2010) and is now commonly used as a research tool to block gap junction channels (Sarihi et al, 2012). Mefloquine also interacts with gamma-aminobutyric acid A (GABA A ) receptors (Amabeoku and Farmer, 2005; Thompson and Loomis, 2008), and interacts with peripheral benzodiazepine receptors (Dzierszinski et al, 2002), adenosine A 1 and A 2A receptors (Weiss et al, 2003; Gillespie et al, 2008), and 5-HT 3 receptors (Thompson et al, 2007; Thompson and Loomis 2008.…”

Section: Introductionmentioning

confidence: 99%

Mefloquine and psychotomimetics share neurotransmitter receptor and transporter interactions in vitro

et al. 2014

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Rationale Mefloquine is used for the prevention and treatment of chloroquine-resistant malaria, but its use is associated with nightmares, hallucinations, and exacerbation of symptoms of post-traumatic stress disorder. We hypothesized that potential mechanisms of action for the adverse psychotropic effects of mefloquine resemble those of other known psychotomimetics. Objectives Using in vitro radioligand binding and functional assays, we examined the interaction of (+)- and (−)-mefloquine enantiomers, the non-psychotomimetic anti-malarial agent, chloroquine, and several hallucinogens and psychostimulants with recombinant human neurotransmitter receptors and transporters. Results Hallucinogens and mefloquine bound stereoselectively and with relatively high affinity (Ki = 0.71–341 nM) to serotonin (5-HT) 2A but not 5-HT1A or 5-HT2C receptors. Mefloquine but not chloroquine was a partial 5-HT2A agonist and a full 5-HT2C agonist, stimulating inositol phosphate accumulation, with similar potency and efficacy as the hallucinogen dimethyltryptamine (DMT). 5-HT receptor antagonists blocked mefloquine’s effects. Mefloquine had low or no affinity for dopamine D1, D2, D3, and D4.4 receptors, or dopamine and norepinephrine transporters. However, mefloquine was a very low potency antagonist at the D3 receptor and mefloquine but not chloroquine or hallucinogens blocked [3H]5-HT uptake by the 5-HT transporter. Conclusions Mefloquine but not chloroquine shares an in vitro receptor interaction profile with some hallucinogens and this neurochemistry may be relevant to the adverse neuropsychiatric effects associated with mefloquine use by a small percentage of patients. Additionally, evaluating interactions with this panel of receptors and transporters may be useful for characterizing effects of other psychotropic drugs and for avoiding psychotomimetic effects for new pharmacotherapies, including antimalarial quinolines.

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“…Additional sharpening of plasticity at the circuit level is provided by differential expression of long-term plasticity (either LTP or LTD, both forms or neither form) at excitatory inputs with specific populations of inhibitory (GABA) interneurons (Chang et al 2010;Nissen et al 2010;Sarih et al 2012). The selective expression of long-term plasticity at these inputs can reduce potential excitotoxic consequences of the activity-dependent plasticity mediating learning and memory expressed by the neurons of the circuit encoding the memory (Lamsa et al 2007;Isaacson and Scanziani 2011).…”

Section: Local Expression Of Zero-sum Long-term Plasticitymentioning

confidence: 99%

The less things change, the more they are different: contributions of long-term synaptic plasticity and homeostasis to memory

Schacher

2014

Learn. Mem.

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An important cellular mechanism contributing to the strength and duration of memories is activity-dependent alterations in the strength of synaptic connections within the neural circuit encoding the memory. Reversal of the memory is typically correlated with a reversal of the cellular changes to levels expressed prior to the stimulation. Thus, for stimulus-induced changes in synapse strength and their reversals to be functionally relevant, cellular mechanisms must regulate and maintain synapse strength both prior to and after the stimuli inducing learning and memory. The strengths of synapses within a neural circuit at any given moment are determined by cellular and molecular processes initiated during development and those subsequently regulated by the history of direct activation of the neural circuit and system-wide stimuli such as stress or motivational state. The cumulative actions of stimuli and other factors on an already modified neural circuit are attenuated by homeostatic mechanisms that prevent changes in overall synaptic inputs and excitability above or below specific set points (synaptic scaling). The mechanisms mediating synaptic scaling prevent potential excitotoxic alterations in the circuit but also may attenuate additional cellular changes required for learning and memory, thereby apparently limiting information storage. What cellular and molecular processes control synaptic strengths before and after experience/activity and its reversals? In this review we will explore the synapse-, whole cell-, and circuit level-specific processes that contribute to an overall zero sum-like set of changes and long-term maintenance of synapse strengths as a consequence of the accommodative interactions between long-term synaptic plasticity and homeostasis.Long-term changes in the strength of synapses-long-term potentiation/facilitation (LTP or LTF) and long-term depression (LTD)-are critical cellular mechanisms in modulating the amplitude and duration of behavioral modifications or the storage of memories (Kandel 2001). These synaptic changes could lead to significant and long-lasting bidirectional changes in the excitability of some neurons within a neural circuit, which under extreme circumstances can lead to excitotoxic or degenerative consequences that impact on cell function or survival, or the storage of memory (Abbott and Nelson 2000;Nelson and Turrigiano 2008). To prevent these maladaptive processes, homeostatic mechanisms restrain the overall weights of synaptic inputs and excitation/ inhibition balance to ensure that neurons remain functional (including the ability to express additional activity-dependent plasticity) while the storage of information acquired by previous activity is maintained (Davis 2006;Marder and Goaillard 2006;Roth-Alpermann et al. 2006;Ibata et al. 2008;Kim and Tsien 2008;Turrigiano 2008).The mechanisms mediating synaptic scaling/homeostasis at the level of individual neurons include those that regulate presynaptic transmitter release by affecting structure/function properties of...

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Cell Type-Specific, Presynaptic LTP of Inhibitory Synapses on Fast-Spiking GABAergic Neurons in the Mouse Visual Cortex

Abstract: Properties and plasticity of inhibitory synapses on fast-spiking (FS) GABAergic (FS-GABA

Cited by 25 publications

References 71 publications

Presynaptic long-term plasticity

Presynaptic long-term plasticity

Mefloquine and psychotomimetics share neurotransmitter receptor and transporter interactions in vitro

The less things change, the more they are different: contributions of long-term synaptic plasticity and homeostasis to memory

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