Reciprocal Homosynaptic and Heterosynaptic Long-Term Plasticity of Corticogeniculate Projection Neurons in Layer VI of the Mouse Visual Cortex

Kourosh-Arami, Masoumeh; Sohya, Kazuhiro; Sarihi, Abdolrahman; Jiang, Bin; Yanagawa, Yuchio; Tsumoto, Tadaharu

doi:10.1523/jneurosci.5350-12.2013

Cited by 20 publications

(23 citation statements)

References 53 publications

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“…The reason for the absence of significant change of group-averages might be the balanced nature of heterosynaptic plasticity. It is also important to note that in articles specifically aimed at investigating heterosynaptic plasticity, it was readily induced by regular pairing (Arami and others 2013; Huang and others 2008; Nishiyama and others 2000), afferent tetanization (Bauer and LeDoux 2004; Chevalyre and others 2003; Cummings and others 1996; Nugent and others 2007; Pascual and others 2005; Royer and Paré 2003; Staubli and Ji 1996; Wöhrl and others 2007), or purely postsynaptic protocols (e.g., Christofi and others 1993; Cummings and others 1996; Pockett and others 1990). This analysis substantiates our conclusion that induction of homosynaptic plasticity by a typical pairing procedure used in STDP studies is accompanied by induction of heterosynaptic plasticity in unpaired inputs.…”

Section: Induction Of Input-specific and Heterosynaptic Plasticity: Smentioning

confidence: 99%

“…Indeed, the rise of [Ca 2+ ] in is sufficient to induce plasticity (Neveu and Zucker 1996; Yang and others 1999). Induction of long-term heterosynaptic plasticity by intracellular tetanization and other protocols was impaired or blocked by chelation of intracellular calcium with EGTA (Arami and others 2013; Bright and Brickley 2008; Han and Heinemann 2013; Lee and others 2012; Nugent and others 2007). Substantial rise of [Ca 2+ ] in is produced by bursts of back-propagating action potentials activating voltage-dependent calcium channels (Miyakawa and others 1992; Petrozzino and Connor 1994; Schiller and others 1995; Schiller and others 1998; Yuste and Denk 1995), and can be further amplified by calcium release from internal stores (Berridge 1998; Fagni and others 2000; Nakamura and others 1999).…”

Section: Induction Of Input-specific and Heterosynaptic Plasticity: Smentioning

confidence: 99%

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Heterosynaptic Plasticity

et al. 2014

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Plasticity is a universal property of synapses. It is expressed in a variety of forms mediated by a multitude of mechanisms. Here we consider two broad kinds of plasticity that differ in their requirement for presynaptic activity during the induction. Homosynaptic plasticity occurs at synapses that were active during the induction. It is also called input specific or associative, and it is governed by Hebbian-type learning rules. Heterosynaptic plasticity can be induced by episodes of strong postsynaptic activity also at synapses that were not active during the induction, thus making any synapse at a cell a target to heterosynaptic changes. Both forms can be induced by typical protocols used for plasticity induction and operate on the same time scales but have differential computational properties and play different roles in learning systems. Homosynaptic plasticity mediates associative modifications of synaptic weights. Heterosynaptic plasticity counteracts runaway dynamics introduced by Hebbian-type rules and balances synaptic changes. It provides learning systems with stability and enhances synaptic competition. We conclude that homosynaptic and heterosynaptic plasticity represent complementary properties of modifiable synapses, and both are necessary for normal operation of neural systems with plastic synapses.

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Section: Induction Of Input-specific and Heterosynaptic Plasticity: Smentioning

confidence: 99%

Section: Induction Of Input-specific and Heterosynaptic Plasticity: Smentioning

confidence: 99%

Heterosynaptic Plasticity

et al. 2014

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“…It has been shown to be concurrently present in the hippocampal dentate gyrus with the perforant afferents [10] [13], while as well in the hippocampal CA1 region [14]. Besides, it has further been reported that the concurrent homosynaptic LTP and heterosynaptic LTD also occur in visual cortex [15]. These are all important regions in brain for memory.…”

Section: Memory As Concurrent Homosynaptic Ltp and Heterosynaptic Ltdmentioning

confidence: 99%

Hypothesis on Remote Memory Forming from Heterosynaptic LTD-Mediated Neuronal Degeneration

Cai¹

2019

OALib

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In this article, it is hypothesized a new mechanism for the formation of stable remote memory in brain comprising the important memory acquired during childhood and the common words in language. It has been demonstrated that the memory forms concurrently at both homosynaptic long term potentiation (LTP) and heterosynaptic long term depression (LTD). It is pointed out that the repeated LTD may result in neuronal degeneration as evidenced at molecular and cellular level, becoming long lasting throughout the lifespan. Besides, it is further supported by the consequent storage of remote memory directly on the information pathway, as evidenced by the degenerative ocular dominance plasticity and the storage of common words/grammar within the linguistic areas of brain. Accordingly, it is herein completed the hypothesis on the formation of remote memory from the heterosynaptic LTD-mediated neuronal degeneration in brain so long as the homosynaptic pathway does not degenerate from such causes as aging and so on, while supplementing a new form of neuronal plasticity for memory in addition to the contemporary LTP and LTD.

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“…LTD is induced by low-frequency protocol in the WM/L-VI to L-IV in younger animals when inhibitory postsynaptic potentials (IPSPs) are blocked (20). Previous studies show that LTD in visual cortex is induced mostly in synapses in layers II/III, IV, and V (17,18). In the authors previous study, in CG neurons of L-VI, it was found that cannabinoid type 1 receptors and calcineurin under-lie the UL-induced and WM-induced het-LTD, respectively.…”

Section: Ltd Of Epspsmentioning

confidence: 99%

“…In the authors previous study, in CG neurons of L-VI, it was found that cannabinoid type 1 receptors and calcineurin under-lie the UL-induced and WM-induced het-LTD, respectively. Therefore, homosynaptic LTP and heterosynaptic LTD in these cells may change the synaptic transmission efficacy by different underlying mechanisms (18).…”

Section: Ltd Of Epspsmentioning

confidence: 99%

Synaptic Neuronal Plasticity

Kourosh-Arami

Jameie

2015

Thrita

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The current study aimed to review research articles concerning cortical representational plasticity following the manipulations of inputs. Evidence Acquisition: This review article compromised previous studies in PubMed, Google Scholar and Scientific Information databases according to the keywords since 1988. Results: CA1 neurons depolarization paired with CA3 presynaptic input result in EPSPs amplitude enhancement called LTP. Theta-burst stimulation of layer IV produced long term potentiation (LTP) in the granular primary motor cortex, but the agranular or primary somatosensory cortex was capable of generating LTP in case of GABAA receptor inhibition. Upper layers (UL)-induced, and White Matter WM-induced plasticity in layer VI corticogeniculate neurons were produced through type-5 metabotropic glutamate and N-methyl-Daspartate (NMDA) receptors, respectively. Calcineurin and cannabinoid type 1 receptors are involved in WM-induced and UL-induced het-LTD, respectively. Long-term potentiation of inhibitory postsynaptic currents (IPSCs) was produced in FS-GABA neurons in layer II/III of the mouse visual cortex by tetanic activation. Conclusions: In summary, the current study presents rational evidences for specific fundamental forms of plasticity, containing associative long-term potentiation and depression of excitatory and inhibitory postsynaptic potentials.

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Reciprocal Homosynaptic and Heterosynaptic Long-Term Plasticity of Corticogeniculate Projection Neurons in Layer VI of the Mouse Visual Cortex

Abstract: Most neurons in layer VI of the visual cortex project to the dorsal lateral geniculate nucleus (dLGN).

Cited by 20 publications

References 53 publications

Heterosynaptic Plasticity

Heterosynaptic Plasticity

Hypothesis on Remote Memory Forming from Heterosynaptic LTD-Mediated Neuronal Degeneration

Synaptic Neuronal Plasticity

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