Endocannabinoid and Nitric Oxide-Dependent IGF-I-Mediated Synaptic Plasticity at Mice Barrel Cortex

Noriega-Prieto, José Antonio; Maglio, Laura E.; Ibáñez-Santana, Sara; Sevilla, David Fernández de

doi:10.3390/cells11101641

Cited by 6 publications

(3 citation statements)

References 43 publications

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“…Even in the same neuronal circuits, the suppression of LTP by L-NAME is through temperature [8]. In the cortices, L-NAME has also been reported to affect the induction of the LTP in the somatosensory cortex, the barrel cortex, and the motor cortex [8,36,37]. It is a major finding that NMDAR and neuronal NOS (nNOS) exist in the postsynaptic site [9][10][11][12].…”

Section: No Is Required For the Lfs-induced Acc-acc Potentiation But ...mentioning

confidence: 99%

The Pathway-Selective Dependence of Nitric Oxide for Long-Term Potentiation in the Anterior Cingulate Cortex of Adult Mice

Chen,

Wan,

et al. 2024

Biomedicines

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Nitric oxide (NO) is a key diffusible messenger in the mammalian brain. It has been proposed that NO may diffuse in retrograde into presynaptic terminals, contributing to the induction of hippocampal long-term potentiation (LTP). Here, we present novel evidence that NO is selectively required for the synaptic potentiation of the interhemispheric projection in the anterior cingulate cortex (ACC). Unilateral low-frequency stimulation (LFS) induced a short-term synaptic potentiation on the contralateral ACC through the corpus callosum (CC). The use of the antagonists of the NMDA receptor (NMDAR), or the inhibitor of the L-type voltage-dependent Ca2+ channels (L-VDCCs), blocked the induction of this ACC-ACC potentiation. In addition, the inhibitor of NO synthase, or inhibitors for its downstream signaling pathway, also blocked this ACC-ACC potentiation. However, the application of the NOS inhibitor blocked neither the local electric stimulation-induced LTP nor the stimulation-induced recruitment of silent responses. Our results present strong evidence for the pathway-selective roles of NO in the LTP of the ACC.

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Section: No Is Required For the Lfs-induced Acc-acc Potentiation But ...mentioning

confidence: 99%

The Pathway-Selective Dependence of Nitric Oxide for Long-Term Potentiation in the Anterior Cingulate Cortex of Adult Mice

Chen,

Wan,

et al. 2024

Biomedicines

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“…Synaptic plasticity is the capacity of neurons to change the synapse in response to external activity over time ( Noriega-Prieto et al, 2022 ). Since memories are thought to be programming of widely linked neuronal circuits, synaptic plasticity is one of the crucial neurochemicals, forming the basis of learning and memory ( Grafe et al, 2022 ).…”

Section: Roles Of Chchd2 and Chchd10 In Physiological And Pathologica...mentioning

confidence: 99%

CHCHD2 and CHCHD10: Future therapeutic targets in cognitive disorder and motor neuron disorder

Jiang

Wang

et al. 2022

Front. Neurosci.

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CHCHD2 and CHCHD10 are homolog mitochondrial proteins that play key roles in the neurological, cardiovascular, and reproductive systems. They are also involved in the mitochondrial metabolic process. Although previous research has concentrated on their functions within mitochondria, their functions within apoptosis, synaptic plasticity, cell migration as well as lipid metabolism remain to be concluded. The review highlights the different roles played by CHCHD2 and/or CHCHD10 binding to various target proteins (such as OPA-1, OMA-1, PINK, and TDP43) and reveals their non-negligible effects in cognitive impairments and motor neuron diseases. This review focuses on the functions of CHCHD2 and/or CHCHD10. This review reveals protective effects and mechanisms of CHCHD2 and CHCHD10 in neurodegenerative diseases characterized by cognitive and motor deficits, such as frontotemporal dementia (FTD), Lewy body dementia (LBD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS). However, there are numerous specific mechanisms that have yet to be elucidated, and additional research into these mechanisms is required.

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“…Additionally, the increase in expression levels of NMDA receptor subunits 2A and 2B at the hippocampus by IGF-I in aged rats (Sonntag et al, 2000) may facilitate the induction of long-term potentiation (LTP). Moreover, a reduction of inhibitory synaptic transmission dependent on the activation of the IGF-I receptor (IGF-IR) on astrocytes (Noriega-Prieto et al, 2021), and on the synthesis of nitric oxide (Noriega-prieto et al, 2022) has been demonstrated in the barrel cortex.…”

Section: Introductionmentioning

confidence: 99%

Bidirectional Modulation Of Synaptic Transmission By Insulin-Like Growth Factor I

Noriega-Prieto,

Maglio,

Dávila

et al. 2023

Preprint

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Insulin-like growth factor-I (IGF-I) plays a key role in the modulation of synaptic plasticity, and is an essential factor in learning and memory processes. Indeed, we have demonstrated that IGF-IR activation induces long-term potentiation (LTP) of synaptic transmission (LTPIGF-I) both in the barrel cortex, improving object recognition (Noriega-Prieto et al., 2021), and in the prefrontal cortex, facilitating the extinction of conditioned fear (Maglio et al., 2021). However, during aging, IGF-I levels are decreased, and the effect of this decrease in the induction of synaptic plasticity remains unknown. Here we show that the induction of NMDAR-dependent LTP at layer 2/3 PNs of the mouse barrel cortex is favored or prevented by IGF-I (10nM) or IGF-I (7nM), respectively, when IGF-I is applied 1 hour before the induction of Hebbian LTP. Analyzing the cellular basis of this bidirectional control of synaptic plasticity, we observed that while 10nM IGF-I generates LTP (LTPIGF-I) of the post-synaptic potentials (PSPs) by inducing LTD of the inhibitory post-synaptic currents (IPSCs), 7nM IGF-I generates LTD of the PSPs (LTDIGF-I) by inducing LTD of the excitatory post-synaptic currents (EPSCs). This bidirectional effect of IGF-I is supported by the observation of IGF-IR immunoreactivity at both excitatory and inhibitory synapses. Therefore, IGF-I controls the induction of Hebbian NMDAR-dependent plasticity depending on its concentration, revealing novel cellular mechanisms of IGF-I on synaptic plasticity and in the learning and memory machinery of the brain.SIGNIFICANCE STATEMENTInsulin-like growth factor-I (IGF-I) signalling plays key regulatory roles in multiple processes of brain physiology, such as learning and memory, and brain pathology, such as Alzheimer disease. Yet, the underlying mechanisms remain largely undefined. Here we demonstrate that IGF-I signalling triggers long-term potentiation (LTP) or long-term depression (LTD) of synaptic transmission at cortical synapses in a concentration dependent manner, thus regulating the induction of Hebbian synaptic plasticity. The present work represents an important conceptual advance in our knowledge of the cellular basis of IGF-I signalling in brain function.

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Endocannabinoid and Nitric Oxide-Dependent IGF-I-Mediated Synaptic Plasticity at Mice Barrel Cortex

Cited by 6 publications

References 43 publications

The Pathway-Selective Dependence of Nitric Oxide for Long-Term Potentiation in the Anterior Cingulate Cortex of Adult Mice

The Pathway-Selective Dependence of Nitric Oxide for Long-Term Potentiation in the Anterior Cingulate Cortex of Adult Mice

CHCHD2 and CHCHD10: Future therapeutic targets in cognitive disorder and motor neuron disorder

Bidirectional Modulation Of Synaptic Transmission By Insulin-Like Growth Factor I

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