Does autophagy work in synaptic plasticity and memory?

Shehata, Mohammad; Inokuchi, Kaoru

doi:10.1515/revneuro-2014-0002

Cited by 32 publications

(27 citation statements)

References 51 publications

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“…Additionally, within individual patients, there is evidence of local hyperconnectivity and long-range hypoconnectivity (Kana et al, 2014; Maximo et al, 2013; Moseley et al, 2015). Synaptic remodeling depends on mTOR-regulated autophagy (Shehata and Inokuchi, 2014; Shehata et al, 2012; Shen et al, 2015; Shen and Ganetzky, 2009; Tang et al, 2014). Thus, insufficient autophagy results in over connection and excessive results in over-pruning.…”

Section: : Discussionmentioning

confidence: 99%

Endosomal system genetics and autism spectrum disorders: A literature review

Patak

Zhang-James

Faraone

2016

Neuroscience & Biobehavioral Reviews

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Autism spectrum disorders (ASDs) are a group of debilitating neurodevelopmental disorders thought to have genetic etiology, due to their high heritability. The endosomal system has become increasingly implicated in ASD pathophysiology. In an attempt to summarize the association between endosomal system genes and ASDs we performed a systematic review of the literature. We searched PubMed for relevant articles. Simons Foundation Autism Research Initiative (SFARI) gene database was used to exclude articles regarding genes with less than minimal evidence for association with ASDs. Our search retained 55 articles reviewed in two categories: genes that regulate and genes that are regulated by the endosomal system. Our review shows that the endosomal system is a novel pathway implicated in ASDs as well as other neuropsychiatric disorders. It plays a central role in aspects of cellular physiology on which neurons and glial cells are particularly reliant, due to their unique metabolic and functional demands. The system shows potential for biomarkers and pharmacological intervention and thus more research into this pathway is warranted.

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Section: : Discussionmentioning

confidence: 99%

Endosomal system genetics and autism spectrum disorders: A literature review

Patak

Zhang-James

Faraone

2016

Neuroscience & Biobehavioral Reviews

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“…Consistent with our previous results, current study revealed that activation of autophagy through metformin can inhibit apoptosis and cell death in hippocampus at day 3. It was accepted that autophagy is the modulator of some behaviors such as cognition and moods (Shehata and Inokuchi 2014). Tang and co-workers revealed that enhanced level of LC3B protein promotes locomotor activity in neuronal injury (Tang et al 2013).…”

Section: Discussionmentioning

confidence: 99%

Metformin improves anxiety-like behaviors through AMPK-dependent regulation of autophagy following transient forebrain ischemia

et al. 2015

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Stroke is one of the main threats to the public health worldwide. Metformin, an anti-diabetic drug, is an activator of AMP-activated protein kinase (AMPK). Metformin plays an important role on improving behavior in neurodegenerative diseases through diverse pathways. In the current study we aimed to investigate the probable effects of metformin on anxiety and autophagy pathway in global cerebral ischemia. Rats were divided into seven groups; Sham, ischemia (I/R), metformin (met), compound c (CC), CC+ischemia, met+ischemia, met+CC+ischemia. Metformin was pretreated for 2 weeks and CC administrated half an hour before global cerebral ischemia. Blood glucose, body weight, sensorimotor scores, elevated plus maze and open field test were evaluated after ischemia. Autophagy related factors were measured by Western blot and immunofluorescent assay in hippocampus of rats. Based on our results, pretreatment of rats by metformin improved sensory motor signs, anxiolytic behavior and locomotion in ischemic rats. CC injection in I/R rats attenuated the therapeutic effects of metformin. Autophagy factors such as light chain 3B, Atg7, Atg5-12 and beclin-1 decreased in ischemic rats compared to the sham group (P < 0.001 in all proteins). Level of autophagic factors increased in metformin pretreated rats compared to global cerebral ischemia (P < 0.001 in all proteins). These data indicated that the beneficial role of metformin in behavior and autophagy flux mediates via AMPK. Our results recommended that metformin therapy could improve psychological disorders and movement disability following I/R and profound understanding of AMPK-dependent autophagy would enhance its development as a promising target for intracellular pathway.

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“…Autophagy can regulate axon morphogenesis and synaptic physiology in neurons (Binotti et al, 2015; Hernandez et al, 2012; Rudolf et al, 2016; Shehata and Inokuchi, 2014; Torres and Sulzer, 2012; Yamamoto and Yue, 2014). For example, knockdown of the autophagic protein Atg7 in murine neurons results in longer axons, while activation of the autophagy pathway with rapamycin results in shorter neurites (Ban et al, 2013; Chen et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

KIF1A/UNC-104 Transports ATG-9 to Regulate Neurodevelopment and Autophagy at Synapses

et al. 2016

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SUMMARY Autophagy is a cellular degradation process essential for neuronal development and survival. Neurons are highly polarized cells in which autophagosome biogenesis is spatially compartmentalized. The mechanisms and physiological importance of this spatial compartmentalization of autophagy in the neuronal development of living animals are not well understood. Here we determine that, in C. elegans neurons, autophagosomes form near synapses and are required for neurodevelopment. We first determine, through unbiased genetic screens and systematic genetic analyses, that autophagy is required cell-autonomously for presynaptic assembly and for axon outgrowth dynamics in specific neurons. We observe autophagosome biogenesis in the axon near synapses, and this localization depends on the synaptic vesicle kinesin, KIF1A/UNC-104. KIF1A/UNC-104 coordinates localized autophagosome formation by regulating the transport of the integral membrane autophagy protein, ATG-9. Our findings indicate that autophagy is spatially regulated in neurons through the transport of ATG-9 by KIF1A/UNC-104 to regulate neurodevelopment.

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Does autophagy work in synaptic plasticity and memory?

Cited by 32 publications

References 51 publications

Endosomal system genetics and autism spectrum disorders: A literature review

Endosomal system genetics and autism spectrum disorders: A literature review

Metformin improves anxiety-like behaviors through AMPK-dependent regulation of autophagy following transient forebrain ischemia

KIF1A/UNC-104 Transports ATG-9 to Regulate Neurodevelopment and Autophagy at Synapses

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