Somatostatin receptor-mediated suppression of gabaergic synaptic transmission in cultured rat retinal amacrine cells

Chen, Wanchun; Ke, Jiang-Bin; Wu, Hang-Jing; Miao, Yanying; Li, F.; Yang, Xiong‐Li; Wang, Z.

doi:10.1016/j.neuroscience.2014.05.013

Cited by 12 publications

(5 citation statements)

References 73 publications

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“…This validated that the IP 3 R was getting inhibited. Xestospongin has been reported in various studies as a potent inhibitor of IP 3 R and its effect is well documented [Szatkowski et al, ; Chen et al, ; Lin et al, ; Xu et al, ].…”

Section: Resultsmentioning

confidence: 99%

Inhibition of Inositol 1, 4, 5-Trisphosphate Receptor Induce Breast Cancer Cell Death Through Deregulated Autophagy and Cellular Bioenergetics

et al. 2017

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Inositol 1,4,5-trisphosphate receptors (IP Rs) regulate autophagy in normal cells and are associated with metastasis in cancer cells. In breast cancer, however, the regulation and role of IP Rs is not clear. To study this, we used MCF-7 breast cancer cell line and mouse model of breast cancer. Inhibiting IP R sub types resulted in compromised bioenergetics both in terms of glucose and mitochondrial metabolism. The siRNA mediated silencing of IP R or its blocking by its inhibitors Xestospongin C and 2-Amino-ethoxy diphenyl borate increased cell death and LC3II expression in MCF-7 cells as well as attenuated cellular bioenergetics. The level of Autophagy related gene, Atg5 was found to be up regulated after pharmacological as well as siRNA blocking of IP R. The specificity of its role in autophagy was confirmed through specific shRNA knockdown of the Atg5 along with IP R inhibitor. Inhibiting as well as silencing of IP R receptor also resulted in increase in ROS production which was abolished after pretreatment with N-acetyl cysteine. Its role in autophagy was confirmed through decrease in the levels of LC3 II after pretreatment with IP R inhibitor and N acetyl cysteine.Moreover, inhibiting as well as silencing IP R-induced cell death in MCF-7 cells was attenuated by autophagic inhibitors (Bafilomycin A1 or 3-Methyladeneine). In mice, blocking of IP Rs by 2-Amino-ethoxy diphenyl borate arrested tumor growth. Overall our findings indicate that IP R blocking resulted in autophagic cell death in breast cancer cells and provides a role of IP Rs in determining the breast cancer cell fate. J. Cell. Biochem. 118: 2333-2346, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Resultsmentioning

confidence: 99%

Inhibition of Inositol 1, 4, 5-Trisphosphate Receptor Induce Breast Cancer Cell Death Through Deregulated Autophagy and Cellular Bioenergetics

et al. 2017

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“…Studies were also dedicated to investigate whether and how somatostatin presynaptically controls the release of GABA but, to the best of our knowledge, the few available data do not support any definitive conclusion [42][43][44].…”

Section: Somatostatin In the Central Nervous System: Synaptic Release And Volume Diffusionmentioning

confidence: 99%

Somatostatin, a Presynaptic Modulator of Glutamatergic Signal in the Central Nervous System

Pittaluga

Roggeri

Vallarino

et al. 2021

IJMS

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Somatostatin is widely diffused in the central nervous system, where it participates to control the efficiency of synaptic transmission. This peptide mainly colocalizes with GABA, in inhibitory, GABA-containing interneurons from which it is actively released in a Ca2+ dependent manner upon application of depolarizing stimuli. Once released in the synaptic cleft, somatostatin acts locally, or it diffuses in the extracellular space through “volume diffusion”, a mechanism(s) of distribution which mainly operates in the cerebrospinal fluid and that assures the progression of neuronal signalling from signal-secreting sender structures towards receptor-expressing targeted neurons located extrasynaptically, in a non-synaptic, inter-neuronal form of communication. Somatostatin controls the efficiency of central glutamate transmission by either modulating presynaptically the glutamate exocytosis or by metamodulating the activity of glutamate receptors colocalized and functionally coupled with somatostatin receptors in selected subpopulations of nerve terminals. Deciphering the role of somatostatin in the mechanisms of “volume diffusion” and in the “receptor-receptor interaction” unveils new perspectives in the central role of this fine tuner of synaptic strength, paving the road to new therapeutic approaches for the cure of central disorders.

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“…In organotypic retinal slices, somatostatin enhances GABA-A responses in rat amacrine cells, suggesting a possible role in facilitating the GABAergic inhibitory transmission in the retinal circuitry [150]. In cultured rat amacrine cells, on the contrary, activation of SST 5 /SST 2 receptors reduces GABA through the inhibition of voltage-gated Ca 2+ channels (L- and N-types) and via negative coupling with cAMP/PKA signaling pathway [151]. PKA downregulation could reduce the phosphorylation of Ca 2+ channels with consequent reduction in Ca 2+ influx and GABA release [115].…”

Section: Molecular and Cellular Physiology Of Somatostatin Action:mentioning

confidence: 99%

Molecular and Cellular Mechanisms Underlying Somatostatin-Based Signaling in Two Model Neural Networks, the Retina and the Hippocampus

Cammalleri

Bagnoli

Bigiani

2019

IJMS

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Neural inhibition plays a key role in determining the specific computational tasks of different brain circuitries. This functional “braking” activity is provided by inhibitory interneurons that use different neurochemicals for signaling. One of these substances, somatostatin, is found in several neural networks, raising questions about the significance of its widespread occurrence and usage. Here, we address this issue by analyzing the somatostatinergic system in two regions of the central nervous system: the retina and the hippocampus. By comparing the available information on these structures, we identify common motifs in the action of somatostatin that may explain its involvement in such diverse circuitries. The emerging concept is that somatostatin-based signaling, through conserved molecular and cellular mechanisms, allows neural networks to operate correctly.

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Somatostatin receptor-mediated suppression of gabaergic synaptic transmission in cultured rat retinal amacrine cells

Cited by 12 publications

References 73 publications

Inhibition of Inositol 1, 4, 5-Trisphosphate Receptor Induce Breast Cancer Cell Death Through Deregulated Autophagy and Cellular Bioenergetics

Inhibition of Inositol 1, 4, 5-Trisphosphate Receptor Induce Breast Cancer Cell Death Through Deregulated Autophagy and Cellular Bioenergetics

Somatostatin, a Presynaptic Modulator of Glutamatergic Signal in the Central Nervous System

Molecular and Cellular Mechanisms Underlying Somatostatin-Based Signaling in Two Model Neural Networks, the Retina and the Hippocampus

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