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

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          Abstract

          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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          Most cited references209

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          Interneurons of the hippocampus.

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            Learning induces long-term potentiation in the hippocampus.

            Years of intensive investigation have yielded a sophisticated understanding of long-term potentiation (LTP) induced in hippocampal area CA1 by high-frequency stimulation (HFS). These efforts have been motivated by the belief that similar synaptic modifications occur during memory formation, but it has never been shown that learning actually induces LTP in CA1. We found that one-trial inhibitory avoidance learning in rats produced the same changes in hippocampal glutamate receptors as induction of LTP with HFS and caused a spatially restricted increase in the amplitude of evoked synaptic transmission in CA1 in vivo. Because the learning-induced synaptic potentiation occluded HFS-induced LTP, we conclude that inhibitory avoidance training induces LTP in CA1.
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              The essential role of hippocampal CA1 NMDA receptor-dependent synaptic plasticity in spatial memory.

              We have produced a mouse strain in which the deletion of the NMDAR1 gene is restricted to the CA1 pyramidal cells of the hippocampus by using a new and general method that allows CA1-restricted gene knockout. The mutant mice grow into adulthood without obvious abnormalities. Adult mice lack NMDA receptor-mediated synaptic currents and long-term potentiation in the CA1 synapses and exhibit impaired spatial memory but unimpaired nonspatial learning. Our results strongly suggest that activity-dependent modifications of CA1 synapses, mediated by NMDA receptors, play an essential role in the acquisition of spatial memories.
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                21 May 2019
                May 2019
                : 20
                : 10
                : 2506
                Affiliations
                [1 ]Dipartimento di Biologia, Università di Pisa, 56127 Pisa, Italy; maurizio.cammalleri@ 123456unipi.it (M.C.); paola.bagnoli@ 123456unipi.it (P.B.)
                [2 ]Dipartimento di Scienze Biomediche, Metaboliche e Neuroscienze, Università di Modena e Reggio Emilia, 41125 Modena, Italy
                Author notes
                [* ]Correspondence: albertino.bigiani@ 123456unimore.it ; Tel.: +39-059-205-5349
                Author information
                https://orcid.org/0000-0001-6987-488X
                Article
                ijms-20-02506
                10.3390/ijms20102506
                6566141
                31117258
                b8a43375-aa20-4535-93e9-4bb17e906811
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 30 April 2019
                : 20 May 2019
                Categories
                Review

                Molecular biology
                somatostatin,retina,hippocampus,ion channels,neurotransmitter release,neuromodulation,information flow,network activity

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