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      Arginine Vasopressin, Synaptic Plasticity, and Brain Networks

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          Abstract

          The arginine vasopressin (AVP), a neurohypophysial hormone, is synthesized within specific sites of the central nervous system and axonally transported to multiple areas, acting as a neurotransmitter/neuromodulator. In this context, AVP acts primarily through vasopressin receptors A and B and is involved in regulating complex social and cognition behaviors and basic autonomic function. Many earlier studies have shown that AVP as a neuromodulator affects synaptic plasticity. This review updates our current understanding of the underlying molecular mechanisms by which AVP affects synaptic plasticity. Moreover, we discuss AVP modulatory effects on event-related potentials and blood oxygen level-dependent responses in specific brain structures, and AVP effects on the network level oscillatory activity. We aimed at providing an overview of the AVP effects on the brain from the synaptic to the network level.

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          Most cited references68

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          Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path.

          1. The after-effects of repetitive stimulation of the perforant path fibres to the dentate area of the hippocampal formation have been examined with extracellular micro-electrodes in rabbits anaesthetized with urethane.2. In fifteen out of eighteen rabbits the population response recorded from granule cells in the dentate area to single perforant path volleys was potentiated for periods ranging from 30 min to 10 hr after one or more conditioning trains at 10-20/sec for 10-15 sec, or 100/sec for 3-4 sec.3. The population response was analysed in terms of three parameters: the amplitude of the population excitatory post-synaptic potential (e.p.s.p.), signalling the depolarization of the granule cells, and the amplitude and latency of the population spike, signalling the discharge of the granule cells.4. All three parameters were potentiated in 29% of the experiments; in other experiments in which long term changes occurred, potentiation was confined to one or two of the three parameters. A reduction in the latency of the population spike was the commonest sign of potentiation, occurring in 57% of all experiments. The amplitude of the population e.p.s.p. was increased in 43%, and of the population spike in 40%, of all experiments.5. During conditioning at 10-20/sec there was massive potentiation of the population spike (;frequency potentiation'). The spike was suppressed during stimulation at 100/sec. Both frequencies produced long-term potentiation.6. The results suggest that two independent mechanisms are responsible for long-lasting potentiation: (a) an increase in the efficiency of synaptic transmission at the perforant path synapses; (b) an increase in the excitability of the granule cell population.
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            Neurophysiological investigation of the basis of the fMRI signal.

            Functional magnetic resonance imaging (fMRI) is widely used to study the operational organization of the human brain, but the exact relationship between the measured fMRI signal and the underlying neural activity is unclear. Here we present simultaneous intracortical recordings of neural signals and fMRI responses. We compared local field potentials (LFPs), single- and multi-unit spiking activity with highly spatio-temporally resolved blood-oxygen-level-dependent (BOLD) fMRI responses from the visual cortex of monkeys. The largest magnitude changes were observed in LFPs, which at recording sites characterized by transient responses were the only signal that significantly correlated with the haemodynamic response. Linear systems analysis on a trial-by-trial basis showed that the impulse response of the neurovascular system is both animal- and site-specific, and that LFPs yield a better estimate of BOLD responses than the multi-unit responses. These findings suggest that the BOLD contrast mechanism reflects the input and intracortical processing of a given area rather than its spiking output.
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              A Brief History of Long-Term Potentiation.

              Since the discovery of long-term potentiation (LTP) in 1973, thousands of papers have been published on this intriguing phenomenon, which provides a compelling cellular model for learning and memory. Although LTP has suffered considerable growing pains over the years, LTP has finally come of age. Here the rich history of LTP is reviewed. These are exciting times and the pace of discovery is remarkable.
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                Author and article information

                Journal
                Curr Neuropharmacol
                Curr Neuropharmacol
                CN
                Current Neuropharmacology
                Bentham Science Publishers
                1570-159X
                1875-6190
                15 November 2022
                15 November 2022
                : 20
                : 12
                : 2292-2302
                Affiliations
                [1 ]deptApplied Cognitive Neuroscience Lab, Department of Human Physiology , Medical University of Gdansk , Gdansk, , Poland;
                [2 ]2-nd Department of Radiology, Medical University of Gdansk , Gdansk, , Poland;
                [3 ]deptDepartment of Anatomy, Physiology, and Pharmacology, Auburn University, and Center for Neurosciences Initiative , Auburn University , Auburn, , USA;
                [4 ]deptDepartment of Human Physiology , Medical University of Gdansk , Gdansk, , Poland
                Author notes
                [* ]Address correspondence to this author at the Department of Human Physiology, Medical University of Gdansk, Tuwima Str. 15, 80-210 Gdansk, Poland; Tel/Fax: +48 58 3491515; E-mail: pawelwinklewski@ 123456wp.pl
                Article
                CN-20-2292
                10.2174/1570159X20666220222143532
                9890292
                35193483
                0750b9da-a144-4f87-976b-82b9688631aa
                © 2022 Bentham Science Publishers

                This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                : 02 November 2021
                : 21 January 2022
                : 10 February 2022
                Categories
                Neurology

                Pharmacology & Pharmaceutical medicine
                arginine-vasopressin,synaptic plasticity,brain networks,neuronal oscillatory activity,blood-oxygen-level-dependent activity,network-level oscillatory activity

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