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Neuron Sep 2012Neuronal computation is energetically expensive. Consequently, the brain's limited energy supply imposes constraints on its information processing capability. Most brain... (Review)
Review
Neuronal computation is energetically expensive. Consequently, the brain's limited energy supply imposes constraints on its information processing capability. Most brain energy is used on synaptic transmission, making it important to understand how energy is provided to and used by synapses. We describe how information transmission through presynaptic terminals and postsynaptic spines is related to their energy consumption, assess which mechanisms normally ensure an adequate supply of ATP to these structures, consider the influence of synaptic plasticity and changing brain state on synaptic energy use, and explain how disruption of the energy supply to synapses leads to neuropathology.
Topics: Animals; Brain; Brain Chemistry; Energy Metabolism; Humans; Neuronal Plasticity; Synaptic Transmission
PubMed: 22958818
DOI: 10.1016/j.neuron.2012.08.019 -
Neuroscience Jan 2019Astrocytes are emerging as important players in synaptic function, and, consequently, on brain function and animal behavior. According to the Tripartite Synapse concept,... (Review)
Review
Astrocytes are emerging as important players in synaptic function, and, consequently, on brain function and animal behavior. According to the Tripartite Synapse concept, astrocytes are integral elements involved in synaptic function. They establish bidirectional communication with neurons, whereby they respond to synaptically released neurotransmitters and, in turn, release gliotransmitters that influence neuronal and synaptic activity. Accumulating evidence is revealing that the mechanisms and functional consequences of astrocyte-neuron signaling are more complex than originally thought. Furthermore, astrocyte-neuron signaling is not based on broad, unspecific interaction; rather, it is a synapse-, cell- and circuit-specific phenomenon that presents a high degree of complexity. This diversity and complexity of astrocyte-synapse interactions greatly enhance the degrees of freedom of the neural circuits and the consequent computational power of the neural systems.
Topics: Animals; Astrocytes; Cell Communication; Humans; Neuronal Plasticity; Neurons; Organ Specificity; Synaptic Transmission
PubMed: 30458223
DOI: 10.1016/j.neuroscience.2018.11.010 -
Frontiers in Neural Circuits 2019
Topics: Animals; Humans; Neurotransmitter Agents; Synaptic Transmission
PubMed: 30971899
DOI: 10.3389/fncir.2019.00019 -
Glia Jan 2023In the last decades, astrocytes have emerged as important regulatory cells actively involved in brain function by exchanging signaling with neurons. The endocannabinoid... (Review)
Review
In the last decades, astrocytes have emerged as important regulatory cells actively involved in brain function by exchanging signaling with neurons. The endocannabinoid (eCB) signaling is widely present in many brain areas, being crucially involved in multiple brain functions and animal behaviors. The present review presents and discusses current evidence demonstrating that astrocytes sense eCBs released during neuronal activity and subsequently release gliotransmitters that regulate synaptic transmission and plasticity. The eCB signaling to astrocytes and the synaptic regulation mediated by astrocytes activated by eCBs are complex phenomena that exhibit exquisite spatial and temporal properties, a wide variety of downstream signaling mechanisms, and a large diversity of functional synaptic outcomes. Studies investigating this topic have revealed novel regulatory processes of synaptic function, like the lateral regulation of synaptic transmission and the active involvement of astrocytes in the spike-timing dependent plasticity, originally thought to be exclusively mediated by the coincident activity of pre- and postsynaptic neurons, following Hebbian rules for associative learning. Finally, the critical influence of astrocyte-mediated eCB signaling on animal behavior is also discussed.
Topics: Animals; Endocannabinoids; Neuronal Plasticity; Synaptic Transmission; Signal Transduction; Astrocytes
PubMed: 36408881
DOI: 10.1002/glia.24256 -
Neural Plasticity 2015
Topics: Animals; Humans; Neuroglia; Neuronal Plasticity; Synaptic Transmission
PubMed: 26346673
DOI: 10.1155/2015/723891 -
Current Opinion in Neurobiology Aug 2017Synaptic adhesion molecules have been extensively studied for their contribution to the regulation of synapse development through trans-synaptic adhesions. However,... (Review)
Review
Synaptic adhesion molecules have been extensively studied for their contribution to the regulation of synapse development through trans-synaptic adhesions. However, accumulating evidence increasingly indicates that synaptic adhesion molecules are also involved in the regulation of excitatory synaptic transmission and plasticity, often through direct or close associations with excitatory neurotransmitter receptors. This review summarizes recent results supporting this emerging concept and underlying mechanisms, and addresses its implications.
Topics: Animals; Cell Adhesion; Humans; Neuronal Plasticity; Synapses; Synaptic Transmission
PubMed: 28390263
DOI: 10.1016/j.conb.2017.03.005 -
International Journal of Molecular... May 2022Unrelated genetic mutations can lead to convergent manifestations of neurological disorders with similar behavioral phenotypes. Experimental data frequently show a lack... (Review)
Review
Unrelated genetic mutations can lead to convergent manifestations of neurological disorders with similar behavioral phenotypes. Experimental data frequently show a lack of dramatic changes in neuroanatomy, indicating that the key cause of symptoms might arise from impairment in the communication between neurons. A transient imbalance between excitatory (glutamatergic) and inhibitory (GABAergic) synaptic transmission (the E/I balance) during early development is generally considered to underlie the development of several neurological disorders in adults. However, the E/I ratio is a multidimensional variable. Synaptic contacts are highly dynamic and the actual strength of synaptic projections is determined from the balance between synaptogenesis and synaptic elimination. During development, relatively slow postsynaptic receptors are replaced by fast ones that allow for fast stimulus-locked excitation/inhibition. Using the binomial model of synaptic transmission allows for the reassessing of experimental data from different mouse models, showing that a transient E/I shift is frequently counterbalanced by additional pre- and/or postsynaptic changes. Such changes-for instance, the slowing down of postsynaptic currents by means of immature postsynaptic receptors-stabilize the average synaptic strength, but impair the timing of information flow. Compensatory processes and/or astrocytic signaling may represent possible targets for medical treatments of different disorders directed to rescue the proper information processing.
Topics: Animals; Astrocytes; Excitatory Postsynaptic Potentials; Mice; Neurons; Signal Transduction; Synaptic Transmission
PubMed: 35628556
DOI: 10.3390/ijms23105746 -
BMC Cell Biology May 2016Electrical synapses are an omnipresent feature of nervous systems, from the simple nerve nets of cnidarians to complex brains of mammals. Formed by gap junction channels... (Review)
Review
Electrical synapses are an omnipresent feature of nervous systems, from the simple nerve nets of cnidarians to complex brains of mammals. Formed by gap junction channels between neurons, electrical synapses allow direct transmission of voltage signals between coupled cells. The relative simplicity of this arrangement belies the sophistication of these synapses. Coupling via electrical synapses can be regulated by a variety of mechanisms on times scales ranging from milliseconds to days, and active properties of the coupled neurons can impart emergent properties such as signal amplification, phase shifts and frequency-selective transmission. This article reviews the biophysical characteristics of electrical synapses and some of the core mechanisms that control their plasticity in the vertebrate central nervous system.
Topics: Animals; Electric Conductivity; Electrical Synapses; Humans; Neuronal Plasticity; Signal Transduction; Synaptic Transmission
PubMed: 27230893
DOI: 10.1186/s12860-016-0091-y -
Progress in Molecular Biology and... 2014In this chapter, we describe how to create mathematical models of synaptic transmission and integration. We start with a brief synopsis of the experimental evidence... (Review)
Review
In this chapter, we describe how to create mathematical models of synaptic transmission and integration. We start with a brief synopsis of the experimental evidence underlying our current understanding of synaptic transmission. We then describe synaptic transmission at a particular glutamatergic synapse in the mammalian cerebellum, the mossy fiber to granule cell synapse, since data from this well-characterized synapse can provide a benchmark comparison for how well synaptic properties are captured by different mathematical models. This chapter is structured by first presenting the simplest mathematical description of an average synaptic conductance waveform and then introducing methods for incorporating more complex synaptic properties such as nonlinear voltage dependence of ionotropic receptors, short-term plasticity, and stochastic fluctuations. We restrict our focus to excitatory synaptic transmission, but most of the modeling approaches discussed here can be equally applied to inhibitory synapses. Our data-driven approach will be of interest to those wishing to model synaptic transmission and network behavior in health and disease.
Topics: Action Potentials; Animals; Computer Simulation; Humans; Models, Neurological; Statistics as Topic; Stochastic Processes; Synaptic Transmission
PubMed: 24560150
DOI: 10.1016/B978-0-12-397897-4.00004-8 -
Frontiers in Neural Circuits 2019The neocortex is densely innervated by basal forebrain (BF) cholinergic neurons. Long-range axons of cholinergic neurons regulate higher-order cognitive function and... (Review)
Review
The neocortex is densely innervated by basal forebrain (BF) cholinergic neurons. Long-range axons of cholinergic neurons regulate higher-order cognitive function and dysfunction in the neocortex by releasing acetylcholine (ACh). ACh release dynamically reconfigures neocortical microcircuitry through differential spatiotemporal actions on cell-types and their synaptic connections. At the cellular level, ACh release controls neuronal excitability and firing rate, by hyperpolarizing or depolarizing target neurons. At the synaptic level, ACh impacts transmission dynamics not only by altering the presynaptic probability of release, but also the magnitude of the postsynaptic response. Despite the crucial role of ACh release in physiology and pathophysiology, a comprehensive understanding of the way it regulates the activity of diverse neocortical cell-types and synaptic connections has remained elusive. This review aims to summarize the state-of-the-art anatomical and physiological data to develop a functional map of the cellular, synaptic and microcircuit effects of ACh in the neocortex of rodents and non-human primates, and to serve as a quantitative reference for those intending to build data-driven computational models on the role of ACh in governing brain states.
Topics: Acetylcholine; Animals; Computer Simulation; Models, Neurological; Neocortex; Synaptic Transmission
PubMed: 31031601
DOI: 10.3389/fncir.2019.00024