FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2010356589> ?p ?o ?g. }

• W2010356589 endingPage "351" @default.
• W2010356589 startingPage "337" @default.
• W2010356589 abstract "Homeostatic synaptic plasticity is a negative feedback mechanism that neurons use to offset excessive excitation or inhibition by adjusting their synaptic strengths. Recent findings reveal a complex web of signaling processes involved in this compensatory form of synaptic strength regulation, and in contrast to the popular view of homeostatic plasticity as a slow, global phenomenon, neurons may also rapidly tune the efficacy of individual synapses on demand. Here we review our current understanding of cellular and molecular mechanisms of homeostatic synaptic plasticity. Homeostatic synaptic plasticity is a negative feedback mechanism that neurons use to offset excessive excitation or inhibition by adjusting their synaptic strengths. Recent findings reveal a complex web of signaling processes involved in this compensatory form of synaptic strength regulation, and in contrast to the popular view of homeostatic plasticity as a slow, global phenomenon, neurons may also rapidly tune the efficacy of individual synapses on demand. Here we review our current understanding of cellular and molecular mechanisms of homeostatic synaptic plasticity. The primary function of a neuron is to receive, integrate, and transmit information as an electrical or chemical signal to other neurons in the brain. In response to extrinsic stimuli, neurons can change and adapt the strength of their connections, or synapses. The most widely studied form of such activity-dependent adaptation of synaptic strength is Hebbian plasticity, which includes long-term potentiation (LTP) and its counterpart, long-term depression (LTD) (Collingridge et al., 2004Collingridge G.L. Isaac J.T.R. Wang Y.T. Receptor trafficking and synaptic plasticity.Nat. Rev. Neurosci. 2004; 5: 952-962Crossref PubMed Scopus (514) Google Scholar, Feldman, 2009Feldman D.E. Synaptic mechanisms for plasticity in neocortex.Annu. Rev. Neurosci. 2009; 32: 33-55Crossref PubMed Scopus (236) Google Scholar, Malenka and Bear, 2004Malenka R.C. Bear M.F. LTP and LTD: an embarrassment of riches.Neuron. 2004; 44: 5-21Abstract Full Text Full Text PDF PubMed Scopus (1641) Google Scholar). In Hebbian plasticity, synaptic changes are associative, rapidly induced, and input specific. Because these hallmark features facilitate reinforcement of synaptic connections that are active with a given set of stimuli or “experience,” Hebbian plasticity has been extensively studied as a cellular basis for learning and memory (Neves et al., 2008Neves G. Cooke S.F. Bliss T.V.P. Synaptic plasticity, memory and the hippocampus: a neural network approach to causality.Nat. Rev. Neurosci. 2008; 9: 65-75Crossref PubMed Scopus (304) Google Scholar, Sjöström et al., 2008Sjöström P.J. Rancz E.A. Roth A. Häusser M. Dendritic excitability and synaptic plasticity.Physiol. Rev. 2008; 88: 769-840Crossref PubMed Scopus (215) Google Scholar). Nevertheless, Hebbian plasticity is a positive feedback process; for example, upon inducing LTP, synapses are more excitable and the same connections have a reduced threshold for undergoing further LTP with a propensity for runaway excitation. In order to prevent neural networks from reaching such extremes, a homeostatic negative feedback regulation that could constrain activity levels would be highly desirable for maintaining network stability, and such an idea has been supported by network models of learning (Turrigiano, 2008Turrigiano G.G. The self-tuning neuron: synaptic scaling of excitatory synapses.Cell. 2008; 135: 422-435Abstract Full Text Full Text PDF PubMed Scopus (428) Google Scholar). Experimental evidence for adaptive compensatory mechanisms suggestive of homeostasis in the central and the peripheral nervous systems was first reported decades ago (Cannon, 1939Cannon W.B. A law of denervation.Am. J. Med. Sci. 1939; 198: 737-750Crossref Google Scholar, Sharpless, 1964Sharpless S.K. Reorganization of function in the nervous system-use and disuse.Annu. Rev. Physiol. 1964; 26: 357-388Crossref PubMed Google Scholar). However, it is only in recent years that homeostatic mechanisms of neural circuit adaptations have been subjected to close scrutiny (reviewed in Burrone and Murthy, 2003Burrone J. Murthy V.N. Synaptic gain control and homeostasis.Curr. Opin. Neurobiol. 2003; 13: 560-567Crossref PubMed Scopus (155) Google Scholar, Davis, 2006Davis G.W. Homeostatic control of neural activity: from phenomenology to molecular design.Annu. Rev. Neurosci. 2006; 29: 307-323Crossref PubMed Scopus (249) Google Scholar, Davis and Bezprozvanny, 2001Davis G.W. Bezprozvanny I. Maintaining the stability of neural function: a homeostatic hypothesis.Annu. Rev. Physiol. 2001; 63: 847-869Crossref PubMed Scopus (184) Google Scholar, Marder and Goaillard, 2006Marder E. Goaillard J.M. Variability, compensation and homeostasis in neuron and network function.Nat. Rev. Neurosci. 2006; 7: 563-574Crossref PubMed Scopus (328) Google Scholar, Pérez-Otaño and Ehlers, 2005Pérez-Otaño I. Ehlers M.D. Homeostatic plasticity and NMDA receptor trafficking.Trends Neurosci. 2005; 28: 229-238Abstract Full Text Full Text PDF PubMed Scopus (213) Google Scholar, Rabinowitch and Segev, 2008Rabinowitch I. Segev I. Two opposing plasticity mechanisms pulling a single synapse.Trends Neurosci. 2008; 31: 377-383Abstract Full Text Full Text PDF PubMed Scopus (37) Google Scholar, Rich and Wenner, 2007Rich M.M. Wenner P. Sensing and expressing homeostatic synaptic plasticity.Trends Neurosci. 2007; 30: 119-125Abstract Full Text Full Text PDF PubMed Scopus (55) Google Scholar, Shah and Crair, 2008Shah R.D. Crair M.C. Retinocollicular synapse maturation and plasticity are regulated by correlated retinal waves.J. Neurosci. 2008; 28: 292-303Crossref PubMed Scopus (36) Google Scholar, Thiagarajan et al., 2007Thiagarajan T.C. Lindskog M. Malgaroli A. Tsien R.W. LTP and adaptation to inactivity: overlapping mechanisms and implications for metaplasticity.Neuropharmacology. 2007; 52: 156-175Crossref PubMed Scopus (51) Google Scholar, Turrigiano, 1999Turrigiano G.G. Homeostatic plasticity in neuronal networks: the more things change, the more they stay the same.Trends Neurosci. 1999; 22: 221-227Abstract Full Text Full Text PDF PubMed Scopus (409) Google Scholar, Turrigiano, 2008Turrigiano G.G. The self-tuning neuron: synaptic scaling of excitatory synapses.Cell. 2008; 135: 422-435Abstract Full Text Full Text PDF PubMed Scopus (428) Google Scholar, Yu and Goda, 2009Yu L.M. Goda Y. Dendritic signalling and homeostatic adaptation.Curr. Opin. Neurobiol. 2009; 19: 327-335Crossref PubMed Scopus (31) Google Scholar). The findings to date point to two major targets to achieve homeostasis: intrinsic excitability and synaptic efficacy. This review will focus on synaptic mechanisms of homeostatic adaptations, primarily at mammalian synapses, mostly drawing on recent developments in this rapidly growing field. Collectively, investigations into the cellular properties and the underlying molecular mechanisms are beginning to unfold a complicated picture in which synapses implement homeostatic adaptations through a variety of cellular processes. The mechanisms appear to differ depending on the developmental stage, the cell type, and the mode of activity manipulation that elicits synaptic homeostasis. Moreover, these differences are further confounded by variables that are introduced by the experimental systems used. In an attempt to simplify the problem, we have divided the review into three main sections. The first part addresses the physiological relevance of homeostatic synaptic plasticity by focusing on studies carried out in preparations that retain the native neural connectivity. In the second section we consider the cellular mechanisms of expression of homeostatic plasticity in the pre- and the postsynaptic neurons. The third part examines the signaling pathways that neurons use to execute homeostatic synaptic adaptations. We conclude the review by reflecting on the overall current state of knowledge and the major issues that remain to be tackled in the future. We apologize to authors whose work could not be cited directly owing to space limitations. In the intact brain, neurons are precisely organized into structured circuits that communicate between each other to perform physiological brain functions. Whereas studies in dissociated neuronal cultures have provided important insights into the cellular and molecular properties of homeostatic synaptic plasticity, a lack of network architecture typical of the intact brain may have obscured some aspects, particularly of mechanisms that rely on precise patterns of synaptic connections. The use of intact in vivo models and organotypic slice cultures that partly preserves the in vivo connectivity and its properties (De Simoni et al., 2003De Simoni A. Griesinger C.B. Edwards F.A. Development of rat CA1 neurones in acute versus organotypic slices: role of experience in synaptic morphology and activity.J. Physiol. 2003; 550: 135-147Crossref PubMed Scopus (142) Google Scholar) provides a complementary approach to further refine findings from dissociated cell culture work. Organotypic slice preparations maintain the ease of pharmacological activity manipulations and single-cell molecular interventions that are typical of neuronal cultures that facilitate studies of detailed mechanisms (e.g., Aptowicz et al., 2004Aptowicz C.O. Kunkler P.E. Kraig R.P. Homeostatic plasticity in hippocampal slice cultures involves changes in voltage-gated Na+ channel expression.Brain Res. 2004; 998: 155-163Crossref PubMed Scopus (35) Google Scholar, Bartley et al., 2008Bartley A.F. Huang Z.J. Huber K.M. Gibson J.R. Differential activity-dependent, homeostatic plasticity of two neocortical inhibitory circuits.J. Neurophysiol. 2008; 100: 1983-1994Crossref PubMed Scopus (31) Google Scholar, Deeg, 2009Deeg K.E. Synapse-specific homeostatic mechanisms in the hippocampus.J. Neurophysiol. 2009; 101: 503-506Crossref PubMed Scopus (3) Google Scholar, Kim and Tsien, 2008Kim J. Tsien R.W. Synapse-specific adaptations to inactivity in hippocampal circuits achieve homeostatic gain control while dampening network reverberation.Neuron. 2008; 58: 925-937Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar). Furthermore, in vivo models permit direct testing of the physiological relevance of mechanisms of homeostatic synaptic plasticity identified in studies in vitro (e.g., Kaneko et al., 2008Kaneko M. Stellwagen D. Malenka R.C. Stryker M.P. Tumor necrosis factor-alpha mediates one component of competitive, experience-dependent plasticity in developing visual cortex.Neuron. 2008; 58: 673-680Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar, Maffei et al., 2006Maffei A. Nataraj K. Nelson S.B. Turrigiano G.G. Potentiation of cortical inhibition by visual deprivation.Nature. 2006; 443: 81-84Crossref PubMed Scopus (185) Google Scholar, Maffei and Turrigiano, 2008Maffei A. Turrigiano G. The age of plasticity: developmental regulation of synaptic plasticity in neocortical microcircuits.Prog. Brain Res. 2008; 169: 211-223Crossref PubMed Scopus (47) Google Scholar, Mrsic-Flogel et al., 2007Mrsic-Flogel T.D. Hofer S.B. Ohki K. Reid R.C. Bonhoeffer T. Hübener M. Homeostatic regulation of eye-specific responses in visual cortex during ocular dominance plasticity.Neuron. 2007; 54: 961-972Abstract Full Text Full Text PDF PubMed Scopus (162) Google Scholar). Here we focus on properties and mechanisms of homeostatic synaptic plasticity pertinent to physiological brain function by highlighting recent findings from preparations that better preserve the native pattern of synaptic connections. In addition, we further consider the pros and cons of native preparations and dissociated neuronal cultures as experimental models for studying homeostatic synaptic adaptations. Homeostatic synaptic plasticity has been studied in vivo in the visual cortex, where experience-dependent scaling of glutamatergic synaptic responses is subject to spatial and developmental regulation (Desai et al., 2002Desai N.S. Cudmore R.H. Nelson S.B. Turrigiano G.G. Critical periods for experience-dependent synaptic scaling in visual cortex.Nat. Neurosci. 2002; 5: 783-789PubMed Google Scholar, Goel et al., 2006Goel A. Jiang B. Xu L.W. Song L. Kirkwood A. Lee H.-K. Cross-modal regulation of synaptic AMPA receptors in primary sensory cortices by visual experience.Nat. Neurosci. 2006; 9: 1001-1003Crossref PubMed Scopus (78) Google Scholar, Goel and Lee, 2007Goel A. Lee H.-K. Persistence of experience-induced homeostatic synaptic plasticity through adulthood in superficial layers of mouse visual cortex.J. Neurosci. 2007; 27: 6692-6700Crossref PubMed Scopus (92) Google Scholar). In this in vivo model, network activity is altered by intraocular injection of tetrodotoxin (TTX) to block action potentials or by manipulating sensory inputs, either by exposing to or depriving animals from light, although there are subtle differences in the mechanisms of homeostatic compensation between those induced by TTX and light deprivation (Maffei and Turrigiano, 2008Maffei A. Turrigiano G. The age of plasticity: developmental regulation of synaptic plasticity in neocortical microcircuits.Prog. Brain Res. 2008; 169: 211-223Crossref PubMed Scopus (47) Google Scholar). In young animals, dark rearing increased glutamatergic quantal size in visual cortical layers 4 and 2/3, which was correlated with an increased abundance of AMPA receptors; re-exposure of animals to light reversed these changes (Desai et al., 2002Desai N.S. Cudmore R.H. Nelson S.B. Turrigiano G.G. Critical periods for experience-dependent synaptic scaling in visual cortex.Nat. Neurosci. 2002; 5: 783-789PubMed Google Scholar, Goel et al., 2006Goel A. Jiang B. Xu L.W. Song L. Kirkwood A. Lee H.-K. Cross-modal regulation of synaptic AMPA receptors in primary sensory cortices by visual experience.Nat. Neurosci. 2006; 9: 1001-1003Crossref PubMed Scopus (78) Google Scholar). Importantly, homeostatic changes in layer 4 were observed only if activity was blocked in early developmental stages before the end of the critical period for ocular dominance plasticity. In contrast, layer 2/3 showed no such restriction, and dark rearing of adult animals produced an increase in AMPA miniature excitatory postsynaptic current (mEPSC) amplitudes (Desai et al., 2002Desai N.S. Cudmore R.H. Nelson S.B. Turrigiano G.G. Critical periods for experience-dependent synaptic scaling in visual cortex.Nat. Neurosci. 2002; 5: 783-789PubMed Google Scholar, Goel and Lee, 2007Goel A. Lee H.-K. Persistence of experience-induced homeostatic synaptic plasticity through adulthood in superficial layers of mouse visual cortex.J. Neurosci. 2007; 27: 6692-6700Crossref PubMed Scopus (92) Google Scholar). Interestingly, the mechanism of homeostatic increase in mEPSCs amplitude could be different between adult and juvenile animals, as only the juvenile animals showed a multiplicative scaling that affected all synapses uniformly (Goel and Lee, 2007Goel A. Lee H.-K. Persistence of experience-induced homeostatic synaptic plasticity through adulthood in superficial layers of mouse visual cortex.J. Neurosci. 2007; 27: 6692-6700Crossref PubMed Scopus (92) Google Scholar). The underlying basis for the layer-specific, developmental differences in the homeostatic scaling mechanisms in the visual cortex remains to be delineated. The spatial specificity of homeostatic synaptic plasticity in the adult cortex is also highlighted in the whisker-to-barrel pathway, although synaptic changes appear to manifest primarily at the level of synapse number (Knott et al., 2002Knott G.W. Quairiaux C. Genoud C. Welker E. Formation of dendritic spines with GABAergic synapses induced by whisker stimulation in adult mice.Neuron. 2002; 34: 265-273Abstract Full Text Full Text PDF PubMed Scopus (252) Google Scholar, Quairiaux et al., 2007Quairiaux C. Armstrong-James M. Welker E. Modified sensory processing in the barrel cortex of the adult mouse after chronic whisker stimulation.J. Neurophysiol. 2007; 97: 2130-2147Crossref PubMed Scopus (18) Google Scholar). In this system, each whisker is connected to layer 4 in the cortical barrel, which integrates signals generated by whisker movement and transduces them to layers 2/3 in the same barrel column. Persistent whisker stimulation produced a compensatory increase in the number of inhibitory synapses in layer 4 neurons; this in turn decreased the spontaneous firing rate of layer 4 neurons and consequently that of layer 2/3 neurons. The effect of enhanced stimulation was confined to the barrel receiving inputs from the stimulated whisker and did not extend to adjacent barrel columns associated to nonstimulated whiskers. Understanding how different synapses within the same network adapt to long-term alterations in activity poses a problem of a higher degree of complexity. Whereas the original studies on modulating network activity in dissociated cultures have revealed uniform multiplicative synaptic scaling (e.g., Turrigiano et al., 1998Turrigiano G.G. Leslie K.R. Desai N.S. Rutherford L.C. Nelson S.B. Activity-dependent scaling of quantal amplitude in neocortical neurons.Nature. 1998; 391: 892-896Crossref PubMed Scopus (958) Google Scholar), recent work in vivo and in organotypic slices indicates that synaptic scaling is not always uniform and suggests that changes in network activity do not affect all synaptic inputs onto a given neuron equally (e.g., Cingolani and Goda, 2008Cingolani L.A. Goda Y. Differential involvement of β3 integrin in pre- and postsynaptic forms of adaptation to chronic activity deprivation.Neuron Glia Biol. 2008; 4: 179-187Crossref PubMed Scopus (22) Google Scholar, Echegoyen et al., 2007Echegoyen J. Neu A. Graber K.D. Soltesz I. Homeostatic plasticity studied using in vivo hippocampal activity-blockade: synaptic scaling, intrinsic plasticity and age-dependence.PLoS ONE. 2007; 2: e700Crossref PubMed Scopus (60) Google Scholar, Goel and Lee, 2007Goel A. Lee H.-K. Persistence of experience-induced homeostatic synaptic plasticity through adulthood in superficial layers of mouse visual cortex.J. Neurosci. 2007; 27: 6692-6700Crossref PubMed Scopus (92) Google Scholar). Moreover, hippocampal and cortical networks display differential regulation of homeostatic synaptic plasticity for specific connections (Bartley et al., 2008Bartley A.F. Huang Z.J. Huber K.M. Gibson J.R. Differential activity-dependent, homeostatic plasticity of two neocortical inhibitory circuits.J. Neurophysiol. 2008; 100: 1983-1994Crossref PubMed Scopus (31) Google Scholar, Kim and Tsien, 2008Kim J. Tsien R.W. Synapse-specific adaptations to inactivity in hippocampal circuits achieve homeostatic gain control while dampening network reverberation.Neuron. 2008; 58: 925-937Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar). For example, in hippocampal slice cultures, TTX treatment strengthened CA3-to-CA1 synapses while inputs onto CA3 cells were regulated differentially depending on their origin: recurrent CA3-to-CA3 inputs were weakened, whereas mossy fiber-to-CA3 connections became stronger (Kim and Tsien, 2008Kim J. Tsien R.W. Synapse-specific adaptations to inactivity in hippocampal circuits achieve homeostatic gain control while dampening network reverberation.Neuron. 2008; 58: 925-937Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar). In the neocortical inhibitory circuits, inputs from two subtypes of inhibitory neurons, parvalbumin-positive (Parv) and somatostatin-positive (Som) neurons, were shown to adapt differentially to chronic action potential blockade (Bartley et al., 2008Bartley A.F. Huang Z.J. Huber K.M. Gibson J.R. Differential activity-dependent, homeostatic plasticity of two neocortical inhibitory circuits.J. Neurophysiol. 2008; 100: 1983-1994Crossref PubMed Scopus (31) Google Scholar). In TTX-treated neocortical slice cultures, the inhibitory drive of Parv neuronal inputs onto excitatory neurons was decreased, at least in part due to reduced synapse number, whereas that of Som neurons remained unchanged. In contrast, when short-term plasticity was examined, Som but not Parv inputs showed enhanced depression following TTX. Notably, Parv neurons preferentially synapse onto the soma and proximal dendrites of excitatory neurons, whereas Som neurons target distal dendrites (e.g., Somogyi and Klausberger, 2005Somogyi P. Klausberger T. Defined types of cortical interneurone structure space and spike timing in the hippocampus.J. Physiol. 2005; 562: 9-26Crossref PubMed Scopus (467) Google Scholar). The differential tuning of two types of inhibitory connections, therefore, supports the idea that the receiving dendrite could homeostatically regulate synaptic strengths in a subcompartment-specific manner (see below: e.g., Branco et al., 2008Branco T. Staras K. Darcy K.J. Goda Y. Local dendritic activity sets release probability at hippocampal synapses.Neuron. 2008; 59: 475-485Abstract Full Text Full Text PDF PubMed Scopus (91) Google Scholar, Sutton et al., 2006Sutton M.A. Ito H.T. Cressy P. Kempf C. Woo J.C. Schuman E.M. Miniature neurotransmission stabilizes synaptic function via tonic suppression of local dendritic protein synthesis.Cell. 2006; 125: 785-799Abstract Full Text Full Text PDF PubMed Scopus (262) Google Scholar). Such local homeostatic adjustments of synaptic strengths might be advantageous for dendritic integration, as it allows for a flexible control of the excitability of each dendritic branch independently of one another (Häusser and Mel, 2003Häusser M. Mel B. Dendrites: bug or feature?.Curr. Opin. Neurobiol. 2003; 13: 372-383Crossref PubMed Scopus (190) Google Scholar, Polsky et al., 2004Polsky A. Mel B.W. Schiller J. Computational subunits in thin dendrites of pyramidal cells.Nat. Neurosci. 2004; 7: 621-627Crossref PubMed Scopus (294) Google Scholar, Rabinowitch and Segev, 2006Rabinowitch I. Segev I. The interplay between homeostatic synaptic plasticity and functional dendritic compartments.J. Neurophysiol. 2006; 96: 276-283Crossref PubMed Scopus (28) Google Scholar, Rabinowitch and Segev, 2008Rabinowitch I. Segev I. Two opposing plasticity mechanisms pulling a single synapse.Trends Neurosci. 2008; 31: 377-383Abstract Full Text Full Text PDF PubMed Scopus (37) Google Scholar). In concert with upregulation of excitatory inputs, modulation of inhibitory synaptic transmission is crucial for restraining network activity and avoiding potential epileptogenic states (Treiman, 2001Treiman D.M. GABAergic mechanisms in epilepsy.Epilepsia. 2001; 42: 8-12Crossref PubMed Google Scholar). For instance, chronic TTX delivery in the intact hippocampus produces an increase in the amplitude and frequency of spontaneous inhibitory currents in addition to enhanced excitation (Echegoyen et al., 2007Echegoyen J. Neu A. Graber K.D. Soltesz I. Homeostatic plasticity studied using in vivo hippocampal activity-blockade: synaptic scaling, intrinsic plasticity and age-dependence.PLoS ONE. 2007; 2: e700Crossref PubMed Scopus (60) Google Scholar). Moreover, in the CA3 region of hippocampal slice cultures, upon activity blockade with glutamate receptor antagonists, the levels of the GABA-synthetic enzyme glutamate decarboxylase isoform, GAD65, and GABAA receptor α1 subunits were maintained rather than being reduced (Buckby et al., 2006Buckby L.E. Jensen T.P. Smith P.J.E. Empson R.M. Network stability through homeostatic scaling of excitatory and inhibitory synapses following inactivity in CA3 of rat organotypic hippocampal slice cultures.Mol. Cell. Neurosci. 2006; 31: 805-816Crossref PubMed Scopus (26) Google Scholar). These observations are in sharp contrast with findings from dissociated cortical and hippocampal cultures, in which activity suppression scales down synaptic GABA currents (Hartman et al., 2006Hartman K.N. Pal S.K. Burrone J. Murthy V.N. Activity-dependent regulation of inhibitory synaptic transmission in hippocampal neurons.Nat. Neurosci. 2006; 9: 642-649Crossref PubMed Scopus (96) Google Scholar, Kilman et al., 2002Kilman V. van Rossum M.C. Turrigiano G.G. Activity deprivation reduces miniature IPSC amplitude by decreasing the number of postsynaptic GABA(A) receptors clustered at neocortical synapses.J. Neurosci. 2002; 22: 1328-1337Crossref PubMed Google Scholar). Inhibitory connections in native circuits may thus be wired to provide an additional layer of negative feedback control that operates in conjunction with homeostatic upregulation of excitatory inputs (Karmarkar and Buonomano, 2006Karmarkar U.R. Buonomano D.V. Different forms of homeostatic plasticity are engaged with distinct temporal profiles.Eur. J. Neurosci. 2006; 23: 1575-1584Crossref PubMed Scopus (50) Google Scholar). In support of such a proposal, in organotypic hippocampal slices, changes in excitation and inhibition elicited by chronic modulation of network activity are dissociable and are expressed in temporally distinct order, with changes in excitation occurring prior to those of inhibition (Karmarkar and Buonomano, 2006Karmarkar U.R. Buonomano D.V. Different forms of homeostatic plasticity are engaged with distinct temporal profiles.Eur. J. Neurosci. 2006; 23: 1575-1584Crossref PubMed Scopus (50) Google Scholar). An additional complexity to the regulation of excitatory-inhibitory balance is suggested by the differential developmental dependence of excitatory and inhibitory inputs to homeostatic modulation (Echegoyen et al., 2007Echegoyen J. Neu A. Graber K.D. Soltesz I. Homeostatic plasticity studied using in vivo hippocampal activity-blockade: synaptic scaling, intrinsic plasticity and age-dependence.PLoS ONE. 2007; 2: e700Crossref PubMed Scopus (60) Google Scholar, Karmarkar and Buonomano, 2006Karmarkar U.R. Buonomano D.V. Different forms of homeostatic plasticity are engaged with distinct temporal profiles.Eur. J. Neurosci. 2006; 23: 1575-1584Crossref PubMed Scopus (50) Google Scholar). In the intact hippocampus, TTX treatment increased mEPSC amplitude only in juvenile animals and mEPSC frequency in both adult and juvenile animals. As for inhibitory inputs, TTX increased mIPSC amplitude in both adult and juvenile animals, while mIPSC frequency was increased only in adult animals (Echegoyen et al., 2007Echegoyen J. Neu A. Graber K.D. Soltesz I. Homeostatic plasticity studied using in vivo hippocampal activity-blockade: synaptic scaling, intrinsic plasticity and age-dependence.PLoS ONE. 2007; 2: e700Crossref PubMed Scopus (60) Google Scholar). Curiously, the age dependency of quantal responses has been demonstrated in dissociated cultures (e.g., Burrone et al., 2002Burrone J. O'Byrne M. Murthy V.N. Multiple forms of synaptic plasticity triggered by selective suppression of activity in individual neurons.Nature. 2002; 420: 414-418Crossref PubMed Scopus (240) Google Scholar, Han and Stevens, 2009Han E.B. Stevens C.F. Development regulates a switch between post- and presynaptic strengthening in response to activity deprivation.Proc. Natl. Acad. Sci. USA. 2009; 106: 10817-10822Crossref PubMed Scopus (29) Google Scholar, Hartman et al., 2006Hartman K.N. Pal S.K. Burrone J. Murthy V.N. Activity-dependent regulation of inhibitory synaptic transmission in hippocampal neurons.Nat. Neurosci. 2006; 9: 642-649Crossref PubMed Scopus (96) Google Scholar, Wierenga et al., 2006Wierenga C.J. Walsh M.F. Turrigiano G.G. Temporal regulation of the expression locus of homeostatic plasticity.J. Neurophysiol. 2006; 96: 2127-2133Crossref PubMed Scopus (87) Google Scholar), albeit not necessarily in the same direction. For instance, in dissociated hippocampal cultures, TTX treatment reduced mIPSC amplitude in both mature and young cultures, whereas it reduced mIPSC frequency significantly in young cultures only (Hartman et al., 2006Hartman K.N. Pal S.K. Burrone J. Murthy V.N. Activity-dependent regulation of inhibitory synaptic transmission in hippocampal neurons.Nat. Neurosci. 2006; 9: 642-649Crossref PubMed Scopus (96) Google Scholar). The observed developmental dependence of homeostatic synaptic changes are not surprising given the higher rate of synapse remodeling in developing networks and GABAA responses that are depolarizing in young neurons. Regardless, many other factors that shape synaptic activity are likely to contribute to the heterogeneity of excitatory and inhibitory homeostatic responses, such as the developmental changes in the spatial distribution of ion channels (Lai and Jan, 2006Lai H.C. Jan L.Y. The distribution and targeting of neuronal voltage-gated ion channels.Nat. Rev. Neurosci. 2006; 7: 548-562Crossref PubMed Scopus (187) Google Scholar) and associated changes in intrinsic excitability (Debanne et al., 2003Debanne D. Daoudal G. Sourdet V. Russier M. Brain plasticity and ion channels.J. Physiol. (Paris). 2003; 97: 403-414Crossref PubMed Scopus (59) Google Scholar, Marder and Goaillard, 2006Marder E. Goaillard J.M. Variability, compensation and homeostasis in neuron and network function.Nat. Rev. Neurosci. 2006; 7: 563-574Crossref PubMed Scopus (328) Google Scholar, Zhang and Linden, 2003Zhang W. Linden D.J. The other side of the engram: experience-driven changes in neuronal intrinsic excitability.Nat. Rev. Neurosci. 2003; 4: 885-900Crossref PubMed Scopus (369) Google Scholar), as well as the vast number of distinct GABAergic cell types with specific functions in influencing circuit behavior (Klausberger and Somogyi, 2008Klausberger T. Somogyi P. Neuronal diversity and temporal dynamics: the unity of hippocampal circuit operations.Science. 2008; 321: 53-57Crossref PubMed Scopus (557) Google Scholar). Hebbian forms of plasticity, such as LTP, rapidly modify the efficacy of individual synapses associatively in an input-specific manner, and they are thought to represent the cellular mechanisms for storing memories (Collingridge et al., 2004Collingridge G.L. Isaac J.T." @default.
• W2010356589 created "2016-06-24" @default.
• W2010356589 creator A5073132799 @default.
• W2010356589 creator A5074324053 @default.
• W2010356589 date "2010-05-01" @default.
• W2010356589 modified "2023-10-18" @default.
• W2010356589 title "Unraveling Mechanisms of Homeostatic Synaptic Plasticity" @default.
• W2010356589 cites W1501886724 @default.
• W2010356589 cites W1514853588 @default.
• W2010356589 cites W1525232496 @default.
• W2010356589 cites W1542136448 @default.
• W2010356589 cites W1548862642 @default.
• W2010356589 cites W1554147846 @default.
• W2010356589 cites W1564467813 @default.
• W2010356589 cites W1576773659 @default.
• W2010356589 cites W1614445885 @default.
• W2010356589 cites W1622692223 @default.
• W2010356589 cites W1647836033 @default.
• W2010356589 cites W1658796519 @default.
• W2010356589 cites W1915062990 @default.
• W2010356589 cites W1963482376 @default.
• W2010356589 cites W1964372429 @default.
• W2010356589 cites W1964914480 @default.
• W2010356589 cites W1965265446 @default.
• W2010356589 cites W1965285506 @default.
• W2010356589 cites W1965513983 @default.
• W2010356589 cites W1965772438 @default.
• W2010356589 cites W1965960354 @default.
• W2010356589 cites W1971156703 @default.
• W2010356589 cites W1971402245 @default.
• W2010356589 cites W1974244318 @default.
• W2010356589 cites W1977637789 @default.
• W2010356589 cites W1981990802 @default.
• W2010356589 cites W1982718099 @default.
• W2010356589 cites W1983897183 @default.
• W2010356589 cites W1984465702 @default.
• W2010356589 cites W1985322212 @default.
• W2010356589 cites W1986120363 @default.
• W2010356589 cites W1986284286 @default.
• W2010356589 cites W1988763174 @default.
• W2010356589 cites W1989133472 @default.
• W2010356589 cites W1990107671 @default.
• W2010356589 cites W1992856813 @default.
• W2010356589 cites W1993020997 @default.
• W2010356589 cites W1993378387 @default.
• W2010356589 cites W1993643645 @default.
• W2010356589 cites W1993782794 @default.
• W2010356589 cites W1994119944 @default.
• W2010356589 cites W1994896596 @default.
• W2010356589 cites W1995680954 @default.
• W2010356589 cites W1996168091 @default.
• W2010356589 cites W1996640377 @default.
• W2010356589 cites W1997278591 @default.
• W2010356589 cites W1999170657 @default.
• W2010356589 cites W2001651016 @default.
• W2010356589 cites W2002734542 @default.
• W2010356589 cites W2003665687 @default.
• W2010356589 cites W2004248029 @default.
• W2010356589 cites W2004784342 @default.
• W2010356589 cites W2004803686 @default.
• W2010356589 cites W2004873650 @default.
• W2010356589 cites W2008027377 @default.
• W2010356589 cites W2008744372 @default.
• W2010356589 cites W2009725257 @default.
• W2010356589 cites W2011046807 @default.
• W2010356589 cites W2013185658 @default.
• W2010356589 cites W2013319759 @default.
• W2010356589 cites W2016032579 @default.
• W2010356589 cites W2016593669 @default.
• W2010356589 cites W2018458016 @default.
• W2010356589 cites W2019808076 @default.
• W2010356589 cites W2020449445 @default.
• W2010356589 cites W2020939800 @default.
• W2010356589 cites W2021024875 @default.
• W2010356589 cites W2021845085 @default.
• W2010356589 cites W2024035512 @default.
• W2010356589 cites W2026599809 @default.
• W2010356589 cites W2027699509 @default.
• W2010356589 cites W2029359382 @default.
• W2010356589 cites W2030040408 @default.
• W2010356589 cites W2031139008 @default.
• W2010356589 cites W2031779883 @default.
• W2010356589 cites W2031898618 @default.
• W2010356589 cites W2034502353 @default.
• W2010356589 cites W2036029991 @default.
• W2010356589 cites W2039187448 @default.
• W2010356589 cites W2039655932 @default.
• W2010356589 cites W2042325100 @default.
• W2010356589 cites W2042604124 @default.
• W2010356589 cites W2043098233 @default.
• W2010356589 cites W2043160791 @default.
• W2010356589 cites W2043921345 @default.
• W2010356589 cites W2047535883 @default.
• W2010356589 cites W2050066016 @default.
• W2010356589 cites W2050519369 @default.
• W2010356589 cites W2051556001 @default.
• W2010356589 cites W2052334135 @default.
• W2010356589 cites W2052707106 @default.

• next