oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
Cortical GABAergic Interneurons in Cross-Modal Plasticity following Early Blindness  [PDF]
Sébastien Desgent,Maurice Ptito
Neural Plasticity , 2012, DOI: 10.1155/2012/590725
Abstract: Early loss of a given sensory input in mammals causes anatomical and functional modifications in the brain via a process called cross-modal plasticity. In the past four decades, several animal models have illuminated our understanding of the biological substrates involved in cross-modal plasticity. Progressively, studies are now starting to emphasise on cell-specific mechanisms that may be responsible for this intermodal sensory plasticity. Inhibitory interneurons expressing γ-aminobutyric acid (GABA) play an important role in maintaining the appropriate dynamic range of cortical excitation, in critical periods of developmental plasticity, in receptive field refinement, and in treatment of sensory information reaching the cerebral cortex. The diverse interneuron population is very sensitive to sensory experience during development. GABAergic neurons are therefore well suited to act as a gate for mediating cross-modal plasticity. This paper attempts to highlight the links between early sensory deprivation, cortical GABAergic interneuron alterations, and cross-modal plasticity, discuss its implications, and further provide insights for future research in the field. 1. Introduction Patterns of activity from the peripheral sensory receptor arrays can dramatically influence the development of connectivity and functional organization of cortical fields in mammals. In some species, evolution in relation to specific environmental cues has nurtured the brain’s blueprint in such a way that a sensory cortex processing specific survival needs has been enlarged over time as compared to other modalities (Figure 1) [1–5]. Similarly, when a sensory function is lost during development, spared senses compensate by taking more cortical space and recruiting the deafferented areas, to maintain homeostasis of sensory function. This reorganization optimizes and secures the individual’s survival and awareness to future environmental changes. For example, the loss of sight at birth or during early life in humans leads to important anatomical and functional reorganization of the visually deprived cortex that will become activated by a wide variety of nonvisual stimuli involving touch, audition, and olfaction [6–11]. Enhanced spatiotemporal functions in the remaining sensory modalities have also been reported [12–16]. It seems therefore that the visual cortex of the blind is not lifeless and is capable of adapting in order to accommodate these nonvisual inputs through cross-modal plasticity. Figure 1: Primary cortical areas in three species of mammals (i.e., Mouse, Ghost Bat and
Fast Homeostatic Plasticity of Inhibition via Activity-Dependent Vesicular Filling  [PDF]
Kristin Hartmann, Claus Bruehl, Tatyana Golovko, Andreas Draguhn
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0002979
Abstract: Synaptic activity in the central nervous system undergoes rapid state-dependent changes, requiring constant adaptation of the homeostasis between excitation and inhibition. The underlying mechanisms are, however, largely unclear. Chronic changes in network activity result in enhanced production of the inhibitory transmitter GABA, indicating that presynaptic GABA content is a variable parameter for homeostatic plasticity. Here we tested whether such changes in inhibitory transmitter content do also occur at the fast time scale required to ensure inhibition-excitation-homeostasis in dynamic cortical networks. We found that intense stimulation of afferent fibers in the CA1 region of mouse hippocampal slices yielded a rapid and lasting increase in quantal size of miniature inhibitory postsynaptic currents. This potentiation was mediated by the uptake of GABA and glutamate into presynaptic endings of inhibitory interneurons (the latter serving as precursor for the synthesis of GABA). Thus, enhanced release of inhibitory and excitatory transmitters from active networks leads to enhanced presynaptic GABA content. Thereby, inhibitory efficacy follows local neuronal activity, constituting a negative feedback loop and providing a mechanism for rapid homeostatic scaling in cortical circuits.
Assortment of GABAergic Plasticity in the Cortical Interneuron Melting Pot  [PDF]
Pablo Méndez,Alberto Bacci
Neural Plasticity , 2011, DOI: 10.1155/2011/976856
Abstract: Cortical structures of the adult mammalian brain are characterized by a spectacular diversity of inhibitory interneurons, which use GABA as neurotransmitter. GABAergic neurotransmission is fundamental for integrating and filtering incoming information and dictating postsynaptic neuronal spike timing, therefore providing a tight temporal code used by each neuron, or ensemble of neurons, to perform sophisticated computational operations. However, the heterogeneity of cortical GABAergic cells is associated to equally diverse properties governing intrinsic excitability as well as strength, dynamic range, spatial extent, anatomical localization, and molecular components of inhibitory synaptic connections that they form with pyramidal neurons. Recent studies showed that similarly to their excitatory (glutamatergic) counterparts, also inhibitory synapses can undergo activity-dependent changes in their strength. Here, some aspects related to plasticity and modulation of adult cortical and hippocampal GABAergic synaptic transmission will be reviewed, aiming at providing a fresh perspective towards the elucidation of the role played by specific cellular elements of cortical microcircuits during both physiological and pathological operations. 1. Introduction The cerebral cortex (which includes the hippocampus, the entorhinal cortex, the piriform cortex, and the neocortex) is the origin of the most sophisticated cognitive functions and complex behaviors. Indeed, the constant computation of incoming sensory information is dynamically integrated to provide a coherent representation of the world, elaborate the past, predict the future, and ultimately develop a consciousness and the self. In particular, the specific activity states of intricate cortical networks often produce a wide range of rhythmic activities, believed to provide the computational substrate for different aspects of cognition and various behaviors [1, 2]. Cortical oscillations range from slow-wave activity (<1?Hz) to ultrafast oscillations (>100?Hz), with several intermediate rhythms (e.g., theta, beta gamma), each of which is considered to underlie specific cognitive aspects, such as non-REM sleep (slow-waves), sensory integration (gamma), working memory (theta), and motor planning (beta) [1]. Importantly, inhibitory neurons were proposed to play a fundamental role in the genesis of most of these rhythms [3–13] through the specialized activity of their GABAergic synapses [7–10]. In fact, it is noteworthy that malfunctioning of specific GABAergic circuits is often indicated as a leading
Meningeal defects alter the tangential migration of cortical interneurons in Foxc1hith/hith mice
Konstantinos Zarbalis, Youngshik Choe, Julie A Siegenthaler, Lori A Orosco, Samuel J Pleasure
Neural Development , 2012, DOI: 10.1186/1749-8104-7-2
Abstract: We studied a unique Foxc1 hypomorph mouse model (Foxc1hith/hith) with meningeal defects and impaired tangential migration of cortical interneurons. We identified a territorial correlation between meningeal defects and disruption of interneuron migration along the adjacent marginal zone in these animals, suggesting that impaired meningeal integrity might be the primary cause for the observed migration defects. Moreover, we postulate that the meningeal factor regulating tangential migration that is affected in homozygote mutants is the chemokine Cxcl12. In addition, by using chromatin immunoprecipitation analysis, we provide evidence that the Cxcl12 gene is a direct transcriptional target of Foxc1 in the meninges. Further, we observe migration defects of a lesser degree in Cajal-Retzius cells migrating within the cortical marginal zone, indicating a less important role for Cxcl12 in their migration. Finally, the developmental migration defects observed in Foxc1hith/hith mutants do not lead to obvious differences in interneuron distribution in the adult if compared to control animals.Our results suggest a critical role for the forebrain meninges to promote during development the tangential migration of cortical interneurons along the cortical marginal zone and Cxcl12 as the factor responsible for this property.The cerebral cortex's proper functioning depends on the balance between excitatory projection neurons and inhibitory interneurons. In rodents, most GABA (γ-aminobutyric acid)-producing interneurons of the cerebral cortex originate in the medial ganglionic eminence of the ventral forebrain and migrate to their cortical destinations using a tangential route [1,2]. The subcortical origin and complex migratory path of cortical interneurons differ greatly from the origin of the cortical projection neurons and their radial migratory route. Once interneurons reach the cortex they follow mostly stereotypical routes in the marginal zone (MZ) and the subventricular zone (S
Long-term down-regulation of GABA decreases orientation selectivity without affecting direction selectivity in mouse primary visual cortex  [PDF]
Kenta M. Hagihara,Kenichi Ohki
Frontiers in Neural Circuits , 2013, DOI: 10.3389/fncir.2013.00028
Abstract: Inhibitory interneurons play important roles in the development of brain functions. In the visual cortex, functional maturation of inhibitory interneurons is essential for ocular dominance plasticity. However, roles of inhibitory interneurons in the development of orientation and direction selectivity, fundamental properties of primary visual cortex, are less understood. We examined orientation and direction selectivity of neurons in GAD67-GFP (Δneo) mice, in which expression of GABA in the brain is decreased in the newborn. We used in vivo two-photon calcium imaging to examine visual response of neurons in these mice and found that long-term decrease of GABA led to increase of response amplitude to non-preferred orientation of visual stimuli, which decreased orientation selectivity. In contrast, direction selectivity was not affected. These results suggest that orientation selectivity is decreased in mice with GABA down-regulation during development.
LTS and FS Inhibitory Interneurons, Short-Term Synaptic Plasticity, and Cortical Circuit Dynamics  [PDF]
Itai Hayut,Erika E. Fanselow,Barry W. Connors,David Golomb
PLOS Computational Biology , 2011, DOI: 10.1371/journal.pcbi.1002248
Abstract: Somatostatin-expressing, low threshold-spiking (LTS) cells and fast-spiking (FS) cells are two common subtypes of inhibitory neocortical interneuron. Excitatory synapses from regular-spiking (RS) pyramidal neurons to LTS cells strongly facilitate when activated repetitively, whereas RS-to-FS synapses depress. This suggests that LTS neurons may be especially relevant at high rate regimes and protect cortical circuits against over-excitation and seizures. However, the inhibitory synapses from LTS cells usually depress, which may reduce their effectiveness at high rates. We ask: by which mechanisms and at what firing rates do LTS neurons control the activity of cortical circuits responding to thalamic input, and how is control by LTS neurons different from that of FS neurons? We study rate models of circuits that include RS cells and LTS and FS inhibitory cells with short-term synaptic plasticity. LTS neurons shift the RS firing-rate vs. current curve to the right at high rates and reduce its slope at low rates; the LTS effect is delayed and prolonged. FS neurons always shift the curve to the right and affect RS firing transiently. In an RS-LTS-FS network, FS neurons reach a quiescent state if they receive weak input, LTS neurons are quiescent if RS neurons receive weak input, and both FS and RS populations are active if they both receive large inputs. In general, FS neurons tend to follow the spiking of RS neurons much more closely than LTS neurons. A novel type of facilitation-induced slow oscillations is observed above the LTS firing threshold with a frequency determined by the time scale of recovery from facilitation. To conclude, contrary to earlier proposals, LTS neurons affect the transient and steady state responses of cortical circuits over a range of firing rates, not only during the high rate regime; LTS neurons protect against over-activation about as well as FS neurons.
Desynchronization of Neocortical Networks by Asynchronous Release of GABA at Autaptic and Synaptic Contacts from Fast-Spiking Interneurons  [PDF]
Frédéric Manseau,Silvia Marinelli,Pablo Méndez,Beat Schwaller,David A. Prince,John R. Huguenard,Alberto Bacci
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1000492
Abstract: Networks of specific inhibitory interneurons regulate principal cell firing in several forms of neocortical activity. Fast-spiking (FS) interneurons are potently self-inhibited by GABAergic autaptic transmission, allowing them to precisely control their own firing dynamics and timing. Here we show that in FS interneurons, high-frequency trains of action potentials can generate a delayed and prolonged GABAergic self-inhibition due to sustained asynchronous release at FS-cell autapses. Asynchronous release of GABA is simultaneously recorded in connected pyramidal (P) neurons. Asynchronous and synchronous autaptic release show differential presynaptic Ca2+ sensitivity, suggesting that they rely on different Ca2+ sensors and/or involve distinct pools of vesicles. In addition, asynchronous release is modulated by the endogenous Ca2+ buffer parvalbumin. Functionally, asynchronous release decreases FS-cell spike reliability and reduces the ability of P neurons to integrate incoming stimuli into precise firing. Since each FS cell contacts many P neurons, asynchronous release from a single interneuron may desynchronize a large portion of the local network and disrupt cortical information processing.
Desynchronization of Neocortical Networks by Asynchronous Release of GABA at Autaptic and Synaptic Contacts from Fast-Spiking Interneurons  [PDF]
Frédéric Manseau,Silvia Marinelli,Pablo Méndez,Beat Schwaller,David A. Prince,John R. Huguenard,Alberto Bacci
PLOS Biology , 2010, DOI: 10.1371/journal.pbio.1000492
Abstract: Networks of specific inhibitory interneurons regulate principal cell firing in several forms of neocortical activity. Fast-spiking (FS) interneurons are potently self-inhibited by GABAergic autaptic transmission, allowing them to precisely control their own firing dynamics and timing. Here we show that in FS interneurons, high-frequency trains of action potentials can generate a delayed and prolonged GABAergic self-inhibition due to sustained asynchronous release at FS-cell autapses. Asynchronous release of GABA is simultaneously recorded in connected pyramidal (P) neurons. Asynchronous and synchronous autaptic release show differential presynaptic Ca2+ sensitivity, suggesting that they rely on different Ca2+ sensors and/or involve distinct pools of vesicles. In addition, asynchronous release is modulated by the endogenous Ca2+ buffer parvalbumin. Functionally, asynchronous release decreases FS-cell spike reliability and reduces the ability of P neurons to integrate incoming stimuli into precise firing. Since each FS cell contacts many P neurons, asynchronous release from a single interneuron may desynchronize a large portion of the local network and disrupt cortical information processing.
Spike-timing dependent plasticity in inhibitory circuits  [PDF]
Karri P. Lamsa,Dimitri M. Kullmann,Melanie A. Woodin
Frontiers in Synaptic Neuroscience , 2010, DOI: 10.3389/fnsyn.2010.00008
Abstract: Inhibitory circuits in the brain rely on GABA-releasing interneurons. For long, inhibitory circuits were considered weakly plastic in the face of patterns of neuronal activity that trigger long-term changes in the synapses between excitatory principal cells. Recent studies however have shown that GABAergic circuits undergo various forms of long-term plasticity. For the purpose of this review, we identify three major long-term plasticity expression sites. The first locus is the glutamatergic synapses that excite GABAergic inhibitory cells and drive their activity. Such synapses, on many but not all inhibitory interneurons, exhibit long-term potentiation (LTP) and depression (LTD). Second, GABAergic synapses themselves can undergo changes in GABA release probability or postsynaptic GABA receptors. The third site of plasticity is in the postsynaptic anion gradient of GABAergic synapses; coincident firing of GABAergic axons and postsynaptic neurons can cause a long-lasting change in the reversal potential of GABAA receptors mediating fast inhibitory postsynaptic potentials. We review the recent literature on these forms of plasticity by asking how they may be triggered by specific patterns of pre- and postsynaptic action potentials, although very few studies have directly examined spike-timing dependent plasticity (STDP) protocols in inhibitory circuits. Plasticity of interneuron recruitment and of GABAergic signaling provides for a rich flexibility in inhibition that may be central to many aspects of brain function. We do not consider plasticity at glutamatergic synapses on Purkinje cells and other GABAergic principal cells.
Molecules and mechanisms involved in the generation and migration of cortical interneurons  [cached]
Luis R Hernández?Miranda,John G Parnavelas,Francesca Chiara
ASN Neuro , 2010, DOI: 10.1042/an20090053
Abstract: The GABA (γ-aminobutyric acid)-containing interneurons of the neocortex are largely derived from the ganglionic eminences in the subpallium. Numerous studies have previously defined the migratory paths travelled by these neurons from their origins to their destinations in the cortex. We review here results of studies that have identified many of the genes expressed in the subpallium that are involved in the specification of the subtypes of cortical interneurons, and the numerous transcription factors, motogenic factors and guidance molecules that are involved in their migration.
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.