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Hilar GABAergic Interneuron Activity Controls Spatial Learning and Memory Retrieval  [PDF]
Yaisa Andrews-Zwilling, Anna K. Gillespie, Alexxai V. Kravitz, Alexandra B. Nelson, Nino Devidze, Iris Lo, Seo Yeon Yoon, Nga Bien-Ly, Karen Ring, Daniel Zwilling, Gregory B. Potter, John L. R. Rubenstein, Anatol C. Kreitzer, Yadong Huang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0040555
Abstract: Background Although extensive research has demonstrated the importance of excitatory granule neurons in the dentate gyrus of the hippocampus in normal learning and memory and in the pathogenesis of amnesia in Alzheimer's disease (AD), the role of hilar GABAergic inhibitory interneurons, which control the granule neuron activity, remains unclear. Methodology and Principal Findings We explored the function of hilar GABAergic interneurons in spatial learning and memory by inhibiting their activity through Cre-dependent viral expression of enhanced halorhodopsin (eNpHR3.0)—a light-driven chloride pump. Hilar GABAergic interneuron-specific expression of eNpHR3.0 was achieved by bilaterally injecting adeno-associated virus containing a double-floxed inverted open-reading frame encoding eNpHR3.0 into the hilus of the dentate gyrus of mice expressing Cre recombinase under the control of an enhancer specific for GABAergic interneurons. In vitro and in vivo illumination with a yellow laser elicited inhibition of hilar GABAergic interneurons and consequent activation of dentate granule neurons, without affecting pyramidal neurons in the CA3 and CA1 regions of the hippocampus. We found that optogenetic inhibition of hilar GABAergic interneuron activity impaired spatial learning and memory retrieval, without affecting memory retention, as determined in the Morris water maze test. Importantly, optogenetic inhibition of hilar GABAergic interneuron activity did not alter short-term working memory, motor coordination, or exploratory activity. Conclusions and Significance Our findings establish a critical role for hilar GABAergic interneuron activity in controlling spatial learning and memory retrieval and provide evidence for the potential contribution of GABAergic interneuron impairment to the pathogenesis of amnesia in AD.
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
Melting Pot Influences on Secondary English Curriculum Policy  [cached]
Allison Skerrett
International Journal of Education Policy and Leadership , 2009,
Abstract: This article explores how racial, cultural, and linguistic diversity are addressed in secondary English curriculum policy in Massachusetts, U.S.A. Data are analyzed through theories of the sociology of knowledge and the myth of the United States melting pot. Analysis revealed that curriculum policy privileged Eurocentric literature and the English language and adhered to a melting pot ideology. The article considers how the international educational policy movement toward post-standardization may afford greater responsiveness to diversity.
Altered GABAergic markers, increased binocularity and reduced plasticity in the visual cortex of Engrailed-2 knockout mice  [PDF]
Sacha Genovesi,Paola Sgadò,Matteo Caleo,Yuri Bozzi
Frontiers in Cellular Neuroscience , 2014, DOI: 10.3389/fncel.2014.00163
Abstract: The maturation of the GABAergic system is a crucial determinant of cortical development during early postnatal life, when sensory circuits undergo a process of activity-dependent refinement. An altered excitatory/inhibitory balance has been proposed as a possible pathogenic mechanism of autism spectrum disorders (ASD). The homeobox-containing transcription factor Engrailed-2 (En2) has been associated to ASD, and En2 knockout (En2?/?) mice show ASD-like features accompanied by a partial loss of cortical GABAergic interneurons. Here we studied GABAergic markers and cortical function in En2?/? mice, by exploiting the well-known anatomical and functional features of the mouse visual system. En2 is expressed in the visual cortex at postnatal day 30 and during adulthood. When compared to age-matched En2+/+ controls, En2?/? mice showed an increased number of parvalbumin (PV+), somatostatin (SOM+), and neuropeptide Y (NPY+) positive interneurons in the visual cortex at P30, and a decreased number of SOM+ and NPY+ interneurons in the adult. At both ages, the differences in distinct interneuron populations observed between En2+/+ and En2?/? mice were layer-specific. Adult En2?/? mice displayed a normal eye-specific segregation in the retino-geniculate pathway, and in vivo electrophysiological recordings showed a normal development of basic functional properties (acuity, response latency, receptive field size) of the En2?/? primary visual cortex. However, a significant increase of binocularity was found in P30 and adult En2?/? mice, as compared to age-matched controls. Differently from what observed in En2+/+ mice, the En2?/? primary visual cortex did not respond to a brief monocular deprivation performed between P26 and P29, during the so-called “critical period.” These data suggest that altered GABAergic circuits impact baseline binocularity and plasticity in En2?/? mice, while leaving other visual functional properties unaffected.
Bulgarian Turks’ Resistance Against 1984-1989 Melting Pot Policy
Zeynep Zafer
Journal of Gazi Academic View , 2010,
Abstract: Serious scientific studies and previously undisclosed archive documents have been published in Bulgaria recently. These publications prepared on the basis of oppression and assimilation contain highly important information in terms of clarifying the forced or ìvoluntary migrations of the Turkish and Muslim populations and the resistance shown by the Bulgarian Turks against the oppression applied. The Bulgarian authorities, who wish to decrease the number of the Turkish population constantly, have never given up the idea of forced assimilation and the forced migration to expel this population they considered dangerous. In this paper, in light of archive documents and sources, the struggle of the Turks in Bulgaria during the 1984-1989 period against the melting pot policy has been emphasized.
As identidades dos imigrantes e o melting pot nacional
Seyferth, Giralda;
Horizontes Antropológicos , 2000, DOI: 10.1590/S0104-71832000001400007
Abstract: the principles behind the idea of brazilian nationality during the period of intense immigration enforced the accomodation of immigrants and their descendants to assimilationist canons contained within the ideals underpinning the formation of the brazilian nation. this in spite of the preponderance of the notion of jus soli within brazilian jurisprudence. primordial sentiments based on notions of jus sanguinis upon wich were founded some of the ethnic identities expressed by groups of immigrants, collided with the precepts of "abrasileiramento" (roughly "becoming brazilianess" or "brazilianization") and its concomitant image of the melting pot. the work presented here discusses different ways of thinking nationality, ethnicity and cultural plurality during the first half of the 20th century. it's empirical reference is the elaboration of ethnic identity within the context of immigration to southern brazil and the concomitant articulations this process maintained with the colonization and occupation of public lands.
Mechanisms of GABAergic Homeostatic Plasticity  [PDF]
Peter Wenner
Neural Plasticity , 2011, DOI: 10.1155/2011/489470
Abstract: Homeostatic plasticity ensures that appropriate levels of activity are maintained through compensatory adjustments in synaptic strength and cellular excitability. For instance, excitatory glutamatergic synapses are strengthened following activity blockade and weakened following increases in spiking activity. This form of plasticity has been described in a wide array of networks at several different stages of development, but most work and reviews have focussed on the excitatory inputs of excitatory neurons. Here we review homeostatic plasticity of GABAergic neurons and their synaptic connections. We propose a simplistic model for homeostatic plasticity of GABAergic components of the circuitry (GABAergic synapses onto excitatory neurons, excitatory connections onto GABAergic neurons, cellular excitability of GABAergic neurons): following chronic activity blockade there is a weakening of GABAergic inhibition, and following chronic increases in network activity there is a strengthening of GABAergic inhibition. Previous work on GABAergic homeostatic plasticity supports certain aspects of the model, but it is clear that the model cannot fully account for some results which do not appear to fit any simplistic rule. We consider potential reasons for these discrepancies. 1. Introduction Alterations in the influence of inhibitory GABAergic circuits can have a profound impact on the excitability of neural network function, and have been associated with hyperexcitable conditions such as epilepsy [1, 2]. Recent work has identified what may be one of the most important processes in ensuring that networks maintain appropriate activity levels; homeostatic plasticity is thought to maintain network spiking activity levels within a physiologically relevant range through compensatory adjustments in intrinsic cellular excitability, as well as excitatory and inhibitory synaptic strength [3–8]. These changes are induced following perturbations in spiking activity levels for many hours. This phenomenon has been identified in several systems, at different developmental stages, in vitro and to a lesser extent in vivo. When activity levels of cultured neuronal networks (cortical, hippocampal, spinal) are altered for days, cellular excitability and synaptic strength within the network are adjusted in a direction that appears to oppose the alteration in activity [9–14]. For instance, when spiking activity is blocked for 2 days, AMPAergic synaptic strength increases and GABAergic synaptic strength decreases in excitatory neurons. When network spiking activity is increased,
Genetic dissection of GABAergic neural circuits in mouse neocortex  [PDF]
Hiroki Taniguchi
Frontiers in Cellular Neuroscience , 2014, DOI: 10.3389/fncel.2014.00008
Abstract: Diverse and flexible cortical functions rely on the ability of neural circuits to perform multiple types of neuronal computations. GABAergic inhibitory interneurons significantly contribute to this task by regulating the balance of activity, synaptic integration, spiking, synchrony, and oscillation in a neural ensemble. GABAergic interneurons display a high degree of cellular diversity in morphology, physiology, connectivity, and gene expression. A considerable number of subtypes of GABAergic interneurons diversify modes of cortical inhibition, enabling various types of information processing in the cortex. Thus, comprehensively understanding fate specification, circuit assembly, and physiological function of GABAergic interneurons is a key to elucidate the principles of cortical wiring and function. Recent advances in genetically encoded molecular tools have made a breakthrough to systematically study cortical circuitry at the molecular, cellular, circuit, and whole animal levels. However, the biggest obstacle to fully applying the power of these to analysis of GABAergic circuits was that there were no efficient and reliable methods to express them in subtypes of GABAergic interneurons. Here, I first summarize cortical interneuron diversity and current understanding of mechanisms, by which distinct classes of GABAergic interneurons are generated. I then review recent development in genetically encoded molecular tools for neural circuit research, and genetic targeting of GABAergic interneuron subtypes, particularly focusing on our recent effort to develop and characterize Cre/CreER knockin lines. Finally, I highlight recent success in genetic targeting of chandelier cells, the most unique and distinct GABAergic interneuron subtype, and discuss what kind of questions need to be addressed to understand development and function of cortical inhibitory circuits.
Acetylcholine release and inhibitory interneuron activity in hippocampal CA1  [PDF]
A. R. McQuiston
Frontiers in Synaptic Neuroscience , 2014, DOI: 10.3389/fnsyn.2014.00020
Abstract: Acetylcholine release in the central nervous system (CNS) has an important role in attention, recall and memory formation. One region influenced by acetylcholine is the hippocampus, which receives inputs from the medial septum and diagonal band of Broca complex (MS/DBB). Release of acetylcholine from the MS/DBB can directly affect several elements of the hippocampus including glutamatergic and GABAergic neurons, presynaptic terminals, postsynaptic receptors and astrocytes. A significant portion of acetylcholine’s effect likely results from the modulation of GABAergic inhibitory interneurons, which have crucial roles in controlling excitatory inputs, synaptic integration, rhythmic coordination of principal neurons and outputs in the hippocampus. Acetylcholine affects interneuron function in large part by altering their membrane potential via muscarinic and nicotinic receptor activation. This minireview describes recent data from mouse hippocampus that investigated changes in CA1 interneuron membrane potentials following acetylcholine release. The interneuron subtypes affected, the receptor subtypes activated, and the potential outcome on hippocampal CA1 network function is discussed.
Development of Cortical GABAergic Innervation  [PDF]
Alex M. Thomson
Frontiers in Cellular Neuroscience , 2011, DOI: 10.3389/fncel.2011.00014
Abstract: The mature neocortex contains many different classes of GABAergic inhibitory interneurons, distributed, with some degree of selectivity, through six layers, and through many different regions. Some of the events in the early lives of these neurones that may determine their ultimate destination, their maturation and their selective innervation of targets appropriate for each subtype, are discussed. Both time and place of birth influence the class of interneuron that an early post-mitotic interneuronal precursor will become, driven by the selective expression of different combinations of transcription factors in different regions of their birth places in the ganglionic eminence and ventricular zone. The long distance migration of these precursors along tangential routes in marginal, subventricular, and intermediate zones and their final radial movement, into the developing cortex, is regulated by chemical cues, both attractant and repellent. Once they arrive at their final destination, they must integrate into the developing circuitry. As they mature within the cortex, their axons grow and branch in highly specific patterns that may be partially determined by the genetic blueprint for each interneuronal class and partly by the environment in which they find themselves. Finally, as each interneuron class begins to form synapses with only certain postsynaptic targets, cell–cell recognition, most probably via protein–protein interactions across the synaptic cleft, facilitate the formation of appropriate synapses.
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