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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
Synaptic Transmission and Plasticity in an Active Cortical Network  [PDF]
Ramon Reig, Maria V. Sanchez-Vives
PLOS ONE , 2007, DOI: 10.1371/journal.pone.0000670
Abstract: Background The cerebral cortex is permanently active during both awake and sleep states. This ongoing cortical activity has an impact on synaptic transmission and short-term plasticity. An activity pattern generated by the cortical network is a slow rhythmic activity that alternates up (active) and down (silent) states, a pattern occurring during slow wave sleep, anesthesia and even in vitro. Here we have studied 1) how network activity affects short term synaptic plasticity and, 2) how synaptic transmission varies in up versus down states. Methodology/Principal Findings Intracellular recordings obtained from cortex in vitro and in vivo were used to record synaptic potentials, while presynaptic activation was achieved either with electrical or natural stimulation. Repetitive activation of layer 4 to layer 2/3 synaptic connections from ferret visual cortex slices displayed synaptic augmentation that was larger and longer lasting in active than in silent slices. Paired-pulse facilitation was also significantly larger in an active network and it persisted for longer intervals (up to 200 ms) than in silent slices. Intracortical synaptic potentials occurring during up states in vitro increased their amplitude while paired-pulse facilitation disappeared. Both intracortical and thalamocortical synaptic potentials were also significantly larger in up than in down states in the cat visual cortex in vivo. These enhanced synaptic potentials did not further facilitate when pairs of stimuli were given, thus paired-pulse facilitation during up states in vivo was virtually absent. Visually induced synaptic responses displayed larger amplitudes when occurring during up versus down states. This was further tested in rat barrel cortex, where a sensory activated synaptic potential was also larger in up states. Conclusions/Significance These results imply that synaptic transmission in an active cortical network is more secure and efficient due to larger amplitude of synaptic potentials and lesser short term plasticity.
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
The brain decade in debate: VI. Sensory and motor maps: dynamics and plasticity
Das, A.;Franca, J.G.;Gattass, R.;Kaas, J.H.;Nicolelis, M.A.L.;Timo-Iaria, C.;Vargas, C.D.;Weinberger, N.M.;Volchan, E.;
Brazilian Journal of Medical and Biological Research , 2001, DOI: 10.1590/S0100-879X2001001200001
Abstract: this article is an edited transcription of a virtual symposium promoted by the brazilian society of neuroscience and behavior (sbnec). although the dynamics of sensory and motor representations have been one of the most studied features of the central nervous system, the actual mechanisms of brain plasticity that underlie the dynamic nature of sensory and motor maps are not entirely unraveled. our discussion began with the notion that the processing of sensory information depends on many different cortical areas. some of them are arranged topographically and others have non-topographic (analytical) properties. besides a sensory component, every cortical area has an efferent output that can be mapped and can influence motor behavior. although new behaviors might be related to modifications of the sensory or motor representations in a given cortical area, they can also be the result of the acquired ability to make new associations between specific sensory cues and certain movements, a type of learning known as conditioning motor learning. many types of learning are directly related to the emotional or cognitive context in which a new behavior is acquired. this has been demonstrated by paradigms in which the receptive field properties of cortical neurons are modified when an animal is engaged in a given discrimination task or when a triggering feature is paired with an aversive stimulus. the role of the cholinergic input from the nucleus basalis to the neocortex was also highlighted as one important component of the circuits responsible for the context-dependent changes that can be induced in cortical maps.
The brain decade in debate: VI. Sensory and motor maps: dynamics and plasticity  [cached]
Das A.,Franca J.G.,Gattass R.,Kaas J.H.
Brazilian Journal of Medical and Biological Research , 2001,
Abstract: This article is an edited transcription of a virtual symposium promoted by the Brazilian Society of Neuroscience and Behavior (SBNeC). Although the dynamics of sensory and motor representations have been one of the most studied features of the central nervous system, the actual mechanisms of brain plasticity that underlie the dynamic nature of sensory and motor maps are not entirely unraveled. Our discussion began with the notion that the processing of sensory information depends on many different cortical areas. Some of them are arranged topographically and others have non-topographic (analytical) properties. Besides a sensory component, every cortical area has an efferent output that can be mapped and can influence motor behavior. Although new behaviors might be related to modifications of the sensory or motor representations in a given cortical area, they can also be the result of the acquired ability to make new associations between specific sensory cues and certain movements, a type of learning known as conditioning motor learning. Many types of learning are directly related to the emotional or cognitive context in which a new behavior is acquired. This has been demonstrated by paradigms in which the receptive field properties of cortical neurons are modified when an animal is engaged in a given discrimination task or when a triggering feature is paired with an aversive stimulus. The role of the cholinergic input from the nucleus basalis to the neocortex was also highlighted as one important component of the circuits responsible for the context-dependent changes that can be induced in cortical maps.
Cross-Modal Plasticity Results in Increased Inhibition in Primary Auditory Cortical Areas  [PDF]
Yu-Ting Mao,Sarah L. Pallas
Neural Plasticity , 2013, DOI: 10.1155/2013/530651
Abstract: Loss of sensory input from peripheral organ damage, sensory deprivation, or brain damage can result in adaptive or maladaptive changes in sensory cortex. In previous research, we found that auditory cortical tuning and tonotopy were impaired by cross-modal invasion of visual inputs. Sensory deprivation is typically associated with a loss of inhibition. To determine whether inhibitory plasticity is responsible for this process, we measured pre- and postsynaptic changes in inhibitory connectivity in ferret auditory cortex (AC) after cross-modal plasticity. We found that blocking GABAA receptors increased responsiveness and broadened sound frequency tuning in the cross-modal group more than in the normal group. Furthermore, expression levels of glutamic acid decarboxylase (GAD) protein were increased in the cross-modal group. We also found that blocking inhibition unmasked visual responses of some auditory neurons in cross-modal AC. Overall, our data suggest a role for increased inhibition in reducing the effectiveness of the abnormal visual inputs and argue that decreased inhibition is not responsible for compromised auditory cortical function after cross-modal invasion. Our findings imply that inhibitory plasticity may play a role in reorganizing sensory cortex after cross-modal invasion, suggesting clinical strategies for recovery after brain injury or sensory deprivation. 1. Introduction Loss of sensory drive as a result of deprivation or deafferentation can lead to a compensatory plastic reorganization of the affected sensory cortex. For example, a homeostatic downregulation of inhibition makes cortical neurons more sensitive to any remaining inputs (see [1], for review). Although the plastic response to the loss of drive can be limited to a single modality, sprouting of inputs responding to other sensory modalities into the deafferented area often results in cross-modal plasticity. For example, in deaf and blind subjects, the spared sensory cortex can be taken over by sensory inputs from other sensory modalities [2–4]. Such cross-modal inputs replace the lost inputs to some extent; thus the mechanisms of recovery might be different from recovery from manipulations affecting a single modality [5]. Because sensory inputs have been changed rather than lost entirely, the loss of inhibition seen after unimodal deprivation may be mitigated. It is important to understand whether cross-modal plasticity has similar or different effects on inhibition than within-modality plasticity because of the prevalence of cross-modal plasticity in patients suffering from
GABA through the Ages: Regulation of Cortical Function and Plasticity by Inhibitory Interneurons  [PDF]
Konrad Lehmann,André Steinecke,Jürgen Bolz
Neural Plasticity , 2012, DOI: 10.1155/2012/892784
Abstract: Inhibitory interneurons comprise only about 20% of cortical neurons and thus constitute a clear minority compared to the vast number of excitatory projection neurons. They are, however, an influential minority with important roles in cortical maturation, function, and plasticity. In this paper, we will highlight the functional importance of cortical inhibition throughout brain development, starting with the embryonal formation of the cortex, proceeding by the regulation of sensory cortical plasticity in adulthood, and finishing with the GABA involvement in sensory information processing in old age. 1. Introduction The functioning of the cerebral cortex depends critically on the precise balance between excitatory and inhibitory neurotransmitter systems. Excitation is mediated via glutamate by pyramidal neurons, the projection neurons of the cortex, and by a special class of local neurons in cortical layer IV, the spiny stellate cells. Inhibition is mediated via γ-aminobutyric acid (GABA) by cortical interneurons, which regulate the degree of glutamatergic excitation, filtering the input and regulate the output of projection neurons. GABAergic interneurons, the “nonpyramidal cells” of the cerebral cortex, take many different forms of dendritic and axonal arborization, which have been used for their morphological classification ever since their first description by Ramon Cajal [1–5]. Moreover, interneurons also differ in their firing patterns, the neuropeptides they express, their calcium-binding protein content, and other molecular markers such as ion channels, receptors, and transporters. Based on the combination of structural, functional, and biochemical criteria, interneurons have been subdivided into many different subclasses and it is still a matter of hot debate among the experts of how many interneuron subtypes exist in the cortices of different species [6–8]. At the circuit level, interneurons control the flow of information and synchronization in the cerebral cortex. There are about five times more glutamatergic neurons than GABAergic neurons in the neocortex; this ratio is consistently observed across many mammalian species. This then suggests that the numerical balance of excitatory and inhibitory neurons may be important for normal brain function and behavior. Even though GABAergic interneurons comprise only a small fraction of the cells in the neocortex, disturbances in their development, and hence the delicate balance between excitation and inhibition, can lead to neurological or neuropsychiatric diseases such as epilepsy, autism, and
Effects of Sensory Behavioral Tasks on Pain Threshold and Cortical Excitability  [PDF]
Magdalena Sarah Volz, Vanessa Suarez-Contreras, Mariana E. Mendonca, Fernando Santos Pinheiro, Lotfi B. Merabet, Felipe Fregni
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0052968
Abstract: Background/Objective Transcutaneous electrical stimulation has been proven to modulate nervous system activity, leading to changes in pain perception, via the peripheral sensory system, in a bottom up approach. We tested whether different sensory behavioral tasks induce significant effects in pain processing and whether these changes correlate with cortical plasticity. Methodology/Principal Findings This randomized parallel designed experiment included forty healthy right-handed males. Three different somatosensory tasks, including learning tasks with and without visual feedback and simple somatosensory input, were tested on pressure pain threshold and motor cortex excitability using transcranial magnetic stimulation (TMS). Sensory tasks induced hand-specific pain modulation effects. They increased pain thresholds of the left hand (which was the target to the sensory tasks) and decreased them in the right hand. TMS showed that somatosensory input decreased cortical excitability, as indexed by reduced MEP amplitudes and increased SICI. Although somatosensory tasks similarly altered pain thresholds and cortical excitability, there was no significant correlation between these variables and only the visual feedback task showed significant somatosensory learning. Conclusions/Significance Lack of correlation between cortical excitability and pain thresholds and lack of differential effects across tasks, but significant changes in pain thresholds suggest that analgesic effects of somatosensory tasks are not primarily associated with motor cortical neural mechanisms, thus, suggesting that subcortical neural circuits and/or spinal cord are involved with the observed effects. Identifying the neural mechanisms of somatosensory stimulation on pain may open novel possibilities for combining different targeted therapies for pain control.
Sensory Adaptation and Short Term Plasticity as Bayesian Correction for a Changing Brain  [PDF]
Ian H. Stevenson,Beau Cronin,Mriganka Sur,Konrad P. Kording
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0012436
Abstract: Neurons in the sensory system exhibit changes in excitability that unfold over many time scales. These fluctuations produce noise and could potentially lead to perceptual errors. However, to prevent such errors, postsynaptic neurons and synapses can adapt and counteract changes in the excitability of presynaptic neurons. Here we ask how neurons could optimally adapt to minimize the influence of changing presynaptic neural properties on their outputs. The resulting model, based on Bayesian inference, explains a range of physiological results from experiments which have measured the overall properties and detailed time-course of sensory tuning curve adaptation in the early visual cortex. We show how several experimentally measured short term plasticity phenomena can be understood as near-optimal solutions to this adaptation problem. This framework provides a link between high level computational problems, the properties of cortical neurons, and synaptic physiology.
Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala  [PDF]
Osvaldo Mirante,Johannes Bohacek,Isabelle M. Mansuy
Frontiers in Molecular Neuroscience , 2014, DOI: 10.3389/fnmol.2014.00062
Abstract: N-methyl-D-aspartate receptor (NMDAR)-dependent long-term depression (LTD) in the lateral nucleus of the amygdala (LA) is a form of synaptic plasticity thought to be a cellular substrate for the extinction of fear memory. The LA receives converging inputs from the sensory thalamus and neocortex that are weakened following fear extinction. Combining field and patch-clamp electrophysiological recordings in mice, we show that a paired-pulse low-frequency stimulation can induce a robust LTD at thalamic and cortical inputs to LA, and we identify different underlying molecular components at these pathways. We show that while LTD depends on NMDARs and activation of the protein phosphatases PP2B and PP1 at both pathways, it requires NR2B-containing NMDARs at the thalamic pathway, but NR2C/D-containing NMDARs at the cortical pathway. LTD appears to be induced postsynaptically at the thalamic input but presynaptically at the cortical input, since postsynaptic calcium chelation and NMDAR blockade prevent thalamic but not cortical LTD. These results highlight distinct molecular features of LTD in LA that may be relevant for traumatic memory and its erasure, and for pathologies such as post-traumatic stress disorder (PTSD).
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