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Excitatory neuronal connectivity in the barrel cortex  [PDF]
Dirk Feldmeyer
Frontiers in Neuroanatomy , 2012, DOI: 10.3389/fnana.2012.00024
Abstract: Neocortical areas are believed to be organized into vertical modules, the cortical columns, and the horizontal layers 1–6. In the somatosensory barrel cortex these columns are defined by the readily discernible barrel structure in layer 4. Information processing in the neocortex occurs along vertical and horizontal axes, thereby linking individual barrel-related columns via axons running through the different cortical layers of the barrel cortex. Long-range signaling occurs within the neocortical layers but also through axons projecting through the white matter to other neocortical areas and subcortical brain regions. Because of the ease of identification of barrel-related columns, the rodent barrel cortex has become a prototypical system to study the interactions between different neuronal connections within a sensory cortical area and between this area and other cortical as well subcortical regions. Such interactions will be discussed specifically for the feed-forward and feedback loops between the somatosensory and the somatomotor cortices as well as the different thalamic nuclei. In addition, recent advances concerning the morphological characteristics of excitatory neurons and their impact on the synaptic connectivity patterns and signaling properties of neuronal microcircuits in the whisker-related somatosensory cortex will be reviewed. In this context, their relationship between the structural properties of barrel-related columns and their function as a module in vertical synaptic signaling in the whisker-related cortical areas will be discussed.
Upregulation of excitatory neurons and downregulation of inhibitory neurons in barrel cortex are associated with loss of whisker inputs  [cached]
Zhang Guanjun,Gao Zilong,Guan Sudong,Zhu Yan
Molecular Brain , 2013, DOI: 10.1186/1756-6606-6-2
Abstract: Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices without receiving inputs undergo the plastic changes. It is not clear how the different types of neurons and synapses in the sensory cortex coordinately change after input deficits in order to prevent loss of their functions and to be used for other modalities. We studied this subject in the barrel cortices from whiskers-trimmed mice vs. controls. After whisker trimming for a week, the intrinsic properties of pyramidal neurons and the transmission of excitatory synapses were upregulated in the barrel cortex, but inhibitory neurons and GABAergic synapses were downregulated. The morphological analyses indicated that the number of processes and spines in pyramidal neurons increased, whereas the processes of GABAergic neurons decreased in the barrel cortex. The upregulation of excitatory neurons and the downregulation of inhibitory neurons boost the activity of network neurons in the barrel cortex to be high levels, which prevent the loss of their functions and enhances their sensitivity to sensory inputs. These changes may prepare for attracting the innervations from sensory cortices and/or peripheral nerves for other modalities during cross-modal plasticity.
Ultrastructural characterization of GABAergic and excitatory synapses in the inferior colliculus  [PDF]
Kyle T. Nakamoto,Jeffrey G. Mellott,Colleen S. Sowick,Brett R. Schofield
Frontiers in Neuroanatomy , 2014, DOI: 10.3389/fnana.2014.00108
Abstract: In the inferior colliculus (IC) cells integrate inhibitory input from the brainstem and excitatory input from both the brainstem and auditory cortex. In order to understand how these inputs are integrated by IC cells identification of their synaptic arrangements is required. We used electron microscopy to characterize GABAergic synapses in the dorsal cortex, central nucleus, and lateral cortex of the IC (ICd, ICc, and IClc) of guinea pigs. Throughout the IC, GABAergic synapses are characterized by pleomorphic vesicles and symmetric junctions. Comparisons of GABAergic synapses with excitatory synapses revealed differences (in some IC subdivisions) between the distributions of these synapse types onto IC cells. For excitatory cells in the IClc and ICd GABAergic synapses are biased toward the somas and large dendrites, whereas the excitatory boutons are biased toward spines and small dendrites. This arrangement could allow for strong inhibitory gating of excitatory inputs. Such differences in synaptic distributions were not observed in the ICc, where the two classes of bouton have similar distributions along the dendrites of excitatory cells. Interactions between excitatory and GABAergic inputs on the dendrites of excitatory ICc cells may be more restricted (i.e., reflecting local dendritic processing) than in the other IC subdivisions. Comparisons across IC subdivisions revealed evidence for two classes of GABAergic boutons, a small GABAergic (SG) class that is present throughout the IC and a large GABAergic (LG) class that is almost completely restricted to the ICc. In the ICc, LG, and SG boutons differ in their targets. SG boutons contact excitatory dendritic shafts most often, but also contact excitatory spines and somas (excitatory and GABAergic). LG synapses make comparatively fewer contacts on excitatory shafts, and make comparatively more contacts on excitatory spines and on somas (excitatory and GABAergic). LG boutons likely have a lemniscal origin.
Remodeling and Tenacity of Inhibitory Synapses: Relationships with Network Activity and Neighboring Excitatory Synapses  [PDF]
Anna Rubinski?,Noam E. Ziv
PLOS Computational Biology , 2015, DOI: 10.1371/journal.pcbi.1004632
Abstract: Glutamatergic synapse size remodeling is governed not only by specific activity forms but also by apparently stochastic processes with well-defined statistics. These spontaneous remodeling processes can give rise to skewed and stable synaptic size distributions, underlie scaling of these distributions and drive changes in glutamatergic synapse size “configurations”. Where inhibitory synapses are concerned, however, little is known on spontaneous remodeling dynamics, their statistics, their activity dependence or their long-term consequences. Here we followed individual inhibitory synapses for days, and analyzed their size remodeling dynamics within the statistical framework previously developed for glutamatergic synapses. Similar to glutamatergic synapses, size distributions of inhibitory synapses were skewed and stable; at the same time, however, sizes of individual synapses changed considerably, leading to gradual changes in synaptic size configurations. The suppression of network activity only transiently affected spontaneous remodeling dynamics, did not affect synaptic size configuration change rates and was not followed by the scaling of inhibitory synapse size distributions. Comparisons with glutamatergic synapses within the same dendrites revealed a degree of coupling between nearby inhibitory and excitatory synapse remodeling, but also revealed that inhibitory synapse size configurations changed at considerably slower rates than those of their glutamatergic neighbors. These findings point to quantitative differences in spontaneous remodeling dynamics of inhibitory and excitatory synapses but also reveal deep qualitative similarities in the processes that control their sizes and govern their remodeling dynamics.
Regulation of Excitatory Synapses and Fearful Memories by Stress Hormones  [PDF]
Harm J. Krugers
Frontiers in Behavioral Neuroscience , 2011, DOI: 10.3389/fnbeh.2011.00062
Abstract: Memories for emotionally arousing and fearful events are generally well retained. From the evolutionary point of view this is a highly adaptive behavioral response aimed to remember relevant information. However, fearful memories can also be inappropriately and vividly (re)expressed, such as in posttraumatic stress disorder. The memory formation of emotionally arousing events is largely modulated by hormones, peptides, and neurotransmitters which are released during and after exposure to these conditions. One of the core reactions in response to a stressful situation is the rapid activation of the autonomic nervous system, which results in the release of norepinephrine in the brain. In addition, stressful events stimulate the hypothalamus–pituitary–adrenal axis which slowly increases the release of glucocorticoid hormones from the adrenal glands. Here we will review how glucocorticoids and norepinephrine regulate the formation of fearful memories in rodents and humans and how these hormones can facilitate the storage of information by regulating excitatory synapses.
Spatial Distribution of Excitatory Synapses on the Dendrites of Ganglion Cells in the Mouse Retina  [PDF]
Yin-Peng Chen, Chuan-Chin Chiao
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0086159
Abstract: Excitatory glutamatergic inputs from bipolar cells affect the physiological properties of ganglion cells in the mammalian retina. The spatial distribution of these excitatory synapses on the dendrites of retinal ganglion cells thus may shape their distinct functions. To visualize the spatial pattern of excitatory glutamatergic input into the ganglion cells in the mouse retina, particle-mediated gene transfer of plasmids expressing postsynaptic density 95-green fluorescent fusion protein (PSD95-GFP) was used to label the excitatory synapses. Despite wide variation in the size and morphology of the retinal ganglion cells, the expression of PSD95 puncta was found to follow two general rules. Firstly, the PSD95 puncta are regularly spaced, at 1–2 μm intervals, along the dendrites, whereby the presence of an excitatory synapse creates an exclusion zone that rules out the presence of other glutamatergic synaptic inputs. Secondly, the spatial distribution of PSD95 puncta on the dendrites of diverse retinal ganglion cells are similar in that the number of excitatory synapses appears to be less on primary dendrites and to increase to a plateau on higher branch order dendrites. These observations suggest that synaptogenesis is spatially regulated along the dendritic segments and that the number of synaptic contacts is relatively constant beyond the primary dendrites. Interestingly, we also found that the linear puncta density is slightly higher in large cells than in small cells. This may suggest that retinal ganglion cells with a large dendritic field tend to show an increased connectivity of excitatory synapses that makes up for their reduced dendrite density. Mapping the spatial distribution pattern of the excitatory synapses on retinal ganglion cells thus provides explicit structural information that is essential for our understanding of how excitatory glutamatergic inputs shape neuronal responses.
New players tip the scales in the balance between excitatory and inhibitory synapses
Joshua N Levinson, Alaa El-Husseini
Molecular Pain , 2005, DOI: 10.1186/1744-8069-1-12
Abstract: In the brain, excitatory and inhibitory synaptic transmission is mainly mediated by two neurotransmitters: glutamate which is released at excitatory glutamatergic synaptic contacts, and γ-amino butyric acid (GABA) which is released at inhibitory GABAergic synapses. Neural information processing is believed to be mediated by integration of excitatory and inhibitory synaptic inputs [1-3]. Therefore, precise controls must exist to maintain an appropriate number of one type of synaptic input relative to the other. This process is thought to be governed by homeostatic feedback mechanisms, however factors involved remain elusive [4,5]. Impressive work carried out in recent years has begun to address the roles of molecules involved in synapse formation. A theme that has emerged from these studies is that glutamatergic and GABAergic synapses consist of complex, yet distinct networks of proteins on the postsynaptic side. The major challenge in this field now is to understand how this molecular machinery is involved in synapse formation and specificity.The discovery of a protein complex that regulates postsynaptic glutamate receptor clustering and the formation of dendritic spines has revealed some of the mechanisms involved in excitatory synapse development. Two main groups of key regulators of excitatory synapse formation have been identified, namely postsynaptic scaffolding proteins and cell adhesion molecules (CAMs). In the first group, several proteins including members of the PSD-95 family, shank, and homer have been shown to promote excitatory synapse maturation (reviewed in [6]). Much work has focused on postsynaptic density protein-95 (PSD-95), one of the most abundant proteins in the PSD [6]. PSD-95 clustering at synapses occurs early in development, prior to other postsynaptic proteins [7], and discs large, a Drosophila homolog of PSD-95, is required for normal neuromuscular junction development in larva [8]. In addition, PSD-95 enhances AMPA-type glutamate recepto
Neuroligin-1 Loss Is Associated with Reduced Tenacity of Excitatory Synapses  [PDF]
Adel Zeidan, Noam E. Ziv
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0042314
Abstract: Neuroligins (Nlgns) are postsynaptic, integral membrane cell adhesion molecules that play important roles in the formation, validation, and maturation of synapses in the mammalian central nervous system. Given their prominent roles in the life cycle of synapses, it might be expected that the loss of neuroligin family members would affect the stability of synaptic organization, and ultimately, affect the tenacity and persistence of individual synaptic junctions. Here we examined whether and to what extent the loss of Nlgn-1 affects the dynamics of several key synaptic molecules and the constancy of their contents at individual synapses over time. Fluorescently tagged versions of the postsynaptic scaffold molecule PSD-95, the AMPA-type glutamate receptor subunit GluA2 and the presynaptic vesicle molecule SV2A were expressed in primary cortical cultures from Nlgn-1 KO mice and wild-type (WT) littermates, and live imaging was used to follow the constancy of their contents at individual synapses over periods of 8–12 hours. We found that the loss of Nlgn-1 was associated with larger fluctuations in the synaptic contents of these molecules and a poorer preservation of their contents at individual synapses. Furthermore, rates of synaptic turnover were somewhat greater in neurons from Nlgn-1 knockout mice. Finally, the increased GluA2 redistribution rates observed in neurons from Nlgn-1 knockout mice were negated by suppressing spontaneous network activity. These findings suggest that the loss of Nlgn-1 is associated with some use-dependent destabilization of excitatory synapse organization, and indicate that in the absence of Nlgn-1, the tenacity of excitatory synapses might be somewhat impaired.
Transitions in Oscillatory Dynamics of Two Connected Neurons with Excitatory Synapses  [PDF]
Yasser Roudi,Shahin Rouhani
Quantitative Biology , 2002,
Abstract: It is shown that long term behavior of two connected Integrate- and- Fire neurons with excitatory synapses is determined by some fixed-points. In the case of equal synaptic weights four different dynamic phases are found. Between these phases there is a specific phase with a global attractor fixed-point, which is of interest from different viewpoints. Simulations support our analytic work. When synaptic weights are equal we observe no synchronization but with different weight we do observe an almost synchronous state. Simulations show that when there is only one non-trivial fixed-point the period of oscillations is stable against small changes in synaptic weights
Noradrenergic System Increases Miniature Excitatory Synaptic Currents in the Barrel Cortex  [cached]
Hashem Haghdoost Yazdi,Mohamad Reza Esmaili,Mohamad Sophiabadi,Christian Stricker
Physiology and Pharmacology , 2007,
Abstract: Introduction: Neurons in layer II and III of the somatosensory cortex in rats show high frequency (33 ± 13 Hz) of miniature excitatory postsynaptic currents (mEPSCs) that their rates and amplitudes are independent of sodium channels. There are some changes in these currents in neurodegenerative and psychological disorders. Regarding to well known roles of the neuromodulatory brain systems in these disorders, study the effects of these systems on the miniature currents provides data to understand more precisely pathogenesis of this disorders. Because cortical neurons receive very dense noradrenergic innervations, we examined effects of noradrenergic system on these currents. Methods: Whole cell patch clamp recordings were made on pyramidal neurons of the barrel cortex from brain slices that continuously superfused with artificial cerebrospinal fluid (ACSF) containing tetrodotoxin, sodium channel blocker and picrotoxin, blocker of the GABA receptors. Results: Application of noradrenalin significantly increased frequency and decreased amplitude of the mEPSCs. Using specific agonists and antagonists of the noradrenergic system, it was determined that the effects are mostly mediated by α1 receptor. Conclusion: Our results showed that noradrenergic system controls sodium channel independent synaptic transmission which can be of importance in regulation and induction of many physiological and pathophysiological conditions.
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