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DP-b99 Modulates Matrix Metalloproteinase Activity and Neuronal Plasticity  [PDF]
Marine Yeghiazaryan, Izabela Rutkowska-Wlodarczyk, Anna Konopka, Grzegorz M. Wilczyński, Armenuhi Melikyan, Eduard Korkotian, Leszek Kaczmarek, Izabela Figiel
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099789
Abstract: DP-b99 is a membrane-activated chelator of zinc and calcium ions, recently proposed as a therapeutic agent. Matrix metalloproteinases (MMPs) are zinc-dependent extracellularly operating proteases that might contribute to synaptic plasticity, learning and memory under physiological conditions. In excessive amounts these enzymes contribute to a number of neuronal pathologies ranging from the stroke to neurodegeneration and epileptogenesis. In the present study, we report that DP-b99 delays onset and severity of PTZ-induced seizures in mice, as well as displays neuroprotective effect on kainate excitotoxicity in hippocampal organotypic slices and furthermore blocks morphological reorganization of the dendritic spines evoked by a major neuronal MMP, MMP-9. Taken together, our findings suggest that DP-b99 may inhibit neuronal plasticity driven by MMPs, in particular MMP-9, and thus may be considered as a therapeutic agent under conditions of aberrant plasticity, such as those subserving epileptogenesis.
Short-term synaptic plasticity in the nociceptive thalamic-anterior cingulate pathway
Bai-Chuang Shyu, Brent A Vogt
Molecular Pain , 2009, DOI: 10.1186/1744-8069-5-51
Abstract: A single nociceptive electrical stimulus to the sciatic nerve induced a prominent sink current in the layer II/III of the ACC in vivo, while high frequency stimulation potentiated the response of this current. Paired-pulse facilitation by electrical stimulation of midline, mediodorsal and intralaminar thalamic nuclei (MITN) suggesting that the MITN projection to ACC mediates the nociceptive short-term plasticity. The short-term synaptic plasticities were evaluated for different inputs in vitro where the medial thalamic and contralateral corpus callosum afferents were compared. Stimulation of the mediodorsal afferent evoked a stronger short-term synaptic plasticity and effectively transferred the bursting thalamic activity to cingulate cortex that was not true for contralateral stimulation. This short-term enhancement of synaptic transmission was mediated by polysynaptic pathways and NMDA receptors. Layer II/III neurons of the ACC express a short-term plasticity that involves glutamate and presynaptic calcium influx and is an important mechanism of the short-term plasticity.The potentiation of ACC neuronal activity induced by thalamic bursting suggest that short-term synaptic plasticities enable the processing of nociceptive information from the medial thalamus and this temporal response variability is particularly important in pain because temporal maintenance of the response supports cortical integration and memory formation related to noxious events. Moreover, these modifications of cingulate synapses appear to regulate afferent signals that may be important to the transition from acute to chronic pain conditions associated with persistent peripheral noxious stimulation. Enhanced and maintained nociceptive activities in cingulate cortex, therefore, can become adverse and it will be important to learn how to regulate such changes in thalamic firing patterns that transmit nociceptive information to ACC in early stages of chronic pain.The cingulate cortex is one of t
Linking Neuronal Ensembles by Associative Synaptic Plasticity  [PDF]
Qi Yuan, Jeffry S. Isaacson, Massimo Scanziani
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0020486
Abstract: Synchronized activity in ensembles of neurons recruited by excitatory afferents is thought to contribute to the coding information in the brain. However, the mechanisms by which neuronal ensembles are generated and modified are not known. Here we show that in rat hippocampal slices associative synaptic plasticity enables ensembles of neurons to change by incorporating neurons belonging to different ensembles. Associative synaptic plasticity redistributes the composition of different ensembles recruited by distinct inputs such as to specifically increase the similarity between the ensembles. These results show that in the hippocampus, the ensemble of neurons recruited by a given afferent projection is fluid and can be rapidly and persistently modified to specifically include neurons from different ensembles. This linking of ensembles may contribute to the formation of associative memories.
Different Modes of Pitch Perception and Learning-Induced Neuronal Plasticity of the Human Auditory Cortex  [PDF]
Michael Schulte,Arne Knief,Annemarie Seither-Preisler,Christo Pantev
Neural Plasticity , 2002, DOI: 10.1155/np.2002.161
Abstract: We designed a melody perception experiment involving eight harmonic complex tones of missing fundamental frequencies (hidden auditory object) to study the short-term neuronal plasticity of the auditory cortex. In this experiment, the fundamental frequencies of the complex tones followed the beginning of the virtual melody of the tune “Frère Jacques”. The harmonics of the complex tones were chosen so that the spectral melody had an inverse contour when compared with the virtual one. Evoked magnetic fields were recorded contralaterally to the ear of stimulation from both hemispheres. After a base line measurement, the subjects were exposed repeatedly to the experimental stimuli for 1 hour a day. All subjects reported a sudden change in the perceived melody, indicating possible reorganization of the cortical processes involved in the virtual pitch formation. After this switch in perception, a second measurement was performed. Cortical sources of the evoked gamma-band activity were significantly stronger and located more medially after a switch in perception. Independent Component Analysis revealed enhanced synchronization in the gamma-band frequency range. Comparing the gamma-band activation of both hemispheres, no laterality effects were observed. The results indicate that the primary auditory cortices are involved in the process of virtual pitch perception and that their function is modifiable by laboratory manipulation.
Neuronal response properties of somatosensory cortex (layer IV) are modulated following experience dependent plasticity in c-fiber depleted rats  [cached]
Ali Shamsizadeh,Vahid Sheibani,Yaghoub Fathollahi,Mohammad Javan
Physiology and Pharmacology , 2007,
Abstract: Previous studies have shown that the receptive field properties, spontaneous activity and spatio-temporal interactions of low-threshold mechanical somatosensory cells in the barrel cortex are influenced by C-fibers. In this study, we examined the effect of C-fiber depletion on response properties of barrel cortex neurons following experience dependent plasticity. Methods: In this study, exteracellular single unit recording was performed on 154 barrel cortex neurons in 70 male Wistar rats (38-41days old). For depleting of C-fibers, neonatal rats received an intra-peritoneal injection of capsaicin solution (50 mg/kg) on the first neonatal day. For induction of experience dependent plasticity, all whiskers but D2 on the left muzzle, were plucked from first neonatal day. Neuronal ON and OFF responses were recorded in right barrel cortex following principal whisker (PW) and its caudal adjacent whisker (AW) deflection. Results: Whisker plucking increased PW–evoked ON responses both in capsaicin and vehicle treated rats (all P<0.05). In vehicle treated rats, AW-evoked ON responses were decreased in plucked animals (P< 0.05). Of particular interest, in capsaicin treated rats, AW-evoked ON responses were not decreased in plucked animals. Analyzing OFF responses showed similar result to ON responses. Conclusion: These findings indicate that c-fibers can modulate neuronal response properties following experience dependent plasticity in layer IV of barrel cortex.
Error correction and fast detectors implemented by ultra-fast neuronal plasticity  [PDF]
Roni Vardi,Hagar Marmari,Ido Kanter
Quantitative Biology , 2014, DOI: 10.1103/PhysRevE.89.042712
Abstract: We experimentally show that the neuron functions as a precise time-integrator, where the accumulated changes in neuronal response latencies, under complex and random stimulation patterns, are solely a function of a global quantity, the average time-lag between stimulations. In contrast, momentary leaps in the neuronal response latency follow trends of consecutive stimulations, indicating ultra-fast neuronal plasticity. On a circuit level, this ultra-fast neuronal plasticity phenomenon implements error-correction mechanisms and fast detectors for misplaced stimulations. Additionally, at moderate/high stimulation rates this phenomenon destabilizes/stabilizes a periodic neuronal activity disrupted by misplaced stimulations.
Pain-related synaptic plasticity in spinal dorsal horn neurons: role of CGRP
Gary C Bird, Jeong S Han, Yu Fu, Hita Adwanikar, William D Willis, Volker Neugebauer
Molecular Pain , 2006, DOI: 10.1186/1744-8069-2-31
Abstract: Whole-cell current- and voltage-clamp recordings were made from substantia gelatinosa (SG) neurons in spinal cord slices from control rats and arthritic rats (> 6 h postinjection of kaolin/carrageenan into the knee). Monosynaptic excitatory postsynaptic currents (EPSCs) were evoked by electrical stimulation of afferents in the dorsal root near the dorsal root entry zone. Neurons in slices from arthritic rats showed increased synaptic transmission and excitability compared to controls. A selective CGRP1 receptor antagonist (CGRP8-37) reversed synaptic plasticity in neurons from arthritic rats but had no significant effect on normal transmission. CGRP facilitated synaptic transmission in the arthritis pain model more strongly than under normal conditions where both facilitatory and inhibitory effects were observed. CGRP also increased neuronal excitability. Miniature EPSC analysis suggested a post- rather than pre-synaptic mechanism of CGRP action.This study is the first to show synaptic plasticity in the spinal dorsal horn in a model of arthritic pain that involves a postsynaptic action of CGRP on SG neurons.Inflammatory processes in peripheral tissues lead to central sensitization in the spinal cord, which contributes to hyperalgesia and allodynia typically associated with inflammatory pain. Although evidence suggests that plastic changes in the spinal dorsal horn account for central sensitization, the relative contribution of pre- and postsynaptic mechanisms and of peripheral and supraspinal factors are not entirely clear. The superficial dorsal horn of the spinal cord, particularly substantia gelatinosa (SG), is a major projection site of small-diameter afferent nerve fibers that predominantly transmit nociceptive signals [1,2]. SG neurons also receive descending inputs from the brainstem [1,3]. Therefore, in addition to intraspinal neuroplastic changes, peripheral as well as supraspinal factors may contribute to central sensitization.Pain-related neuroplastic cha
Cross-modal plasticity in cuban visually-impaired child cochlear implant candidates: topography of somatosensory evoked potentials
Charroó-Ruíz,Lidia E.; Pérez-Abalo,María C.; Hernández,María C.; álvarez,Beatriz; Bermejo,Beatriz; Bermejo,Sandra; Galán,Lídice; Díaz-Comas,Lourdes;
MEDICC Review , 2012, DOI: 10.1590/S1555-79602012000200007
Abstract: introduction: studies of neuroplasticity have shown that the brain's neural networks change in the absence of sensory input such as hearing or vision. however, little is known about what happens when both sensory modalities are lost (deaf-blindness). hence, this study of cortical reorganization in visually-impaired child cochlear implant (ci) candidates. objective: assess cross-modal plasticity, specifically cortical reorganization for tactile representation in visually-impaired child ci candidates, through study of topography of somatosensory evoked potentials (sep). methods: from april through september 2005, sep from median and tibial nerve electrical stimulation were studied in 12 visually-impaired child ci candidates aged 3-15 years and 23 healthy controls. following placement of 19 recording electrodes using the international 10-20 system , sep were recorded and then processed. topographic maps were obtained for sep n20 (median nerve) and sep p40 (tibial nerve), permitting assessment of cortical reorganization by comparing visually-impaired, deaf children's maps with those of healthy children by means of visual inspection and statistical comparison using a permutation test. results: sep n20 topography was significantly more extensive in visually-impaired child ci candidates than in healthy children. an asymmetrical pattern occurred from the expansion of hand tactile activation into the temporal and occipital regions in the left hemisphere on right median nerve stimulation. this did not occur for sep p40 on tibial nerve stimulation (right and left). magnitude of expanded sep n20 response was related to severity of visual impairment and longer duration of dual sensory loss. conclusions: changes in sep n20 topography are evidence of cross-modal plasticity in visually-impaired child ci candidates, appearing to result from a complex interaction between severity of visual impairment and duration of multisensory deprivation.
Cross-modal plasticity in cuban visually-impaired child cochlear implant candidates: topography of somatosensory evoked potentials
Lidia E. Charroó-Ruíz,María C. Pérez-Abalo,María C. Hernández,Beatriz álvarez
MEDICC Review , 2012,
Abstract: INTRODUCTION: Studies of neuroplasticity have shown that the brain's neural networks change in the absence of sensory input such as hearing or vision. However, little is known about what happens when both sensory modalities are lost (deaf-blindness). Hence, this study of cortical reorganization in visually-impaired child cochlear implant (CI) candidates. OBJECTIVE: Assess cross-modal plasticity, specifically cortical reorganization for tactile representation in visually-impaired child CI candidates, through study of topography of somatosensory evoked potentials (SEP). METHODS: From April through September 2005, SEP from median and tibial nerve electrical stimulation were studied in 12 visually-impaired child CI candidates aged 3-15 years and 23 healthy controls. Following placement of 19 recording electrodes using the International 10-20 System , SEP were recorded and then processed. Topographic maps were obtained for SEP N20 (median nerve) and SEP P40 (tibial nerve), permitting assessment of cortical reorganization by comparing visually-impaired, deaf children's maps with those of healthy children by means of visual inspection and statistical comparison using a permutation test. RESULTS: SEP N20 topography was significantly more extensive in visually-impaired child CI candidates than in healthy children. An asymmetrical pattern occurred from the expansion of hand tactile activation into the temporal and occipital regions in the left hemisphere on right median nerve stimulation. This did not occur for SEP P40 on tibial nerve stimulation (right and left). Magnitude of expanded SEP N20 response was related to severity of visual impairment and longer duration of dual sensory loss. CONCLUSIONS: Changes in SEP N20 topography are evidence of cross-modal plasticity in visually-impaired child CI candidates, appearing to result from a complex interaction between severity of visual impairment and duration of multisensory deprivation.
Metabolic Regulation of Neuronal Plasticity by the Energy Sensor AMPK  [PDF]
Wyatt B. Potter,Kenneth J. O'Riordan,David Barnett,Susan M. K. Osting,Matthew Wagoner,Corinna Burger,Avtar Roopra
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0008996
Abstract: Long Term Potentiation (LTP) is a leading candidate mechanism for learning and memory and is also thought to play a role in the progression of seizures to intractable epilepsy. Maintenance of LTP requires RNA transcription, protein translation and signaling through the mammalian Target of Rapamycin (mTOR) pathway. In peripheral tissue, the energy sensor AMP-activated Protein Kinase (AMPK) negatively regulates the mTOR cascade upon glycolytic inhibition and cellular energy stress. We recently demonstrated that the glycolytic inhibitor 2-deoxy-D-glucose (2DG) alters plasticity to retard epileptogenesis in the kindling model of epilepsy. Reduced kindling progression was associated with increased recruitment of the nuclear metabolic sensor CtBP to NRSF at the BDNF promoter. Given that energy metabolism controls mTOR through AMPK in peripheral tissue and the role of mTOR in LTP in neurons, we asked whether energy metabolism and AMPK control LTP. Using a combination of biochemical approaches and field-recordings in mouse hippocampal slices, we show that the master regulator of energy homeostasis, AMPK couples energy metabolism to LTP expression. Administration of the glycolytic inhibitor 2-deoxy-D-glucose (2DG) or the mitochondrial toxin and anti-Type II Diabetes drug, metformin, or AMP mimetic AICAR results in activation of AMPK, repression of the mTOR pathway and prevents maintenance of Late-Phase LTP (L-LTP). Inhibition of AMPK by either compound-C or the ATP mimetic ara-A rescues the suppression of L-LTP by energy stress. We also show that enhanced LTP via AMPK inhibition requires mTOR signaling. These results directly link energy metabolism to plasticity in the mammalian brain and demonstrate that AMPK is a modulator of LTP. Our work opens up the possibility of using modulators of energy metabolism to control neuronal plasticity in diseases and conditions of aberrant plasticity such as epilepsy.
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