Добірка наукової літератури з теми "Glycinergic synaptic transmission"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Зміст
Ознайомтеся зі списками актуальних статей, книг, дисертацій, тез та інших наукових джерел на тему "Glycinergic synaptic transmission".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Статті в журналах з теми "Glycinergic synaptic transmission"
Betz, H., J. Gomeza, W. Armsen, P. Scholze, and V. Eulenburg. "Glycine transporters: essential regulators of synaptic transmission." Biochemical Society Transactions 34, no. 1 (January 20, 2006): 55–58. http://dx.doi.org/10.1042/bst0340055.
Повний текст джерелаAwatramani, Gautam B., Rostislav Turecek, and Laurence O. Trussell. "Staggered Development of GABAergic and Glycinergic Transmission in the MNTB." Journal of Neurophysiology 93, no. 2 (February 2005): 819–28. http://dx.doi.org/10.1152/jn.00798.2004.
Повний текст джерелаZhang, Bo, Ozgun Gokce, W. Dylan Hale, Nils Brose, and Thomas C. Südhof. "Autism-associated neuroligin-4 mutation selectively impairs glycinergic synaptic transmission in mouse brainstem synapses." Journal of Experimental Medicine 215, no. 6 (May 3, 2018): 1543–53. http://dx.doi.org/10.1084/jem.20172162.
Повний текст джерелаDonato, Roberta, and Andrea Nistri. "Relative Contribution by GABA or Glycine to Cl−-Mediated Synaptic Transmission on Rat Hypoglossal Motoneurons In Vitro." Journal of Neurophysiology 84, no. 6 (December 1, 2000): 2715–24. http://dx.doi.org/10.1152/jn.2000.84.6.2715.
Повний текст джерелаUmemiya, M., and A. J. Berger. "Presynaptic inhibition by serotonin of glycinergic inhibitory synaptic currents in the rat brain stem." Journal of Neurophysiology 73, no. 3 (March 1, 1995): 1192–201. http://dx.doi.org/10.1152/jn.1995.73.3.1192.
Повний текст джерелаDonato, Roberta, and Andrea Nistri. "Differential Short-Term Changes in GABAergic or Glycinergic Synaptic Efficacy on Rat Hypoglossal Motoneurons." Journal of Neurophysiology 86, no. 2 (August 1, 2001): 565–74. http://dx.doi.org/10.1152/jn.2001.86.2.565.
Повний текст джерелаLiu, Tao, Tsugumi Fujita, Terumasa Nakatsuka, and Eiichi Kumamoto. "Phospholipase A2 Activation Enhances Inhibitory Synaptic Transmission in Rat Substantia Gelatinosa Neurons." Journal of Neurophysiology 99, no. 3 (March 2008): 1274–84. http://dx.doi.org/10.1152/jn.01292.2007.
Повний текст джерелаSebe, Joy Y., Erika D. Eggers, and Albert J. Berger. "Differential Effects of Ethanol on GABAA and Glycine Receptor-Mediated Synaptic Currents in Brain Stem Motoneurons." Journal of Neurophysiology 90, no. 2 (August 2003): 870–75. http://dx.doi.org/10.1152/jn.00119.2003.
Повний текст джерелаOda, Y., S. Charpier, Y. Murayama, C. Suma, and H. Korn. "Long-term potentiation of glycinergic inhibitory synaptic transmission." Journal of Neurophysiology 74, no. 3 (September 1, 1995): 1056–74. http://dx.doi.org/10.1152/jn.1995.74.3.1056.
Повний текст джерелаLiu, Tao, Tsugumi Fujita, and Eiichi Kumamoto. "Acetylcholine and norepinephrine mediate GABAergic but not glycinergic transmission enhancement by melittin in adult rat substantia gelatinosa neurons." Journal of Neurophysiology 106, no. 1 (July 2011): 233–46. http://dx.doi.org/10.1152/jn.00838.2010.
Повний текст джерелаДисертації з теми "Glycinergic synaptic transmission"
Singer, Joshua H. "Postnatal development of glycinergic synaptic transmission and biophysical properties of glycine receptor-channels /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/10535.
Повний текст джерелаZhu, Hongmei. "Prenatal dysfunctions of chloride-related inhibition in lumbar motoneurons of the SOD1G93A ALS." Electronic Thesis or Diss., Bordeaux, 2023. http://www.theses.fr/2023BORD0026.
Повний текст джерелаAmyotrophic lateral sclerosis (ALS) is a fatal and adult-onset neurodegenerative disease characterized by a progressive degeneration of motoneurons (MNs) with complex multifactorial aetiology. Most ALS studies have focused on symptomatic stages based on the hypothesis that ALS pathogenesis occurs when the disease becomes symptomatic. However, growing evidence indicates that ALS pathogenesis might start long before symptom onset. My PhD thesis work was based on the hypothesis that ALS - familial and sporadic - stems from deficits taking place during early development. With the aim of identifying early changes underpinning ALS neurodegeneration, the first part of my thesis analysed the GABAergic/glycinergic inhibitory postsynaptic currents (IPSCs) to embryonic (E) E17.5 MNs located in the ventro-lateral motor column from SOD1G93A (SOD) mice, in parallel with the analyse of chloride homeostasis. Our results showed that IPSCs are less frequent in SOD animals in accordance with a reduction of synaptic VIAAT-positive terminals in the close proximity of MN somata. SOD MNs exhibited an ECI 10 mV more depolarized than wild type (WT) MNs. This deficit in GABA/glycine inhibition was due to a reduction of the neuronal chloride transporter KCC2. SOD spontaneous IPSCs and evoked GABAAR-currents exhibited a slower decay correlated to elevated [Cl-]i. Using computer modelling approach, we revealed that the slower relaxation of synaptic inhibitory events acts as a compensatory mechanism to strengthen or increase the efficacy of GABA/glycine inhibition when ECI is more depolarized. Interestingly, simulations revealed an excitatory effect of low frequency (<50Hz) depolarizing GABA/glycine post-synaptic potentials (dGPSPs) in SOD-like MNs but not in WT-like littermates. At high frequency, dGPSPs switched to inhibitory effect resulting from the summation of the shunting components. The second part of my PhD thesis focussed on the effect of electrically evoked-dGPSPs, at different frequencies (7.5 to 100 Hz), on real lumbar E17.5 MNs in which a depolarized ECI (below spike threshold) was imposed. The aim was to examine whether the excitatory effect could be linked to morphological changes previously described in E17.5 SOD MNs. Results showed that some MNs were excited by low frequency dGPSPs and inhibited by high frequency dGPSPs (Dual MNs) and others were inhibited at all frequencies (Inhibited MNs). Dual effect was more often detected in SOD MNs. WT MNs were classified into two clusters according to their input resistance (Rin), Dual MNs being specific to high Rin and Inhibited MNs to low Rin. Morphometric data pointed out a reduced dendritic tree in high Rin WT Dual MNs and a large dendritic tree in low Rin Inhibited MNs. This was not the case in SOD MNs that were excited or inhibited whatever their morphology and Rin. In agreement with simulation showing that a less density of inhibitory current on MNs soma favours excitatory dGPSPs, we found less synaptic VIAAT terminals on the soma and proximal dendrites of SOD MNs, compared to littermate WT MNs, as well as a lower frequency of spontaneous dGPSPs. Altogether, my thesis data emphasize a prenatal defect in the CI- homeostasis and GABA/glycine innervation in the SOD1G93A ALS MNs. Before birth, a dominant population of MNs with low Rin emerges in WT animals. These MNs that are inhibited by dGPSPs could represent future ALS vulnerable fast MNs (putative FF). Interestingly, those MNs are not inhibited in SOD animals. The inhibitory dysfunction could be attributed to two distinct factors: morphology and perisomatic inhibitory synapse density. Of these two factors, the latter plays a major role by controlling capability of GABAergic/glycinergic neurons for shaping spinal motor output