Dissertations / Theses on the topic 'Synaptic transmission'
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1
Warren, Darren A. (Darren Allen). "Mechanisms of Synaptic Transmission." Thesis, The University of Sydney, 1996. https://hdl.handle.net/2123/27620.
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In this work we have presented the results of studies into the mechanisms of synaptic transmission in the sympathetic
nervous sytem. This work has involved calcium imaging on chick ciliary ganglion cells, intracellular recording from rat
main pelvic ganglion cells and extracellular recordings from visualised boutons in the rat main pelvic ganglion.
Using digital imaging techniques, we studied the changes in cell calcium concentration in the avian ciliary ganglion
following tetanic stimulation. The results showed a 3 fold increase for a short tetanus or a 4 fold increase for a long
tetanus in the calcium concentration of both the calyx and soma. After a long tetanus the calcium concentration then
declined along a double exponential with a time course similar to that of post-tetanic potentiation and long term
potentiation in the ganglia.
A new technique has been developed for recording the electrical signs of transmission at single boutons in the sympathetic nervous system. This technique allows recording and
comparison of the relative amplitude of the presynaptic action potential, electrical signs of transmitter release and
postsynaptic action potential from single or small groups of boutons. The preparation used for this work was the rat main pelvic ganglion.
Extracellular electrodes placed over visualized boutons revealed evoked excitatory postsynaptic potentials (extracellular EPSP's) with amplitude histograms that were best described by single gamma distributions in most cases inlow [Ca2+]o (less than 0.5 mM). However, in some cases the gamma distribution had a very large variance which may
have been due to the synchronous release of transmitter from closely apposed boutons which were observed under a
confocal microscope. Intracellular electrodes used on the same preparation revealed spontaneous excitatory
postsynaptic potentials (EPSP’S) with amplitude histograms which were in general well fitted by a Poisson mixtures of
gamma distributions over a wide range of calcium concentrations.
Using the technique of extracellular recording from single boutons or small numbers of boutons we were able to
conclude that K-opioid receptors are located on the boutons of the hypogastric nerve. When activated by K—opioid
receptor agonists they reduce quantal secretion without affecting the propagation of the nerve impulse along the
hypogastric nerve.
2
Mackenzie, Paul James. "Mechanisms regulating the reliability of synaptic transmission." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0020/NQ46382.pdf.
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Yang, Yuanjing. "ATP modulatory actions on hippocampal synaptic transmission." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ59415.pdf.
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Wahl, Linda Marie. "Sources of quantal variance in synaptic transmission." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318451.
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Nishimune, Atsushi. "NSF binding to GluR2 regulates synaptic transmission." Kyoto University, 2000. http://hdl.handle.net/2433/180867.
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Jeffry, Joseph August. "Modulation of synaptic transmission by TRP channels." OpenSIUC, 2010. https://opensiuc.lib.siu.edu/dissertations/121.
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The first sensory synapse is the site where sensory afferent fibers make synaptic connections with second order neurons. Somatic and craniofacial afferents terminate in spinal cord dorsal horn (SDH) and caudal spinal trigeminal nucleus (CSTN). Neurotransmitter release from first order nerve terminals regulates ascending sensory transmission. Several lines of evidence indicate that plasticity in the spinal cord dorsal horn underlies secondary hyperalgesia. The sensory receptors, Transient Receptor Potential (TRP) channels, are expressed not only at peripheral terminals, but also at the central terminals of sensory neurons. While the role of these channels at the periphery is detecting environmental stimuli, their function at central terminals is not fully understood. Furthermore, TRP channel expression has been shown in CNS nuclei like hippocampus that are not tightly linked to somatosensation. In this study, I first determined the functionality of TRP channels at the first sensory synapse and hippocampus using pharmacological activators. I then determined if putatively endogenous TRP channel activators modulate synaptic transmission at the first sensory synapse. Lastly, I determined if recordings that respond to capsaicin demonstrate synaptic plasticity in either hippocampus or spinal cord, in an attempt to attribute synaptic plasticity mechanisms to TRPV1 activity at glutamatergic terminals. I have used slice patch-clamp technique to record miniature, spontaneous and evoked currents in lamina II neurons of spinal cord dorsal horn, CSTN and hippocampus. In lamina II neurons of SDH and CSTN, capsaicin, a TRPV1 agonist, robustly increased the frequency of mEPSCs and sEPSCs in a dose dependant manner. Although capsaicin increased m/sEPSC frequency, eEPSC amplitude, which reflects synchronous action potential propagation at glutamatergic terminals, was markedly depressed by capsaicin. Our studies indicate capsaicin inhibits action potential dependant transmission at central terminals. Resiniferatoxin (RTX) is a TRPV1 agonist that displays higher potency (>100 fold) compared to capsaicin, and deactivation with this agonist is minimal. RTX also depressed eEPSC amplitude in lamina II neurons of SDH and CSTN; unexpectedly, RTX increased m/sEPSC frequency to lesser extent compared to capsaicin. The TRPA1 agonist, N-methyl maleimide (NMM), increased s/mEPSC frequency in lamina II neurons; however, NMM did not depress eEPSC amplitude like capsaicin and RTX. It is possible that inhibition of nerve terminal firing is a unique property of TRPV1 agonists compared to other noxious chemicals. To justify a physiological relevance for nociceptive TRP channel expression at the first sensory synapse, I studied the effect of endogenous TRP channel agonists on synaptic transmission at the first sensory synapse. Anandamide (AEA) is an agonist of CB1/CB2 and TRPV1 receptors; it is less potent at TRPV1 receptors than capsaicin. AEA increased sEPSC frequency in 70% of neurons, whereas the remainder of neurons showed a decrease in sEPSC frequency. Unlike capsaicin and RTX, anandamide did not dramatically depress eEPSC amplitude. Methyl glyoxal (MG) is a putative TRPA1 agonist produced during conditions of hyperglycemia. MG increased the frequency of sEPSCs in SDH lamina II neurons. I next used high frequency synaptic stimulation (HFS-100 Hz, 1s) to model synaptic activity during pain transmission. HFS induced a modest increase in sEPSC frequency and minimally changed eEPSC amplitude; patches that showed HFS modulation also responded to capsaicin. In studying the role of TRP channels in modulating synaptic transmission at central synapses, I finally performed experiments in hippocampus with 2 objectives; 1) to determine extent of capsaicin responsiveness as an indicator of TRPV1 functionality, and 2) to evaluate synaptic plasticity in response to HFS. Capsaicin effect on sEPSC frequency in CA1 and CA3 neurons was minimal in comparison to its effect in dorsal horn neurons. HFS at schaffer collateral region caused LTP in CA1 neurons that was more pronounced than for spinal cord. In conclusion, TRP channels are expressed at central terminals of nociceptors where they modulate glutamatergic transmission. Studying their role at the first sensory synapse enhances our understanding of nociceptive transmission, and this study suggests this receptor for a target for intervening in pathological pain transmission at the level of spinal cord.
7
Rizvi, Nisha. "NOVEL DOPAMINERGIC SIGNALING MODULATING HIPPOCAMPAL SYNAPTIC TRANSMISSION." OpenSIUC, 2015. https://opensiuc.lib.siu.edu/dissertations/1082.
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Dopaminergic systems regulate many brain functions and dysfunction of dopaminergic neurotransmission is thought to underlie numerous disorders, including schizophrenia, attention deficit hyperactivity disorder (ADHD), depression and Alzheimer’s disease. In the hippocampus, a dopaminergic projection from the ventral tegmental area (VTA) is proposed to be essential for controlling entry of sensory information into long-term memory through novelty and salience detection. However, the effects of the VTA-dopamine system on hippocampal synaptic transmission are largely under-explored and the underlying mechanisms are unclear. The goal of this project was to investigate mechanisms involved in dopaminergic modulation of hippocampal neurophysiology. Specifically, I (1) examined if dopamine modulates hippocampal synaptic transmission in a region- and input-specific manner, and (2) studied the signaling mechanisms underlying such modulation. In the first aim for the study, I tested whether SKF38393, a dopamine D1-like receptor agonist, differentially affects excitatory synaptic transmission in perforant path synapses onto dentate gyrus granule cells and whether such effects differ from those at area CA1 synapses. I found that SKF38393 produced a concentration-dependent increase in field excitatory postsynaptic potential (fEPSP) in both subregions, but that higher concentrations were needed in the dentate gyrus to produce comparable effects. This synaptic enhancement was long-lasting and largely irreversible which suggests it may be a form of long term enhancement (LTP). Also, the increase in synaptic transmission at medial perforant path synapses was larger than in the lateral perforant path. Importantly, effects in the dentate gyrus, unlike those in CA1, differed substantially along the dorsoventral axis, with effects being significantly larger at the dorsal compared to the ventral pole. In the second aim, various combinations of D1 and D2-like receptor agonists and antagonists as well as inhibitors of second messenger systems, demonstrated that differential mechanisms were required for initiation and maintenance of SKF38393-mediated early and late-phase enhancement and that a novel non-canonical phospholipase-C (PLC) dependent signaling pathway may be involved. Based on recent discoveries in other brain regions, we hypothesized that multiple subcellular signaling pathways may contribute to PLC activation which may include but are not limited to D1(5)-D2 heteromers and Gβγ complex. In conclusion, this work uncovers novel dopaminergic signaling pathways regulating hippocampal physiology, which will lead to development of better (functionally selective) therapeutic agents.
8
Kuczewski, Nicola. "Cholinergic modulation of synaptic transmission and plasticity." Doctoral thesis, SISSA, 2004. http://hdl.handle.net/20.500.11767/3976.
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The physiological and cognitive states of the brain are influenced by variations
in the activity of the cholinergic systems. For example, changes in the levels of ACh
have been associated with arousal/sleep cycle, sustained and focal attention. Moreover
interfering with cholinergic transmission affects learning and cellular plasticity.
Despite cholinergic system exerts its action by modifying the extracellular cortical
concentration of acetylcholine (ACh) few investigations have until now tested if and
how variation in ACh concentrations could influence neuronal synaptic efficacy and
plasticity in acute brain preparation. In order to investigate this aspect we have used a
quantitative experimental approach (variations in the levels of cholinergic activity)
rather than a simply qualitative (absence or presence of cholinergic activity) on rodent
visual cortex slices. We found that the extracellular ACh concentration affected in
opposite way cortical synaptic efficacy, producing either an enhancement or an
inhibition of evoked field potentials (FPs) respectively with low or high concentrations
of exogenously applied ACh. The versus of ACh modulatory action was dependent on
the activity of AChE and relayed on specific subtypes of muscarinic acetylcholine
receptors (mAChRs), thus linking the action of ACh to the activation of particular
receptor subtypes. The demonstration of a synaptic-pathway specificity of ACh
modulatory action, suggests that cholinergic release could control, in a dynamic way,
the flow of cortical information. Moreover, we showed that ACh concentration in
cortical tissue contributes to modulate long term changes of synaptic efficacy, such as
LTP or LTD induced by specific patterns of afferent neuronal activity. We found that:
1) in the absence of muscarinic receptors activation LTP is not inducible as shown in
slices treated with atropine, 2)cholinergic action on cortical L TP depends on the
activation of the even (M2, M,i) mAChRs. In addition, the sign of long term change,
whether L TP or LTD, appears to be depend on the endogenous level of ACh; indeed,
we reported that burst stimulation of afferent neurons, in rats with reduced cortical
cholinergic innervation, induces an LTD instead of LTP. These results suggest that the
degree of activation of cholinergic system could control cortical the direction of
synaptic plasticity in visual cortex.
9
Uteshev, Vladimir V. "A vision of synaptic transmission between central neurons." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0004/NQ27745.pdf.
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S, Mathew Seena. "Kainate receptor modulation of synaptic transmission in neocortex." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007p/mathew.pdf.
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Okorocha, Albert Egwu. "Fluorescent protein calcium sensor for monitoring synaptic transmission." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/37615.
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Monitoring Ca²⁺ in intracellular compartments remains an uphill task. Fluorescent, organic calcium dyes and genetically encoded calcium indicators (GECIs) have been widely used to increase our understanding of neural activity. Notable among the GECIs is the GCaMP family. The first versions of this family showed potential but were relatively dim and had poor signal to noise ratios. To overcome these weaknesses, our laboratory developed three new ratiometric versions of the SyGCaMP2 family called SyGCaMP2-mCherry, SyGCaMP2-mCherry⁺ and GCaMP2-mCherry. The purpose of the work presented here was to establish whether these sensors were functional and to then use them to examine calcium signalling within the presynaptic terminals of cultured hippocampal and cerebral cortical neurones. The sensors were expressed in HEK 293T cells and their sensitivities to changes in intracellular free Ca²⁺concentration ascertained. The dissociation constants calculated for SyGCaMP2-mCherry⁺ and SyGCaMP2-mCherry were 140 ± 3.1 nM and 149 ± 3.3 nM respectively, but GCaMP2-mCherry was not accurately measured. Sensors were expressed in cortical and hippocampal neurones using lipofection based transfection methods and the expression patterns of each recorded. Both SyGCaMP2-mCherry and SyGCaMP2-mCherry⁺ were expressed in puncta that co-localised with presynaptic markers bassoon and VGlut1. Neurones were activated using field stimulation and the responses to different intensities and patterns of stimulation evaluated. Using the Thy1.2 promotor for neuronal expression, two transgenic mice (SyG 14 and SyG 37) were engineered in our lab that expressed SyGCaMP2-mCherry and responses to electrical stimulation were characterised in hippocampal brain slices. The roles of intracellular Ca²⁺stores in shaping the presynaptic Ca²⁺dynamics were examined and results demonstrated that inhibiting the sarcoendoplasmic reticulum calcium transport ATPase (SERCA pump) with Cyclopiazonic acid (CPA) and thapsigargin led to an enhancement in synaptic strength. In addition, activating ryanodine receptors (RYRs) with caffeine and low concentrations of ryanodine altered presynaptic Ca²⁺ dynamics.
12
Knight, David. "Pre-synaptic regulation of transmitter release probability /." St. Lucia, Qld, 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16101.pdf.
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MOSCHETTA, MATTEO. "Removal of the calcium-dependent regulation of ATP binding in Synapsin I has distinct effects at excitatory and inhibitory synapses." Doctoral thesis, Università degli studi di Genova, 2020. http://hdl.handle.net/11567/993830.
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Synapsins are the most abundant family of neuro-specific phosphoproteins associated with the cytoplasmic surface of the synaptic vesicle membrane. These proteins actively regulate synaptic transmission at the level of the presynaptic terminal by controlling the storage and mobilization of synaptic vesicles within a reserve pool. However, it is hypothesized that synapsins could be involved in other stages of synaptic vesicle dynamics such as trafficking, docking, fusion with the plasma membrane and consequent recycling. Synapsin I (SynI) in particular is expressed two isoforms (Ia and Ib) at the presynaptic compartment of all neurons in the adult brain. Several studies suggest that SynI is also involved in axon elongation and synaptic vesicle fusion kinetics. In human, nonsense and missense mutations of SYN1 gene are related to several diseases such as epilepsy and autism spectrum disorder; in fact, SynI knockout (KO) mice show an epileptic and autism-like phenotype. To carry out its functions, SynI requires to bind ATP in a Ca2+-dependent manner thanks to the coordination of a glutamate residue (E373). As ATP binding regulates SynI oligomerization and SV clustering, we analyzed the effect of E373K mutation on neurotransmitter release and short-term plasticity in excitatory and inhibitory synapses. We coupled electrophysiology (patch-clamp recordings) with electron microscopy in primary SynI KO hippocampal neurons in which either the human wild type or the E373K mutant SynI were re-introduced by infection with lentiviral vectors. Our data indicate that E373K mutation affects predominantly excitatory synapses. The frequency of miniature excitatory postsynaptic currents (mEPSCs) was enhanced, without changes in the amplitude and in the number of excitatory synapses. The increment of mEPSCs frequency was totally abolished after acute injection of BAPTA-AM (a specific Ca2+ chelator), suggesting a possible alteration of Ca2+ homeostasis at the presynaptic terminal. Excitatory E373K-Syn I neurons showed reduced evoked EPSC amplitude attributable to a reduction of the readily releasable pool (RRP), while, on the contrary, inhibitory E373K-Syn I neurons did not show any difference both in miniature, evoked IPSC amplitude and RRP size. While no effects in the dynamics and steady state of depression were detected, both excitatory and inhibitory E373K-Syn I neurons failed to recover after stimulation with long high-frequency trains. No mutation-induced changes were observed in network firing/bursting activity as determined with multi-electrode extracellular recordings. Our data suggest that the Ca2+-dependent regulation of ATP-binding to SynI plays important roles in spontaneous and evoked neurotransmitter release that differentially affect the strength of excitatory and inhibitory transmission.
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Trommershäuser, Julia. "A semi-microscopic model of synaptic transmission and plasticity." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=963474626.
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Bird, Alex. "Temporal and spatial factors affecting synaptic transmission in cortex." Thesis, University of Warwick, 2016. http://wrap.warwick.ac.uk/80032/.
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Synaptic transmission in cortex depends on both the history of synaptic activity and the location of individual anatomical contacts within the dendritic tree. This thesis analyses key aspects of the roles of both these factors and, in particular, extends many of the results for deterministic synaptic transmission to a more naturalistic stochastic framework. Firstly, I consider how correlations in neurotransmitter vesicle occupancy arising from synchronous activity in a presynaptic population interact with the number of independent release sites, a parameter recently shown to be modified during long-term plasticity. I study a model of multiple-release-site short-term plasticity and derive exact results for the postsynaptic voltage variance. Using approximate results for the postsynaptic firing rate in the limits of low and high correlations, I demonstrate that short-term depression leads to a maximum response for an intermediate number of presynaptic release sites, and that this in turn leads to a tuning-curve response peaked at an optimal presynaptic synchrony set by the number of neurotransmitter release sites per presynaptic neuron. As the nervous system operates under constraints of efficient metabolism it is likely that this phenomenon provides an activity-dependent constraint on network architecture. Secondly, I consider how synapses exhibiting short-term plasticity transmit spike trains when spike times are autocorrelated. I derive exact results for vesicle occupancy and postsynaptic voltage variance in the case that spiking is a renewal process, with uncorrelated interspike intervals (ISIs). The vesicle occupancy predictions are tested experimentally and shown to be in good agreement with the theory. I demonstrate that neurotransmitter is released at a higher rate when the presynaptic spike train is more regular, but that positively autocorrelated spike trains are better drivers of the postsynaptic voltage when the vesicle release probability is low. I provide accurate approximations to the postsynaptic firing rate, allowing future studies of neuronal circuits and networks with dynamic synapses to incorporate physiologically relevant spiking statistics. Thirdly, I develop a Bayesian inference method for synaptic parameters. This expands on recent Bayesian approaches in that the likelihood function is exact for both the quantal and dynamic synaptic parameters. This means that it can be used to directly estimate parameters for common synaptic models with few release sites. I apply the method to simulated and real data; demonstrating a substantial improvement over analysis techniques that are based around the mean and variance. Finally, I consider a spatially extended neuron model where the dendrites taper away from the soma. I derive an accurate asymptotic solution for the voltage profile in a dendritic cable of arbitrary radius profile and use this to determine the profile that optimally transfers voltages to the soma. I find a precise quadratic form that matches results from non-parametric numerical optimisation. The equation predicts diameter profiles from reconstructed cells, suggesting that dendritic diameters optimise passive transfer of synaptic currents.
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Smith, Amanda Jane. "Synaptic transmission in the rat medial superior olivary nucleus." Thesis, University of Leicester, 1998. http://hdl.handle.net/2381/29917.
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The medial superior olivary (MSO) nucleus forms part of the binaural auditory pathway in the brain stem where it is involved in sound source localisation. It detects interaural time differences (ITDs) of sounds arriving at the two ears by functioning as a coincidence detector of the bilateral excitatory inputs from spherical bushy cells of the anterior ventral cochlear nuclei (AVCN). The MSO also receives a unilateral inhibitory synaptic input from globular bushy cells of the contralateral AVCN, via the medial nucleus of the trapezoid body (MNTB). Investigations in this thesis focus on the inhibitory synaptic input. Transverse brain stem slices were prepared from 6-13 day old Lister Hooded rats and whole cell patch clamp recordings were made from visually identified MSO neurones. Synaptic currents were evoked using a bipolar platinum stimulating electrode positioned over the ipsilateral MNTB. The excitatory synaptic input from the contralateral AVCN was mediated by glutamate receptors. Inhibitory postsynaptic currents (IPSCs), generated by stimulation of the ipsilateral MNTB reversed around the chloride equilibrium potential and were blocked by 1microM strychnine, suggesting them to be glycine receptor mediated. The EPSCs had a mean 10-90% rise time of 0.71+/-0.12ms (n=9) and decayed over a double exponential time course with time constants of 8.54+/-0.44ms and 41.50+/-1.84ms (n=81) at 25°C. The decay time course of the IPSC had a Q10 of ~2 and was slightly voltage-dependent. The IPSCs were also modulated by 5HT, metabotropic glutamate and GABA B receptors, the latter of which, based on miniature current analysis was suggested to be via a presynaptic site. This work confirms that there is a functional synapse between the MNTB and MSO which is mediated by the inhibitory transmitter, glycine and hence suggests that models of sound source localisation should incorporate this important observation.
17
Zhang, Jingfei. "Neuroinflammation rapidly triggers long-term modulation of synaptic transmission." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43253.
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Cognitive dysfunction and abnormal synaptic transmission are main characteristics of various brain disorders, including stroke, trauma and various neurodegenerative diseases. Neuroinflammation, known to influence synaptic function, plays an important role in all these brain disorders. Hypoxia is usually concurrent with neuroinflammation in these brain disorders. In peripheral systems, inflammation and hypoxia are interdependent on each other by sharing pathways at the initiation of downstream pathways leading to inflammatory responses. However, the interaction of inflammation and hypoxia in the CNS, and more importantly, whether this interaction can affect synaptic function, is still largely unknown.
In Chapter 3, I performed field recording, whole cell recording, 2 photon imaging and biochemical measurements in acute hippocampal slices and found that inflammatory stimuli, either LPS or Aβ, interact with hypoxia to trigger a fast-onset (within 15 min) LTD of synaptic transmission. This neuroinflammation+hypoxia LTD is unusual in that it is independent of NMDARs, mGluRs or patterned synaptic activity. Neuroinflammatory stimulus activates NADPH oxidase by triggering subunits assembly and translocation to the plasma membrane. Hypoxia increases the level of lactic acid via glycolysis, resulting in an increase of lactic acid/pyruvate ratio and a consequent increase of NADPH/NADP⁺ ratio, which in turn boosts production of superoxide by NADPH oxidase. Superoxide subsequently activates PP2A, and ultimately leads to GluR2-mediated AMPAR endocytosis, resulting in LTD of synaptic transmission.
In Chapter 4, I performed field recording and biochemical measurements in acute hippocampal slices and showed that LPS can impair the induction of LTP in a relatively rapid way (1 h pre-incubation). This blockage of LTP is mediated by the activation of microglial TLR4 and its associated MyD88-dependent signaling pathway. IL-1β released from microglia is the major factor in LPS-induced impairment of LTP.
Taken together, our study discovered that neuroinflammation can rapidly induce long-term modulation of synaptic transmission through two distinct pathways. These findings represent novel mechanisms in which environmental stressors modulate synaptic transmission. Furthermore, our study contributes to our understanding of synaptic and cognitive dysfunctions in various brain disorders and suggests new therapeutic targets to alleviate memory loss in these disorders.
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Park, Yun Kyung. "Long-term depression of Kainate receptor-mediated synaptic transmission." Thesis, University of Sheffield, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500258.
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Billups, Daniela. "Modulation of synaptic transmission by interacting proteins and transporters." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271306.
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Mellor, Jack Robert. "Electrophysiological investigation of the mechanisms underlying GABAergic synaptic transmission." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624122.
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Andrew-Adiamah, Jemma. "The P2X receptor mediated regulation of inhibitory synaptic transmission." Thesis, University of Warwick, 2012. http://wrap.warwick.ac.uk/59614/.
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In the central nervous system ATP can be released by neurons and glial cells through similar pathways as other neurotransmitters. Extracellular ATP targets P2X purinoreceptors, causing an influx of Ca2+ ions which transmit very important messages for neurons and glial cells. Ionic signals modulated by P2X receptors can be transformed into the modulation of GABAA receptors. This work describes the universal interaction of P2X receptors downregulating GABAA mediated currents via a Ca2+-dependent mechanism. I have shown that the postsynaptic modulation of GABA currents by P2X receptors is present in both the peripheral (DRG neurons) and central nervous system (cortical neurons). This effect is strongly regulated by an intracellular signalling cascade involving Protein Kinase C. Furthermore, tonically-activated GABAA receptors expressed on central neurons, containing alpha5 and delta subunits are also affected by this P2X and GABAA receptor interaction. The purinergic modulation of GABAA receptors has significant implications for synaptic plasticity, an important mechanism of learning and memory in the central nervous system. The down-regulation of GABAA receptors on the postsynaptic membrane enhances the activity of NMDA receptors and thus increases synaptic efficacy. The study of the purinergic involvement in the induction of Long Term Potention is far from being understood. Ionotrophic purinoceptors represent a novel pathway of GABAA receptor modulation: release of ATP from neurons and astrocytes activates Ca2+- signalling via purinergic P2X receptors, which can regulate GABAA receptors activity in both peripheral and central nervous system compartments. The physiological implications of this regulatory pathway are yet to be investigated.
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Needham, E. L. "AMPA receptors and auxiliary subunits in central synaptic transmission." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1380162/.
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AMPA receptors (AMPARs) mediate the majority of fast excitatory synaptic transmission in the central nervous system (CNS). AMPARs are tetrameric assemblies of AMPAR subunits forming a functional ion channel gated by the binding of glutamate. The functional properties of AMPARs dictate key features of the excitatory postsynaptic current and they differ with receptor subunit composition (GluA1-4). The incorporation of GluA2 determines many key properties of AMPARs including their permeability to calcium. GluA2-lacking AMPARs are calcium permeable and their expression is tightly regulated. Transmembrane AMPAR regulatory proteins (TARPs) also play a vital role in the regulation of AMPAR properties. TARPs aid the trafficking of AMPARs to the neuronal surface and their synaptic targeting. They also regulate AMPAR channel properties and their gating. AMPARs are known to be dynamic at the neuronal surface. AMPAR density at the synapse changes with synaptic strength, as does their subunit composition. These regulated changes modify the AMPAR-mediated postsynaptic response. While these changes in synaptic AMPARs and synaptic strength are vital for functions such as learning and memory, the altered regulation of AMPARs is implicated in many pathophysiological states including many neurodegenerative diseases. By investigating the properties of AMPARs in central synaptic transmission, and in recombinant expression systems, I have examined the role of AMPARs in a specific disease, the expression of calcium-permeable AMPARs, and the role of TARPs in regulating AMPAR properties. The aim of this thesis was to investigate the function of AMPARs at intact synapses formed in vivo and in recombinant expression systems. My experiments have shown that excitatory and inhibitory synaptic transmission are both altered in the cerebellum of a mouse model of the most common progressive neurodegenerative disease of childhood, Batten disease. I have also shown that spinal motor neurons express a mixture of calcium permeable- and calcium impermeable AMPARs at the synapse. Additionally, my results suggest that the prototypical TARP, stargazin, appears to regulate a proportion of these AMPARs. Finally, I have considered the role of a protein related to the TARP family, γ-6, in the regulation of recombinant AMPAR properties. γ-6 was found to regulate AMPAR trafficking and pharmacology, but is unable to modify single-channel conductance.
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Morton, Robin A. "Modulation of cholinergic synaptic transmission in the rat hippocampus." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/22509.
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Intracellular recordings were made from pyramidal neurones in the CA1 region of the rat hippocampus to investigate aspects of cholinergic synaptic transmission in the mammalian brain. In the presence of ionotropic glutamate and GABA receptor antagonists, single shock stimulation of the septohippocampal cholinergic input in stratum oriens evoked a slow excitatory postsynaptic potential (EPSP) which was associated with an increase in input resistance. Stimulation at intensities sub-threshold for evoking a slow EPSP caused a reduction of spike frequency adaptation. Pharmacological analysis of these responses revealed that they were mediated by muscarinic acetylcholine receptors (mAChRs). Having established a protocol for evoking reproducible mAChR-mediated EPSPs (EPSPMs) and mAChR-mediated inhibition of spike frequency adaptation, experiments were conducted to investigate the modulation of these responses by other neurotransmitter receptors. In this respect, activation of adenosine receptors by the broad spectrum adenosine receptor agonist 2-chloroadenosine (CADO) reversibly inhibited mAChR-mediated synaptic responses in a concentration dependent manner. The pharmacological profile of this effect established that it was mediated by adenosine A1 receptors. In conclusion, it is possible to evoke isolated muscarinic acetylcholine receptor mediated synaptic responses with a single stimulus in the CA1 region of the rat hippocampus. Adenosine A1 receptors are present on cholinergic terminals in this region and act to inhibit these responses by an unknown mechanism. GABAB receptor activation also inhibits cholinergic synaptic transmission although the mechanism and site of action of this is unclear. Finally, endogenous adenosine and GABA, acting at adenosine A1 and GABAB receptors respectively, inhibit cholinergic synaptic transmission in vitro. This modulation provides a potentially important mechanism for the control of neuronal excitability in the hippocampus in vivo.
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Sims-Robinson, Catrina Suppiramaniam Vishnu. "Differential modulation of glutamatergic synaptic transmission by polysialic acid." Auburn, Ala, 2007. http://hdl.handle.net/10415/1352.
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FENG, LIN. "MODULATION OF SYNAPTIC TRANSMISSION AT THE NUCLEUS TRACTUS SOLITARIUS." OpenSIUC, 2014. https://opensiuc.lib.siu.edu/dissertations/816.
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The caudal nucleus tractus solitarius (cNTS) is the key recipient of the primary afferents from visceral sensory neurons and also an important site that processes and integrates gastrointestinal, cardiovascular and respiratory functions. Glutamate and gamma-aminobutyric acid are the major neurotransmitters within the NTS, but studies have suggested that nicotinic acetylcholine receptors (nAChRs) and transient receptor potential (TRP) channels can modulate excitatory/inhibitory neurotransmission. I have designed studies to understand the role of nAChRs and TRP channels in the modulation of neurotransmission in the cNTS. In the first aim, experiments were designed to test the hypothesis that the cNTS contains function-specific subsets of neurons whose responsiveness to nicotine correlates with the target of their axonal projections. cNTS neurons send axonal projections to brain regions such as parabrachial nucleus (PBN), hypothalamic paraventricular nucleus (PVN), nucleus ambiguous (NA), dorsal motor nucleus of the vagus (DMV) and the caudal ventrolateral medulla (CVLM) and are involved in integrating autonomic and neuroendocrine functions. Presynaptic/postsynaptic modulation by nAChRs differ in the axonal projections of cNTS neurons, studying of which would provide better understanding of this complex integration. In vivo fluorescent tracing combined with in vitro slice patch-clamp electrophysiological recordings from anatomically identified caudal NTS neurons were used to study the expression and function of nAChRs (mainly á3â4 containing nAChRs) in the cNTS. Results from these studies demonstrate that presynaptic and postsynaptic responsiveness of caudal NTS neurons to nicotine correlates with the areas the neurons project to in the following order of prevalence: DMV>PVN>NA>CVLM>PBN (for presynaptic responses) and DMV>CVLM>PBN>NA>PVN (for postsynaptic responses). In the second aim, experiments were designed to test the hypothesis that nociceptive TRP channels TRPV1 (vanilloid) and TRPA1 (ankyrin) modulate synaptic transmission in the NTS. As a result of this modulation, the efferent functions that control autonomic and visceral functions will be regulated and account for the changes in autonomic neuropathy as patients with diabetes develop significant alterations in blood pressure and heart rate as well as silent myocardial ischemia as a result of blunted pain carrying ability. Results obtained from these studies demonstrated that TRPV1 and TRPA1 mRNA were detected in the dorsal root ganglion (DRG), but not in the NTS. Immunofluorescence studies revealed that TRPV1 and TRPA1 were expressed in the solitary tract central sensory terminals inputs to NTS but not in NTS neurons. This suggests that TRPV1 and TRPA1 are expressed only in solitary tract. Administration of capsaicin (TRPV1 agonist) and allyl isothiocyanate (AITC, TRPA1 agonist) both increased the frequency of s/mEPSCs without affecting spontaneous and miniature inhibitory postsynaptic currents (s/mIPSCs). Next, the modulation of TRPV1- and TRPA1-induced responses by utilizing a PKC activator (PDBu) was examined. Incubation of slices with PDBu synergistically increased the mEPSC frequency following capsaicin application suggesting an increased receptor affinity; however following application of AITC there was no significant change, suggesting that activation by covalent modification does not enhance binding affinity. Finally, the specificity of TRPV1 and TRPA1 effect on synaptic transmission by ablating TRPV1 and TRPA1were tested. There was no modulation of synaptic transmission in these animals, further confirming that capsaicin- and AITC-mediated modulation of synaptic transmission are specifically mediated by TRPV1 and TRPA1, respectively. Furthermore, animals with painful diabetic peripheral neuropthy exhibited enhanced synaptic activity at the NTS, suggesting a role in nociception and other visceral functions. In summary, nAChRs, TRPV1 and TRPA1 are expressed in the NTS and activation of which modulate excitatory synaptic transmission. The results obtained from these studies and their interpretation may provide a better understanding of the central mechanism of modulation on efferent functions from NTS that regulate cardiovascular, respiratory and gastrointestinal functions.
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Stanback, Alexandra Elizabeth. "The Effects of a Ketone Body on Synaptic Transmission." UKnowledge, 2019. https://uknowledge.uky.edu/biology_etds/57.
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The ketogenic diet is commonly used to control epilepsy, especially in cases when medications cannot. The diet typically consists of high fat, low carb, and adequate protein and produces a metabolite called acetoacetate. Seizure activity is characterized by glutamate excitotoxicity and therefore glutamate regulation is a point of research for control of these disorders. Acetoacetate is heavily implicated as the primary molecule responsible for decreasing glutamate in the synapse; it is believed that acetoacetate interferes with the transport of glutamate into the synaptic vesicles. The effects on synaptic transmission at glutamatergic synapses was studied in relation to the ketogenic diet in Drosophila larvae for this thesis. Various measures of synaptic transmission were conducted. Acetoacetate decreased neurotransmission at the synapse. It was also found that acetoacetate has direct effects on the postsynaptic membrane, which indicates a novel role for the metabolite.
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Sorensen, Staci A. "Afferent input regulates dendritic structure in nucleus laminaris /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/10668.
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Nicol, Scott. "The synapsins : interactions with calmodulin." Thesis, University of Kent, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244329.
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Mitchell, Simon James. "Modulation of transmitter release at a glomerular synapse in the central nervous system." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251826.
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De, La Rue Sarah Anne. "Development and use of a tool for real-time imaging of surface expression of the AMPA-type ionotropic glutamate receptors." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247181.
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Yuan, Ning. "DISTINCT MODULATORY EFFECTS OF DOPAMINE ON EXCITATORY CHOLINERGIC AND INHIBITORY GABAERGIC SYNAPTIC TRANSMISSION IN DROSOPHILA." Ohio University / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1149001533.
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Kan, Ho Man. "The novel synaptic scaffold protein--SHANK /." View Abstract or Full-Text, 2002. http://library.ust.hk/cgi/db/thesis.pl?BICH%202002%20KAN.
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Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2002.Includes bibliographical references (leaves 78-91). Also available in electronic version. Access restricted to campus users.
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Greget, Renaud. "Modélisation et simulation informatique de la transmission nerveuse." Thesis, Mulhouse, 2011. http://www.theses.fr/2011MULH6252.
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Au cours des dernières années, la biologie et plus généralement la recherche médicale, a connu des avancées majeures grâce aux nombreux progrès de la microscopie, de la génétique, de la biologie moléculaire, de la protéomique, et du séquençage à haut débit. Il s’agit maintenant d’identifier à partir de toutes ces données gigantesques, les grandes lois de la biologie. Le principe de la biologie intégrative ou systémique est de poser les bases d'une véritable théorie de l'organisation fonctionnelle du vivant à partir des différents mécanismes découverts expérimentalement. De la même manière que l'on décrit la matière par les théories des mathématiques, de la physique, et de la chimie, on veut pouvoir comprendre, formaliser et modéliser le fonctionnement des mécanismes du vivant. Cette thèse a consisté à réaliser une bibliothèque de modèles fonctionnels des réactions chimiques qui prennent place dans les cellules nerveuses aussi appelés modèles élémentaires et de les assembler afin d’obtenir un système mimant le plus finement possible les mécanismes de la propagation du signal électrique au sein d’une synapse. Les travaux réalisés jusqu'alors ont permis de modéliser les mécanismes essentiels et de reconstituer le comportement d’une synapse glutamatergique. En particulier, l’utilisation de cette nouvelle méthode de recherche et de développement de médicaments a pour objectif de proposer des molécules innovantes, en optimisant leurs propriétés biochimiques. Cette technique permettra, dans un futur proche, l'avènement d'une nouvelle génération de pharmaceutiques, dit multi-cibles, c'est-à-dire permettant d'intervenir sur les différents mécanismes d'une pathologieIn recent years, biology and medical research more generally, has seen major advances in microscopy, genetics, molecular biology, proteomics, and high-throughput sequencing. We now identify from these huge data, the great laws of biology. The principle of integrative biology or systemic is to defined the basis of the foundations for a theory of the functional organization of living from different mechanisms discovered experimentally. In the same way that matter is described by the theories of mathematics, physics, and chemistry, we want to understand, formalize and model the functioning of living mechanisms. This thesis has been to achieve a library of functional models of chemical reactions that take place in nerve cells also called elementary models and assemble them to obtain a system mimicking the finest possible mechanisms of electrical signal propagation within of a synapse. The work done so far allow us to model the essential mechanisms and reconstruct the behavior of a glutamatergic synapse. In particular, the use of this new method of research and drug development aims to offer innovative molecules by optimizing their biochemical properties. This technique will, in the near future, the advent of a new generation of pharmaceuticals, said multi-target, able to intervene on the different mechanisms of disease
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Englitz, Bernhard. "Synaptic transmission and signal representation at the calyx of Held." Leipzig Leipziger Uni.-Verl, 2009. http://d-nb.info/1000423956/04.
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Owens, Steven. "Aspects of inhibitory synaptic transmission to the medial superior olive." Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/29939.
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The medial superior olive (MSO) is a nucleus located in the auditory brainstem receiving binaural input to detect inter-aural time differences of sounds arriving at the two ears. It receives binaural excitatory inputs from the anteroventral cochlear nucleus and a monaural inhibitory input from the ipsilateral medial nucleus of the trapezoid body (MNTB). Investigations in this thesis concentrate on the inhibitory synaptic input and introduce aspects of the excitatory input. Lister Hooded rats aged 3-14 day old were killed by decapitation and transverse brainstem slices (150-200 urn) were prepared. Whole-cell voltage clamp recordings were made from visually identified MSO neurones and synaptic currents evoked by a bipolar stimulating electrode placed across the ipsilateral MNTB. The inhibitory postsynaptic current (IPSC) had a GABAergic component in animals under 6 days old and negligible there after. After 6 days the IPSC was predominantly glycine mediated. The decay time course of the glycinergic IPSC had two components in animals under 11 days old. After 11 days the glycinergic IPSC decay time course accelerated accompanied by a loss of the second slower component. IPSCs were modulated by metabotropic glutamate and GABAb receptors with GABAb receptors acting presynaptically to inhibit neurotransmitter release. Glycine release from the MNTB synapse was mediated predominantly by P/Q-type Ca++ channels, but with a significant contribution from N-type Ca++ channels. Spontaneous miniature IPSCs were variable in amplitude and were of large conductance. Excitatory inputs were mediated by AMPA and NMDA receptors. Excitatory postsynaptic currents (EPSCs) displayed fast decay kinetics compared to EPSCs from other regions of the brain. These studies describe evidence detailing the development and modulation of inhibitory synaptic input to the MSO.
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Geddes, Sean D. "Dynamic Regulation of Synaptic Transmission onto Serotonin Neurons by Antidepressants." Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23532.
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Antidepressants are generally believed to exert their clinical efficacy by enhancing 5-HT transmission. Interestingly, sustained administration of selective serotonin (5-HT) reuptake inhibitors (SSRIs) strongly suppresses in the first few days the firing activity of 5-HT neurons in the dorsal raphe nucleus (DRN), thereby severely hampering the increase of 5-HT in target regions. Remarkably, the firing activity of 5-HT neurons gradually recovers over the time course of treatment and this recovery is believed to be accounted for by the desensitization of 5-HT1A somatodendritic autoreceptors. Here, we sought to investigate whether additional mechanisms might contribute to the dynamic regulation of excitability of 5-HT neurons during the course of SSRI treatments. Borrowing from the well-described homeostatic strengthening of glutamatergic synapses onto cortical pyramidal neurons following prolonged periods of inactivity, we hypothesized that a similar homeostatic-like regulation of synaptic strength might be operant on 5-HT cells during an SSRI treatment. To test this possibility, we used whole-cell electrophysiological recordings on acute midbrain slices to monitor glutamatergic synapses onto 5-HT neurons. We found that a two-day treatment with the SSRI citalopram induced a robust reduction in both the amplitude and frequency of AMPAR-mediated mEPSCs. We also show that this depression in synaptic strength, induced by an SSRI, is transient since excitatory drive onto 5-HT neurons was enhanced by 7 days of treatments. Altogether, these results document a dynamic regulation of glutamatergic synaptic transmission during the time course of a prolonged treatment with an SSRI. Further elucidation of the cellular and molecular mechanisms driving this synaptic plasticity might identify novel pharmacological target to shorten the delay of antidepressant action.
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Paßlick, Stefan [Verfasser]. "Functional characterization of neuron-NG2 cell synaptic transmission / Stefan Paßlick." Bonn : Universitäts- und Landesbibliothek Bonn, 2014. http://d-nb.info/1060787210/34.
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Neale, Stuart Andrew. "Metabotropic glutamate receptors and synaptic transmission in the cerebellar cortex." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271219.
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Lalic, Tatjana. "Synaptic transmission of hippocampal mossy fibres in health and disease." Thesis, University of Oxford, 2009. http://ora.ox.ac.uk/objects/uuid:cb37e4ad-f00a-4fb5-b4b4-5f8a55c3c64c.
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Dentate microcircuitry is thought to be involved in filtering, integrating, and relaying extrinsic hippocampal inputs to the hippocampus proper, which contributes to memory formation and retrieval. The axons of granule cells are called mossy fibres (MFs), and contain multiple terminal types that form characteristic synaptic connections with their postsynaptic targets. This diversity of presynaptic release sites that exists on the same MF provides an extremely interesting axonal type to study the organizing principles of presynaptic release regulation. A remarkable set of neurotransmitters and receptors present at the MF synaptic complex allow diverse computational modification of information from the dentate gyrus to the hippocampus. There are several types of glutamate receptors expressed at MF, such as group II/III mGluRs and kainate receptors (KARs). Presynaptic KARs modulate transmission at MF-CA3 pyramidal cell synapses; however, it is not known whether presynaptic KARs affect other synapses made by MFs. The aim of the first part of this thesis was to establish the principles of synapse-specific actions of presynaptic KARs in MFs. Combining electrophysiology and calcium imaging, this study provides compelling evidence that presynaptic KARs and Ca2+ stores can be activated by glutamate release from a single action potential in a single MF axon. This contributes to short-term, use-dependent facilitation of presynaptic Ca2+ entry and glutamate release exclusively at MF-CA3 pyramidal cell synaps, but not at other MF synapses, on hilar mossy cells or interneurons. Thus, our findings indicate that the presynaptic KARs, coupled with intracellular stores, exist in a synapse-specific autoreceptor mechanism. Activation of KARs strengthened MF-CA3 pyramidal cell synapses by increasing the Ca2+ influx at giant boutons, which might also contribute to the KAR-dependent hyper-excitability of the MF circuitry related to the mechanisms of temporal lobe epilepsy (TLE). This makes KARs good potential targets for therapies in CNS disorders such as epilepsy and other neurological and psychiatric disorders. The second part of this thesis was to explore the actions on the hippocampus of purified antibodies from a limbic encephalitis (LE) patient. LE is a CNS disease characterized by subacute onset of memory loss and temporal lobe seizures. The serum of these patients strongly labels MFs apparently co-localizing with the VGKC. The patients improve with immunotherapies that reduce the VGKC antibody levels in the serum, thus, strongly suggesting that these antibodies cause the condition. We found that LE serum IgGs enhance CA3 pyramidal cell excitability by blocking α-DTX sensitive VGKCs, which results in the increased release of glutamate. This, in turn, strengthens and desynchronizes MF and CA3 pyramidal cells synaptic transmission. However, these effects were occluded by α-DTX, a Kv1.1, Kv1.2 and Kv1.6 antagonist which, when applied alone, mimicked the action of the LE IgG, suggesting that they may share similar mechanisms of action. In contrast serum taken from healthy control patients had no significant effect under same recording conditions. Thus, this study provides the first evidence that the LE IgG functionally affects VGKC containing Kv1.1, Kv1.2 and/or Kv1.6 at both presynaptic MF axon terminals as well as the postsynaptic somatodendritic domain of CA3 pyramidal cells. Whatever defines the exact nature of LE IgG action, our results suggest that drugs acting specifically as openers of VGKC might help to protect the hippocampus from immune-mediated damage. In conclusion my data is consistent with the increasingly documented idea that MFs play a critical role in regulating the excitability of the hippocampal circuits and the dysfunction of MF transmission profoundly impairs hippocampal function.
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Wardle, Rinda A. "Modulation of inhibitory synaptic transmission by brain-derived neurotrophic factor /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2003. http://wwwlib.umi.com/cr/ucsd/fullcit?p3094613.
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Fan, Kai Yoon. "GABAergic synaptic transmission, plasticity and integration in the subthalamic nucleus." Thesis, University of Sheffield, 2012. http://etheses.whiterose.ac.uk/3167/.
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Hoang, Caroline J. "The role of metabotropic glutamate receptors in baroreceptor neurotransmission." free to MU campus, others may purchase free online, 2002. http://wwwlib.umi.com/cr/mo/preview?3074406.
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Parker, David. "The physiology and pharmacology of direct central connections between the fast extensor and flexor tibiae motor neurones in the locust." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318422.
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Cheung, Helen. "Pharmacology of acetylcholine receptors in the cockroach (Periplaneta americana L.) CNS." Thesis, Oxford Brookes University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279155.
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Fleming, John. "Molecular characterisation of ion-channel receptor mutants." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240915.
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Babcock, Michael Cameron. "Forward and reverse genetic approaches to studying synaptic transmission in Drosophila melanogaster /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/10289.
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Vasileva, Mariya [Verfasser], and Thomas [Akademischer Betreuer] Kuner. "Function of Synapsin Proteins in Synaptic Transmission at a Giant CNS Synapse / Mariya Vasileva ; Betreuer: Thomas Kuner." Heidelberg : Universitätsbibliothek Heidelberg, 2012. http://d-nb.info/1179785940/34.
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Lucas, Sarah Jane. "The role of group II metabotropic glutamate receptors in synaptic transmission and synaptic plasticity in the lateral amygdala." Thesis, University of Bristol, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544343.
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Li, Jingjun Bhat Manzoor A. "Crucial role of Drosophila neurexin in proper active zone apposition to postsynaptic densities, synaptic growth and synaptic transmission." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1919.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.Title from electronic title page (viewed Dec. 11, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum of Neurobiology, School of Medicine." Discipline: Neurobiology; Department/School: Medicine.
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Mahmoud, Ghada Saad Zaglool Ahmed. "Mechanisms of growth hormone enhancement of excitatory synaptic transmission in hippocampus /." Huntington, WV : [Marshall University Libraries], 2005. http://www.marshall.edu/etd/descript.asp?ref=532.
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Theses (Ph. D.)--Marshall University, 2005.Title from document title page. Includes abstract. Document formatted into pages: contains xiii, 156 pages including illustrations. Bibliography: p. 118-156.