Amplitude fluctuations in synaptic potentials evoked in cat spinal motoneurones at identified group Ia synapses.

Redman, S. J.; Walmsley, Bruce

doi:10.1113/jphysiol.1983.sp014885

Cited by 132 publications

(82 citation statements)

References 17 publications

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“…58 In the transverse plane of all levels of the spinal cord, the centrifugal dendritic branches in the white matter run parallel with the centripetal propriospinal and bulbospinal fibers, and serial contact and synapses are formed between the dendrites and the axons. 27 This powerful anatomical organization is further supported by the distribution of high-conductance excitatory synapses in distal dendrites of motoneurons, 37,38 and the extensive 5-HT receptor expression along the entire dendritic tree. 59 Therefore, the transmission failure in white matter dendrites could possibly contribute to the movement dysfunction in EAE.…”

Section: Discussionmentioning

confidence: 96%

“…First, in spinal motoneurons, the conductance of excitatory synapses on distal dendrites may be many times higher than that on proximal dendrites. 38,39 Therefore, similar levels of excitotoxic conditions may more severely damage distal dendrites. Secondly, the gray matter may have higher capacity to clear the extracellular glutamate because the gray matter contains much more synapses than does the white matter.…”

Section: Discussionmentioning

confidence: 99%

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Dendritic and Synaptic Pathology in Experimental Autoimmune Encephalomyelitis

Zhu

Luo

Moore

et al. 2003

The American Journal of Pathology

110

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Evidence has shown that excitotoxicity may contribute to the loss of central nervous system axons and oligodendrocytes in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). Because dendrites and synapses are vulnerable to excitotoxicity, we examined these structures in acute and chronic models of EAE. Immunostaining for microtubule-associated protein-2 showed that extensive dendritic beading occurred in the white matter of the lumbosacral spinal cord (LSSC) during acute EAE episodes and EAE relapses. Retrograde labeling confirmed that most motoneuron dendrites were beaded in the white matter of the LSSC in acute EAE. In contrast, only mild swelling was observed in the gray matter of the LSSC. Dendritic beading showed marked recovery during EAE remission and after EAE recovery. In addition, synaptophysin, synapsin I, and PSD-95 immunoreactivities were significantly reduced in both the gray and white matter of the LSSC during acute EAE episodes and EAE relapses, but showed partial recovery during EAE remission and after EAE recovery. Pathologically, both dendritic beading and the reduction in synaptic protein immunoreactivity were well correlated with inflammatory cell infiltration in the LSSC at different EAE stages. We propose that dendritic and synaptic damage in the spinal cord may contribute to the neurological deficits in EAE. Central nervous system (CNS) inflammation and neurodegeneration are two major pathological processes in multiple sclerosis (MS). Understanding the pathology and mechanisms of CNS degeneration in MS is essential for protecting neural structures and functions in MS patients. In addition to the demyelination and the loss of oligodendrocytes, axonal degeneration in MS has received substantial attention. It has been realized that axonal loss starts early in the disease course, 1,2 and that the accumulation of axonal damage parallels in general the progressive neurological dysfunction in MS patients.3

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Dendritic and Synaptic Pathology in Experimental Autoimmune Encephalomyelitis

Zhu

Luo

Moore

et al. 2003

The American Journal of Pathology

110

View full text Add to dashboard Cite

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“…(1) Glutamate is released into the synaptic cleft by fusion of vesicles, each saturating the receptors at the release site (Jack, Redman & Wong, 1981;Redman & Walmsley, 1983), and each producing a sEPSC. (2) The glutamate concentration transient due to each vesicle is rapid, in the order of a millisecond (Clements, Lester, Tong, Jahr & Westbrook, 1992 Fig.…”

Section: Methodsmentioning

confidence: 99%

Characterization of spontaneous excitatory synaptic currents in salamander retinal ganglion cells.

Taylor¹,

Chen²,

Copenhagen³

1995

The Journal of Physiology

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1. Spontaneous excitatory postsynaptic currents (sEPSCs) were recorded under voltage-clamp conditions. Consistent with activation of non-NMDA-type glutamate receptors, the sEPSCs reversed at potentials above 0 mV, were blocked by 1 UM CNQX and prolonged by 2 mm aniracetam. 2. The peak conductance of the averaged sEPSCs (n = 70-400) was 130 + 60 pS (mean + S.D.; 17 cells, ranging from 70 to 290 pS). Amplitude distributions were skewed towards larger amplitudes. 3. The decay of individual and mean sEPSCs was exponential with a mean time constant (Td) of 3.75 + 0-84 ms (n = 13), which was voltage independent. The 10-90% rise time of the sEPSCs was 1-30 + 0 44 ms (n = 13). There was no correlation between sEPSC rise time and Td suggesting that dendritic filtering alone did not shape the time course of sEPSCs. Light-evoked EPSCs in these retinal ganglion cells are mediated by concomitant activation ofNMDA and non-NMDA receptors; however, no NMDA component was discerned in the sEPSCs, even when recording at -96 mV in Mg2+-free solutions. The decay time course was not altered by 20 uM AP7, an NMDA antagonist, nor was an NMDA component unmasked by adding glycine or D-serine. These results suggest that NMDA and non-NMDA receptors are not coactivated by a single vesicle of transmitter during spontaneous release, and thus are probably not colocalized in the postsynaptic membrane at the sites of spontaneous release. 5. The sEPSCs were an order of magnitude faster than the non-NMDA receptor-mediated EPSCs evoked by light stimuli, and it is proposed that the EPSC time course is determined largely by the extended time course of release of synaptic vesicles from bipolar cells. The quantal content of a light-evoked non-NMDA receptor-mediated EPSC in an on-off cell is about 200 quanta.Bipolar cells provide the major presynaptic excitatory inputs to retinal ganglion cells (Wong-Riley, 1974 (Finch, Fischer & Jackson, 1990;LoTurco, Mody & Kriegstein, 1990). Although the time course of sEPSCs can directly reflect the kinetics of activated channels, it may also be affected by the membrane properties of the neurone. In some neurones, correlation between rise and decay times indicates that electrotonic decay along the dendrites filters sEPSCs recorded at the cell soma (McBain & Dingledine, 1993;Ulrich & Luscher, 1993). In this study, using the whole-cell patch-clamp technique to study sEPSCs in retinal ganglion cells of tiger salamander, we investigated whether sEPSCs are solely glutamatergic and whether there are dual NMDA and non-NMDA components in the sEPSCs consistent with a colocalization of receptor subtypes. In addition, we characterized the amplitude distribution and time course of sEPSCs and computed the approximate number of glutamate channels activated by a typical sEPSC. We also tested the possibility that sEPSC time courses were shaped primarily by filtering due to conduction along the dendritic process. Some of the results have been presented in abstract form (Taylor, Chen & Copenhagen, 1991). This is the first study to ch...

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“…This result implied that release was limited to a single vesicle per synapse. Studies examining transmission at other central synapses have bolstered support for UVR (Redman and Walmsley, 1983;Gulyás et al, 1993;Lawrence et al, 2003;Silver et al, 2003;Murphy et al, 2004;Biró et al, 2005). Given that numerous vesicles are ultrastructurally docked at many presynaptic active zones and constitute a readily releasable pool of functional vesicles (Lenzi et al, 1999;Schikorski and Stevens, 2001;XuFriedman et al, 2001), a mechanism must exist to prevent multiple fusion events at synapses limited to UVR.…”

Section: Ubiquity Of Mvrmentioning

confidence: 99%

Multivesicular Release at Schaffer Collateral–CA1 Hippocampal Synapses

Christie¹,

Jahr²

2006

J. Neurosci.

144

156

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Whether an individual synapse releases single or multiple vesicles of transmitter per action potential is contentious and probably depends on the type of synapse. One possibility is that multivesicular release (MVR) is determined by the instantaneous release probability (P r ) and therefore can be controlled by activity-dependent changes in P r . We investigated transmitter release across a range of P r at synapses between Schaffer collaterals (SCs) and CA1 pyramidal cells in acute hippocampal slices using patch-clamp recordings. The size of the synaptic glutamate transient was estimated by the degree of inhibition of AMPA receptor EPSCs with the rapidly equilibrating antagonist ␥-D-glutamylglycine. The glutamate transient sensed by AMPA receptors depended on P r but not spillover, indicating that multiple vesicles are essentially simultaneously released from the same presynaptic active zone. Consistent with an enhanced glutamate transient, increasing P r prolonged NMDA receptor EPSCs when glutamate transporters were inhibited. We suggest that MVR occurs at SC-CA1 synapses when P r is elevated by facilitation and that MVR may be a phenomenon common to many synapses throughout the CNS.

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Amplitude fluctuations in synaptic potentials evoked in cat spinal motoneurones at identified group Ia synapses.

Abstract: SUMMARY1. Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in spinal motoneurones (of anaesthetized cats) by impulses in single group la axons. The morpho-

Cited by 132 publications

References 17 publications

Dendritic and Synaptic Pathology in Experimental Autoimmune Encephalomyelitis

Dendritic and Synaptic Pathology in Experimental Autoimmune Encephalomyelitis

Characterization of spontaneous excitatory synaptic currents in salamander retinal ganglion cells.

Multivesicular Release at Schaffer Collateral–CA1 Hippocampal Synapses

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