Spinal Interneurons (spinal + interneuron)

Distribution by Scientific Domains


Selected Abstracts


Functional subdivision of feline spinal interneurons in reflex pathways from group Ib and II muscle afferents; an update

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2010
Elzbieta Jankowska
Abstract A first step towards understanding the operation of a neural network is identification of the populations of neurons that contribute to it. Our aim here is to reassess the basis for subdivision of adult mammalian spinal interneurons that mediate reflex actions from tendon organs (group Ib afferents) and muscle spindle secondary endings (group II afferents) into separate populations. Re-examining the existing experimental data, we find no compelling reasons to consider intermediate zone interneurons with input from group Ib afferents to be distinct from those co-excited by group II afferents. Similar patterns of distributed input have been found in subpopulations that project ipsilaterally, contralaterally or bilaterally, and in both excitatory and inhibitory interneurons; differences in input from group I and II afferents to individual interneurons showed intra- rather than inter-population variation. Patterns of reflex actions evoked from group Ib and II afferents and task-dependent changes in these actions, e.g. during locomotion, may likewise be compatible with mediation by premotor interneurons integrating information from both group I and II afferents. Pathological changes after injuries of the central nervous system in humans and the lineage of different subclasses of embryonic interneurons may therefore be analyzed without need to consider subdivision of adult intermediate zone interneurons into subpopulations with group Ib or group II input. We propose renaming these neurons ,group I/II interneurons'. [source]


Activity-dependent modulation of GABAergic synapses in developing rat spinal networks in vitro

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2002
Marcelo Rosato-Siri
Abstract The role of activity-dependent plasticity in modulating inhibitory synapses was investigated in embryonic rat spinal cord slice cultures, by chronic exposure to non-NMDA receptor blockers. GABAergic synaptic efficacy in control and chronic-treated cultures was investigated by patch-recordings from visually identified spinal interneurons. In both culture groups proximal stimulation induced the appearance of postsynaptic currents (PSCs), which were fully antagonized by 20 µM bicuculline application and reverse polarity at potential values close to those reported for spontaneous GABAergic PSCs. In chronically treated cells GABAergic evoked PSCs displayed a larger failure rate and a smaller coefficient of variation of mean PSC amplitude, when compared to controls. As opposed to controls, chronic GABAergic evoked PSCs did not facilitate upon paired-pulse stimulation. Facilitation at chronic synapses was observed when extracellular calcium levels were decreased below physiological values (< 2 mM). Kainate was used to disclose any functional differences between control and treated slices. In accordance with the presynaptic action of kainate, the application of this drug along with GYKI, an AMPA receptor selective antagonist, changed, with analogous potency, short-term plasticity of GABAergic synapses from control and treated cultures. Nevertheless, in chronic cultures, the downstream effects of such activation unmasked short-term depression. Ultrastructural analysis of synapses in chronically treated cultures showed a reduction both in symmetric synapses and in the number of vesicles at symmetric terminals. Thus, based on electrophysiological and ultrastructural data, it could be suggested that during the development of spinal circuits, GABAergic synapses are modulated by glutamatergic transmission, and thus implying that excitatory transmission regulates the strength of GABAergic synapses. [source]


What Does the Mechanism of Spinal Cord Stimulation Tell Us about Complex Regional Pain Syndrome?

PAIN MEDICINE, Issue 8 2010
Joshua P. Prager MD
Abstract Spinal cord stimulation (SCS) can have dramatic effects on painful, vascular, and motor symptoms of complex regional pain syndrome (CRPS), but its precise mechanism of action is unclear. Better understanding of the physiologic effects of SCS may improve understanding not only of this treatment modality but also of CRPS pathophysiology. Effects of SCS on pain perception are likely to occur through activation of inhibitory GABA-ergic and cholinergic spinal interneurons. Increased release of both neurotransmitters has been demonstrated following SCS in animal models of neuropathic pain, with accompanying reductions in pain behaviors. Effects of SCS on vascular symptoms of CRPS are thought to occur through two main mechanisms: antidromic activation of spinal afferent neurons and inhibition of sympathetic efferents. Cutaneous vasodilation following SCS in animal models has been shown to involve antidromic release of calcitonin gene-related peptide and possibly nitric oxide, from small-diameter sensory neurons expressing the transient receptor potential V1 (TRPV1) receptor. The involvement of sympathetic efferents in the effects of SCS has not been studied in animal models of neuropathic pain, but has been demonstrated in models of angina pectoris. In conclusion, SCS is of clinical benefit in CRPS, and although its mechanism of action merits further elucidation, what little we do know is informative and can partially explain some of the pathophysiology of CRPS. [source]


Neurotransmitter properties of spinal interneurons in embryonic and larval zebrafish

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2004
Shin-Ichi Higashijima
Abstract Many classes of spinal interneurons in zebrafish have been described based on morphology, but their transmitter phenotypes are largely unknown. Here we combine back-filling or genetic labeling of spinal interneurons with in situ staining for markers of neurotransmitter phenotypes, including the vesicular glutamate transporter (VGLUT) genes for glutamatergic neurons, the neuronal glycine transporter (GLYT2) for glycinergic neurons, and glutamic acid decarboxylase (GAD) for GABAergic neurons. Neurons positive for VGLUT include the commissural CoPA, MCoD, UCoD, and some of the CoSA neurons. The CiD interneurons, which have ipsilateral descending axons, were also VGLUT -positive, as were the ventrally located VeMe interneurons, whose descending axonal trajectory has not been clearly revealed. Cells positive for GLYT2 include the commissural CoLAs as well as some of the CoBL and CoSA neurons. The CiA cells were the only GLYT2 -positive cells with an ipsilateral axon. Cells staining for GAD included, most notably, the dorsal longitudinal ascending (DoLA) and KA interneurons. Our approach allowed us to define the likely transmitter phenotypes of most of the known classes of spinal interneurons. These data provide a foundation for understanding the functional organization of the spinal networks in zebrafish. J. Comp. Neurol. 480:19,37, 2004. © 2004 Wiley-Liss, Inc. [source]