Immunohistochemical evidence for coexistence of glycine and GABA in nerve terminals on cat spinal motoneurones

Örnung, Göran; Shupliakov, Oleg; Ottersen, Ole Petter; Storm‐Mathisen, Jon; Cullheim, Staffan

doi:10.1097/00001756-199404000-00009

Cited by 84 publications

(53 citation statements)

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“…There is strong anatomical evidence for the colocalization of GABA A and glycine receptors at single postsynaptic densities (115, 1252, 1270) and for GABA and glycine colocalization in presynaptic terminals (937,941,942,1150,1205,1252). Electrophysiological measurements are consistent with GABAergic and glycinergic contributions to IPSP/C in cranial motoneurons (656), as well as recurrent (1099), afferent, and descending inhibitory inputs to spinal motoneurons (412,413,991,992,1191,1389).…”

Section: B) Colocalization/corelease Of Gaba and Glycinementioning

confidence: 86%

Synaptic Control of Motoneuronal Excitability

Rekling

Funk

Bayliss

et al. 2000

Physiological Reviews

537

482

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Movement, the fundamental component of behavior and the principal extrinsic action of the brain, is produced when skeletal muscles contract and relax in response to patterns of action potentials generated by motoneurons. The processes that determine the firing behavior of motoneurons are therefore important in understanding the transformation of neural activity to motor behavior. Here, we review recent studies on the control of motoneuronal excitability, focusing on synaptic and cellular properties. We first present a background description of motoneurons: their development, anatomical organization, and membrane properties, both passive and active. We then describe the general anatomical organization of synaptic input to motoneurons, followed by a description of the major transmitter systems that affect motoneuronal excitability, including ligands, receptor distribution, pre-and postsynaptic actions, signal transduction, and functional role. Glutamate is the main excitatory, and GABA and glycine are the main inhibitory transmitters acting through ionotropic receptors. These amino acids signal the principal motor commands from peripheral, spinal, and supraspinal structures. Amines, such as serotonin and norepinephrine, and neuropeptides, as well as the glutamate and GABA acting at metabotropic receptors, modulate motoneuronal excitability through pre-and postsynaptic actions. Acting principally via second messenger systems, their actions converge on common effectors, e.g., leak K + current, cationic inward current, hyperpolarization-activated inward current, Ca 2+ channels, or presynaptic release processes. Together, these numerous inputs mediate and modify incoming motor commands, ultimately generating the coordinated firing patterns that underlie muscle contractions during motor behavior.

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Section: B) Colocalization/corelease Of Gaba and Glycinementioning

confidence: 86%

Synaptic Control of Motoneuronal Excitability

Rekling

Funk

Bayliss

et al. 2000

Physiological Reviews

537

482

View full text Add to dashboard Cite

show abstract

“…Colocalization of the two neurotransmitters is prominent in the spinal cord (Todd and Sullivan, 1990;Ornung et al, 1994;Taal and Holstege, 1994;Yang et al, 1997) and other sensory and motor centers (Wenthold et al, 1987;Ottersen et al, 1988;Wentzel et al, 1993). The observation of GABAergic terminals facing glycine receptor (GlyR) clusters (Triller et al, 1987) and of mixed boutons presynaptic to domains containing GABA A receptor (GABA A R) and probably GlyR (Todd et al, 1996) first suggested that the two transmitters might be coreleased at the same synapse.…”

Section: Abstract: Serotonin; Cerebellum; Gaba; Glycine; Viaat; Glytmentioning

confidence: 99%

“…In the spinal cord and brainstem, the only places where cotransmission of GABA and glycine is formally demonstrated (Jonas et al, 1998;O'Brien and Berger, 1999), pure glycinergic transmission and pure GABAergic transmission also occur (Ornung et al, 1994;Yang et al, 1997). Thus, networks of inhibitory interneurons using GABA and glycine as their transmitters have a complex and versatile functional organization.…”

Section: Abstract: Serotonin; Cerebellum; Gaba; Glycine; Viaat; Glytmentioning

confidence: 99%

IPSC Kinetics at Identified GABAergic and Mixed GABAergic and Glycinergic Synapses onto Cerebellar Golgi Cells

2001

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In the rat cerebellum, Golgi cells receive serotonin-evoked inputs from Lugaro cells (L-IPSCs), in addition to spontaneous inhibitory inputs (S-IPSCs). In the present study, we analyze the pharmacology of these IPSCs and show that S-IPSCs are purely GABAergic events occurring at basket and stellate cell synapses, whereas L-IPSCs are mediated by GABA and glycine. Corelease of the two transmitters at Lugaro cell synapses is suggested by the fact that both GABA A and glycine receptors open during individual L-IPSCs. Double immunocytochemical stainings demonstrate that GABAergic and glycinergic markers are coexpressed in Lugaro cell axonal varicosities, together with the mixed vesicular inhibitory amino acid transporter. Lugaro cell varicosities are found apposed to glycine receptor (GlyR) clusters that are localized on Golgi cell dendrites and participate in postsynaptic complexes containing GABA A receptors (GABA A Rs) and the anchoring protein gephyrin. GABA A R and GlyR/gephyrin appear to form segregated clusters within individual postsynaptic loci. Basket and stellate cell varicosities do not face GlyR clusters. For the first time the characteristics of GABA and glycine cotransmission are compared with those of GABAergic transmission at identified inhibitory synapses converging onto the same postsynaptic neuron. The ratio of the decay times of L-IPSCs and of S-IPSCs is a constant value among Golgi cells. This indicates that, despite a high cell-to-cell variability of the overall IPSC decay kinetics, postsynaptic Golgi cells coregulate the kinetics of their two main inhibitory inputs. The glycinergic component of L-IPSCs is responsible for their slower decay, suggesting that glycinergic transmission plays a role in tuning the IPSC kinetics in neuronal networks.

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“…The predominant adult isoform of the GlyR is composed of three ␣1 and two ␤ subunits (Legendre, 2001). In spinal motoneurons, the coexistence of GABA and glycine in axon terminals (Ornung et al, 1994;Taal and Holstege, 1994), their core-lease (Jonas et al, 1998) and the colocalization of postsynaptic GABA A and GlyR (Baer et al, 2003) have been established. Both postsynaptic GABA A and GlyR at inhibitory synapses are aggregated in clusters whose formation is regulated by gephyrin, a submembrane scaffolding protein (Pfeiffer et al, 1984, Triller at al., 1985.…”

Section: Introductionmentioning

confidence: 99%

Differential Plasticity of the GABAergic and Glycinergic Synaptic Transmission to Rat Lumbar Motoneurons after Spinal Cord Injury

Sadlaoud

Tazerart²,

Brocard³

et al. 2010

J. Neurosci.

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Maturation of inhibitory postsynaptic transmission onto motoneurons in the rat occurs during the perinatal period, a time window during which pathways arising from the brainstem reach the lumbar enlargement of the spinal cord. There is a developmental switch in miniature IPSCs (mIPSCs) from predominantly long-duration GABAergic to short-duration glycinergic events. We investigated the effects of a complete neonatal [postnatal day 0 (P0)] spinal cord transection (SCT) on the expression of Glycine and GABA A receptor subunits (GlyR and GABA A R subunits) in lumbar motoneurons. In control rats, the density of GlyR increased from P1 to P7 to reach a plateau, whereas that of GABA A R subunits dropped during the same period. In P7 animals with neonatal SCT (SCT-P7), the GlyR densities were unchanged compared with controls of the same age, while the developmental downregulation of GABA A R was prevented. Whole-cell patch-clamp recordings of mIPSCs performed in lumbar motoneurons at P7 revealed that the decay time constant of miniature IPSCs and the proportion of GABAergic events significantly increased after SCT. After daily injections of the 5-HT 2 R agonist DOI, GABA A R immunolabeling on SCT-P7 motoneurons dropped down to values reported in control-P7, while GlyR labeling remained stable. A SCT made at P5 significantly upregulated the expression of GABA A R 1 week later with little, if any, influence on GlyR. We conclude that the plasticity of GlyR is independent of supraspinal influences whereas that of GABA A R is markedly influenced by descending pathways, in particular serotoninergic projections.

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Immunohistochemical evidence for coexistence of glycine and GABA in nerve terminals on cat spinal motoneurones

Cited by 84 publications

References 0 publications

Synaptic Control of Motoneuronal Excitability

Synaptic Control of Motoneuronal Excitability

IPSC Kinetics at Identified GABAergic and Mixed GABAergic and Glycinergic Synapses onto Cerebellar Golgi Cells

Differential Plasticity of the GABAergic and Glycinergic Synaptic Transmission to Rat Lumbar Motoneurons after Spinal Cord Injury

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