Qualitative and quantitative analysis of glycine‐ and GABA‐immunoreactive nerve terminals on motoneuron cell bodies in the cat spinal cord: A postembedding electron microscopic study

Örnung, Göran; Shupliakov, Oleg; Lindå, Hans; Ottersen, Ole Petter; Storm‐Mathisen, Jon; Ulfhake, Brun; Cullheim, Staffan

doi:10.1002/(sici)1096-9861(19960212)365:3<413::aid-cne6>3.3.co;2-n

Cited by 24 publications

(43 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

“…Early protocols for post-embedding immuno-gold studies allowed for the detection of amino acid transmitters, including glutamate, GABA, and glycine in the brain and spinal cord (Ottersen, 1987; Örnung, 1996, 1998). Alternatively, freeze-substitution and embedding of fixed brain tissue in Lowicryl HM20 has demonstrated excellent antigen preservation and suitability for immunogold localization of neural antigens in the electron microscope (van Lookeren Campagne et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Retrogradely transported fluorogold accumulates in lysosomes of neurons and is detectable ultrastructurally using post-embedding immuno-gold methods

Persson

Havton

2009

Journal of Neuroscience Methods

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For ultrastructural studies, it is of great interest to be able to combine anatomical tracer techniques with sensitive immunohistochemical methods. Fluorogold (FG) is a fluorescent and retrogradely transported anatomical tracer, which is commonly used to label neurons in the brain and spinal cord for light microscopic studies. We here describe a method for detecting FG-labeled somata in the electron microscope using a high resolution post-embedding immuno-gold method. For this purpose, spinal motoneurons were retrogradely labeled by an intraperitoneal injection of FG in the adult rat. The rats were intravascularly perfused with a fixative solution containing 2% paraformaldehyde and 1-2% glutaraldehyde. Vibratome sections of spinal cord tissues were cryo-protected in glycerol, freeze-substituted in methanol containing uranyl acetate, and embedded in the Lowicryl HM20 resin at low temperatures. Electron microscopic analysis demonstrated atypical lysosome-like structures in the cytoplasm of FG-labeled motoneurons. Subsequent post-embedding immuno-gold labeling demonstrated prominent accumulation of FG in numerous lysosomes but not in other organelles or cytoplasmic compartments of the labeled neurons. The protocol is versatile and allows for combining anatomical tracing of neurons with e.g. neuro-transmitter studies in the electron microscope. We suggest that the described method for sensitive detection of FG in the spinal cord may also have broad applicability to other areas of the central nervous system.

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“…Studies using intracellular recording in rodent in vitro preparation showed that glycine and GABA are either colocalized and coreleased from the same presynaptic vesicle or released from the separate terminals onto spinal and cranial motoneurons (Jonas et al, 1998;O'Brien and Berger, 1999;Russier et al, 2002). Anatomical studies also demonstrated that input terminals on spinal motoneurons contain GABA, glycine, or both (Taal and Holstege, 1994;Ornung et al, 1996). The present study suggests that both glycine and GABA release contribute to the active inhibition of muscle tone during electrical stimulation and after ACh stimulation of PIA, as well as during the normal release of ACh on the PIA in REM sleep (Kodama et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

2003

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We hypothesized that cessation of brainstem monoaminergic systems and an activation of brainstem inhibitory systems are both involved in pontine inhibitory area (PIA) stimulation-induced muscle atonia. In our previous study (Lai et al., 2001), we found a decrease in norepinephrine and serotonin release in motoneuron pools during PIA stimulation-induced muscle tone suppression. We now demonstrate an increase in inhibitory amino acid release in motor nuclei during PIA stimulation in the decerebrate cat using in vivo microdialysis and HPLC analysis techniques. Microinjection of acetylcholine into the PIA elicited muscle atonia and simultaneously produced a significant increase in both glycine and GABA release in both the hypoglossal nucleus and the lumbar ventral horn. Glycine release increased by 74% in the hypoglossal nucleus and 50% in the spinal cord. GABA release increased by 31% in the hypoglossal nucleus and 64% in the spinal cord during atonia induced by cholinergic stimulation of the PIA. As with cholinergic stimulation, 300 msec train electrical stimulation of the PIA elicited a significant increase in glycine release in the hypoglossal nucleus and ventral horn. GABA release was significantly increased in the hypoglossal nucleus but not in the spinal cord during electrical stimulation of the PIA. Glutamate release in the motor nuclei was not significantly altered during atonia induced by electrical or acetylcholine stimulation of the PIA. We suggest that both glycine and GABA play important roles in the regulation of upper airway and postural muscle tone. A combination of decreased monoamine and increased inhibitory amino acid release in motoneuron pools causes PIA-induced atonia and may be involved in atonia linked to rapid eye-movement sleep.

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Qualitative and quantitative analysis of glycine‐ and GABA‐immunoreactive nerve terminals on motoneuron cell bodies in the cat spinal cord: A postembedding electron microscopic study

Cited by 24 publications

References 0 publications

Synaptic Control of Motoneuronal Excitability

Synaptic Control of Motoneuronal Excitability

Retrogradely transported fluorogold accumulates in lysosomes of neurons and is detectable ultrastructurally using post-embedding immuno-gold methods

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

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