Inhibitory of glycine on spinal neurons in the cat.

Werman, R.; Davidoff, Robert A.; Aprison, M. H.

doi:10.1152/jn.1968.31.1.81

Cited by 414 publications

(97 citation statements)

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“…Systemic infusion of GABA and glycine agonists produces a decrease, whereas antagonist perfusion generates an increase in the frequency and amplitude of hypoglossal nerve activity in the decerebrate rat (Hayashi and Lipski, 1992). Iontophoretic application of glycine and GABA into the spinal cord blocks motoneuron discharge induced by DL-homocysteic acid (Werman et al, 1968). ten Bruggencate and Sonnhof (1972) demonstrated that iontophoretic application of glycine and GABA generates IPSPs in hypoglossal motoneurons, and this hyperpolarization can be blocked by glycine and GABA antagonists, strychnine and picrotoxin, respectively.…”

Section: Discussionmentioning

confidence: 98%

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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Section: Discussionmentioning

confidence: 98%

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

2003

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“…(Curtis & Watkins, 1960), the crayfish stretch receptor (Edwards & Kuffler, 1959) and earlier work on frog spinal cord (Curtis et al 1961), and indicate that a compound with positively charged and negatively charged groups separated by three carbon atoms is necessary for optimal activity. However, the depolarizing potency of glycine relative to GABA on primary afferents was considerably less than its hyperpolarizing potency on mammalian neurones (Curtis & Watkins, 1960;Werman et al 1968). The extremely potent depolarizing action of imidazoleacetic on primary afferent fibres agrees with the strong post-synaptic inhibitory action of this substance (McGeer, McGeer & McLennan, 1961;Phillis, Tebecis & York, 1968;Haas, Anderson & Hosli, 1972;Godfraind, Krnjevic, Maretic & Pumain, 1973;Swagel, Ikeda & Roberts, 1973).…”

Section: Discussionmentioning

confidence: 97%

“…(e.g. Curtis, Hosli & Johnston, 1968;Galindo, 1969;Obata & Highstein, 1970;Nicoll, 1971) has provided evidence to support the hypothesis that glycine is a principal inhibitory transmitter in the spinal cord (Werman, Davidoff & Aprison, 1968), while GABA is a major inhibitory transmitter at supraspinal sites (Krnjevic & Schwartz, 1967;Obata, Ito, Ochi & Sato, 1967).…”

Section: Introductionmentioning

confidence: 98%

Studies on convulsants in the isolated frog spinal cord. I. Antagonism of amino acid responses.

Barker¹,

Nicoll²,

Padjen³

1975

The Journal of Physiology

141

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SUMMARY1. The isolated frog spinal cord was used to study the effects of picrotoxin, bicuculline, and strychnine on the responses of primary afferents to amino acids. Recording was by sucrose gap technique.2. A series of neutral amino acids was found to depolarize primary afferents. Optimal activity was obtained by an amino acid whose carboxyl and amino groups were separated by a three-carbon chain length (i.e. GABA). Amino acids with shorter (i.e. f-alanine, glycine) or longer (i.e. a-aminovaleric acid, e-aminocaproic acid) distances between the charged groups were less potent. Imidazoleacetic acid was the most potent depolarizing agent tested.3. Picrotoxin and bicuculline antagonized the primary afferent depolarizations of a number of amino acids tested with equal specificity.Depolarizing responses to standard (10-3 M) concentrations of fl-alanine and taurine were completely blocked by these convulsants, while depolarizations to 103 M y-aminobutyric acid (GABA) were only partially antagonized. Glycine responses were unaffected by these agents.4. Strychnine completely blocked ,8-alanine and taurine depolarizations and incompletely antagonized several other neutral amino acids. GABA, glutamate, and glycine depolarizations were not affected.5. These results suggest that there are at least three distinct populations of neutral amino acid receptors on primary afferent terminals: a GABAlike receptor, a taurine/f,-alanine receptor, and a glycine-like receptor. The

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“…Cells equally sensitive to GABA and glycine are of special interest since they may resemble motoneurones where both GABA and glycine can mimic the action of the inhibitory transmitter by hyperpolarizing the membrane potential towards the same equilibrium level by selectively increasing the membrane conductance to certain ions (Curtis, Hosli, Johnston & Johnston, 1968;Werman, Davidoff & Aprison, 1968). Indeed glycine may be a more potent depressant of spinal motoneurones than GABA (Curtis, Hosli & Johnston, 1968;Curtis et al, 1968b).…”

Section: Discussionmentioning

confidence: 99%

On the pharmacology of the γ‐aminobutyric acid receptors on the cuneo‐thalamic relay cells of the cat

Kelly

Renaud

1973

British J Pharmacology

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Summary1. y-Aminobutyric acid (GABA) and glycine applied by iontophoresis were equipotent depressants of cuneo-thalamic relay neurones isolated from the middle third of the cuneate nucleus of cats either decerebrated or anaesthetized with sodium pentobarbitone. 2. Glycine 13+2 nA and GABA 20+2 nA were equipotent depressors of hair cells (n=22) and, bicuculline applied by iontophoresis caused a parallel shift to the right of the GABA but not the glycine log-current response curves. The GABA equipotent dose-ratio was 20 + 0-2 for bicuculline currents of approximately 144 nA lasting about 11 min in cells excited either transynaptically by peripheral stimulation or postsynaptically by glutamate. 3. Although a maximal bicuculline current seldom caused a significant shift of the glycine-log current response curve, many of our records show the onset of the glycine response to be slowed by doses in excess of 84 nA.4. Bicuculline also antagonized depressions by fl-guanidinopropionic acid, and 8-aminovaleric acid which mimicked the action of GABA. 5. When tested on the same neurone, bicuculline and picrotoxin applied by iontophoresis were equipotent and their effects appear to be additive. 6. The GABA sensitivity was not modified by repetitive (5 or 6) doses of i.v. bicuculline (0-2 mg/kg). 7. The antagonism of GABA by bicuculline and picrotoxin appears to be of sufficient specificity to enable the separate roles of GABA and glycine as putative inhibitory transmitters of cuneo-thalamic relav cells to be determined.

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Inhibitory of glycine on spinal neurons in the cat.

Cited by 414 publications

References 0 publications

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

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

Studies on convulsants in the isolated frog spinal cord. I. Antagonism of amino acid responses.

On the pharmacology of the γ‐aminobutyric acid receptors on the cuneo‐thalamic relay cells of the cat

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