Amino‐acid induced depression of cortical neurones

Johnson, E. S.; Roberts, M. W.; Straughan, Donald W.

doi:10.1111/j.1476-5381.1970.tb09875.x

Cited by 43 publications

(11 citation statements)

References 11 publications

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“…The reduction in staining intensity in rostra1 brain regions compared with the spinal cord was due both to a decrease in the number of stained profiles and to a decrease in the intensity of staining of individual the activity of the natural transmitter, and this depression can profiles. Since the structures stained with antisera used in the be selectively blocked by strychnine ; Curtis present study are regions of the postsynaptic specialization (auet al, 1968;Johnson et al, 1970). The addition of the present ditory system: Altschuler et al, 1986;spinal cord: Triller et al, data demonstrating high amounts of glycine in a select popu-1985 and present study; olfactory bulb: present study), smaller lation of presynaptic axons further supports the role of glycine synaptic specializations would result in a smaller fluorescent as a neurotransmitter candidate.…”

Section: Subcellular Localization Of Glycine Immunoreactivitymentioning

confidence: 90%

“…Strychnine, which in low doses binds selectively to glycine re-ceptors (Young and Snyder, 1974), binds to specific regions of the rat nervous system (Zarbin et al,198 1) and to homologous areas of the human nervous system (Probst et al, 1986). Electrophysiological responses to glycine have been recorded, generally of an inhibitory nature Curtis et al, 1968), and these can be blocked by strychnine (Curtis et al, 1968;Johnson et al, 1970). Pronounced release of glycine from spinal cord slices, but not from cerebral cortex, can be induced with potassium (Mulder and Snyder, 1974).…”

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confidence: 99%

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Glycine and glycine receptor immunoreactivity in brain and spinal cord

1988

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To study the distribution of glycine immunoreactive neurons in the spinal cord and brain, antisera were raised against glycine conjugated to protein carriers. High-titer rabbit glycine antiserum was purified by affinity chromatography. Testing against other amino acids and peptides with immuno dot blots and ELISA assays showed little apparent cross-reaction with glutamate, aspartate, glutamine, taurine, and 17 other amino acids and related compounds. Similarly, the antiserum showed little apparent recognition of glycine when glycine was incorporated into peptides. A slight cross-reactivity with GABA, beta- alanine, and cysteine was found. Immunocytochemical labeling of tissue sections could be blocked with glycine conjugated to a heterologous carrier protein but not by other amino acids conjugated to that protein. Immunocytochemistry at the light microscope level with immunofluorescence and silver-intensified colloidal gold revealed a wide distribution of glycine-like immunoreactivity throughout all laminae of the rat spinal cord and in all segments studied from the cervical, thoracic, lumbar, and sacral cord. Immunoreactive boutons were found terminating on both cell bodies and on dendrites. Ultrastructural analysis with postembedding colloidal gold immunocytochemistry demonstrated large numbers of immunoreactive boutons making symmetrical type synapses with neuronal perikarya, including motor neurons, and with proximal and distal dendrites. Presynaptic glycine immunoreactive boutons were found in both ventral and dorsal horn. Immunoreactivity was concentrated over regions rich in vesicles, and over mitochondria in immunoreactive boutons, but not over mitochondria in postsynaptic dendrites. Glycine-immunoreactive perikarya were identified both in the dorsal horn and in the ventral horn. Myelinated and unmyelinated glycine-immunoreactive axons were noted both in the gray and white matter of the cord. The density of immunoreactive axons varied in the white matter, with the greatest number of immunoreactive axons found in the white matter adjacent to the gray matter in lateral and ventral white. Significantly fewer immunoreactive axons were found in the white matter of the dorsal columns. Myelin sheaths around axons were unlabeled. The distribution of glycine-immunoreactive boutons correlated well with the distribution of glycine receptor immunoreactivity on postsynaptic elements of the spinal cord, tested with different monoclonal antisera against strychnine-purified glycine receptor. Glycine receptor immunoreactivity was found throughout the gray matter of both rat and primate.

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Section: Subcellular Localization Of Glycine Immunoreactivitymentioning

confidence: 90%

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confidence: 99%

Glycine and glycine receptor immunoreactivity in brain and spinal cord

1988

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“…More recently, following the introduction of bicuculline as a specific GABA antagonist, Curtis and his colleagues (Curtis & Felix, 1971) have extended their studies to show that motoneurones are inhibited by at least two separate pathways terminating on two distinct populations of interneurones capable of releasing either GABA or glycine. In the cortex, however, where GABA is about 4 times more potent than glycine (Krnjevic & Phillis, 1963;Curtis et al, 1968a;Kelly & Krnjevic, 1969;Johnson, Roberts & Straughan, 1970), Kelly & Kmjevic (1969) found that only GABA mimicked the effect of the inhibitory transmitter on the cell membrane. GABA was also considered a more effective depressant than glycine on the spike-discharge of Deiters' neurones (Bruggencate & Engberg, 1969Obata, Takeda & Shinozaki, 1970), Purkinje cells of the cerebellum (Kawamura & Provini, 1970;Curtis et al, 1971b) and the mitral cells of the olfactory bulb (Nicoll, 1971), three situations where the inhibitory transmitter may well be GABA.…”

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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“…This effect was the principal reason for the rather lower percentage utility of bicuculline as compared with some of the other substances examined (Table 1). R. G. Hill, M. A. Simmonds and D. W. S!raughan Strychnine has been shown to antagonize glycine depression of spinal and cortical neurones (Curtis, Hosli & Johnston, 1968;Johnson et al, 1970) and, in addition, large currents of strychnine can have some antagonistic effects on GABA responses in the cortex (Johnson et al, 1970;Biscoe et al, 1972). The present study confirms that strychnine can exert a weak GABA antagonist action and also indicates that it may sometimes potentiate GABA depressions.…”

Section: Control Agonistsmentioning

confidence: 99%

A comparative study of some convulsant substances as γ‐aminobutyric acid antagonists in the feline cerebral cortex

Hill

Simmonds

Straughan

1973

British J Pharmacology

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Summary1. By the use of microiontophoretic techniques, quantitative estimates were obtained of the depressant effects of y-aminobutyric acid (GABA) on single feline cortical neurones. 2. Picrotoxin, bicuculline, strychnine, ( +)-tubocurarine, penicillin and leptazol were also applied microiontophoretically to single neurones. Sequential GABA applications were made before, during and after the microiontophoresis of these substances and any effects on the time course of the GABA depression were measured as an estimate of antagonism or potentiation of GABA. 3. (+ )-Tubocurarine was found to be a potent GABA antagonist. Picrotoxin and bicuculline were rather less potent and strychnine and penicillin only weakly active as GABA antagonists. Leptazol appeared to be inactive against GABA depressions. 4. In addition, bicuculline and strychnine were found to be capable of potentiating the depressant action of GABA. This property was not shared by the other substances studied. 5. All the substances studied produced changes in neuronal firing rate that did not correlate with GABA antagonism. 6. In conclusion, several potent convulsants have been shown to be capable or GABA antagonism. It is not yet clear that this effect, rather than a direct effect on neuronal excitability, is the prime mechanism behind their convulsant properties.

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Amino‐acid induced depression of cortical neurones

Cited by 43 publications

References 11 publications

Glycine and glycine receptor immunoreactivity in brain and spinal cord

Glycine and glycine receptor immunoreactivity in brain and spinal cord

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

A comparative study of some convulsant substances as γ‐aminobutyric acid antagonists in the feline cerebral cortex

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