Effect of frontal cortex ablation on striatal glutamic acid level in rat

Kim, J S; Hasller, R; Hau, Peter; Paik, Kwang Se

doi:10.1016/0006-8993(77)90430-9

Cited by 303 publications

(54 citation statements)

References 17 publications

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“…Biochemical investigations employing cortical lesions have suggested that glutamic acid is the natural synaptic transmitter for this afferent pathway (Divac et al, 1977;Kim et al, 1977;McGeer et al, 1977;Reubi & Cuenod, 1979). The cerebral cortex is therefore a possible source for the afferent fibres producing the N-2 response.…”

Section: Discussionmentioning

confidence: 99%

Non‐cholinergic synaptic excitation in neostriatum: pharmacological evidence for mediation by a glutamate‐like transmitter

Cordingley

Weight

1986

British J Pharmacology

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We studied the synaptic pharmacology of an excitatory pathway in the neostriatum using electrophysiological techniques in tissue slices from rats. In response to single electrical stimuli, two negative, extracellular potentials (N‐1 and N‐2) were recorded through micropipette electrodes within 150–450 μm of the stimulating cathode. N‐2 was reversibly reduced or abolished by reducing the concentration of calcium in the bathing medium, while N‐1 was unaffected. Both N‐1 and N‐2 were reversibly abolished by the local anaesthetic procaine. Single‐unit, extracellular action potentials were, at times, associated with either N‐1 or N‐2. Intracellular recordings showed action potentials at N‐2 latency arising from graded, monophasic, depolarizing potentials. Bath‐applied cholinoceptor and dopamine receptor antagonists failed to reduce N‐2. By contrast, antagonists of excitatory amino acid transmitters reversibly reduced or abolished N‐2. γ‐d‐Glutamylglycine (GG), (±)‐cis‐2,3‐piperidine dicarboxylic acid (PDA) and dL‐2‐amino‐4‐phosphonobutyric acid (APB) blocked N‐2 with ED50s of 0.79 mm, 1.0 mm and 1.1 mm, respectively. (−)−Baclofen reversibly blocked N‐2 with an ED50 of 0.79 μm; (+)‐baclofen was 330 times less potent. The results suggest that N‐1 results from direct activation of fibre tracts or cell bodies, while N‐2 is a population spike mediated by excitatory synapses whose natural transmitter pharmacologically resembles glutamate.

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Section: Discussionmentioning

confidence: 99%

Non‐cholinergic synaptic excitation in neostriatum: pharmacological evidence for mediation by a glutamate‐like transmitter

Cordingley

Weight

1986

British J Pharmacology

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“…These effects were of long duration and persisted for 1 h after cessation of stimulation. They seem to result from a presynaptic influence mediated by a bilateral corticostriatal projection which is very probably glutamatergic [1]. In fact, the activa tion of 3H-DA release in the contralateral caudate nucleus was abolished by acute transection of the rostral part of the corpus callosum.…”

mentioning

confidence: 92%

Control of the Activity of the Two Dopaminergic Systems by Cortical, Cerebellar and Sensory Afferents in the Cat

Nieoullon¹,

Chéramy²,

Głowiński³

1979

Stereotact Funct Neurosurg

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“…The monosynaptic cortico-caudate projection (Kitai, Kocsis, Preston & Sugimori, 1976;Vandermaelen & Kitai, 1980;Webster, 1965) is a neuronal pathway which may use an excitatory amino acid as a transmitter (Divac, Fonnum & Storm-Mathisen, 1977;Fonnum, Storm-Mathisen & Divac, 1981;Kim, Hassler, Haug & Paik, 1977;McGeer, McGeer, Scherer & Singh, 1977;Roberts, McBean, Sharif & Thomas, 1982). Although there have been a number ofelectrophysiological studies using extracellular recording where excitatory amino acids have been applied by micro-ionophoresis to neurones in the caudate nucleus, most of these agents were used in order to create a background of firing against which inhibitory drugs could be tested (Ben-Ari & Kelly, 1976;Davies & Tongroach, 1978, 1979Fry, Zieglgaensberger & Herz, 1980;Jones, 1981;McLennan & York, 1966;Norcross & Spehlmann, 1981;Woodruff, McCarthy & Walker, 1976).…”

Section: Introductionmentioning

confidence: 99%

Effects of excitatory amino acids and their antagonists on membrane and action potentials of cat caudate neurones.

Herrling¹,

Morris²,

Salt³

1983

The Journal of Physiology

174

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SUMMARY1. The electrical activity of caudate neurones was recorded with intracellular electrodes in halothane anaesthetized cats. Agonists and antagonists of excitatory amino acid receptors were applied by micro-ionophoresis and their effects on membrane-and action potentials and on cortically evoked synaptic potentials evaluated.2. The agonists, L-aspartate (asp), L-glutamate (glu), N-methyl-DL-aspartate (NMA), quinolinate and quisqualate all depolarized the membrane, caused repetitive firing, reduced the apparent amplitude of the cortically evoked excitatory postsynaptic potentials (e.p.s.p.s) and increased the amplitude of the associated inhibitory post-synaptic potential. Two of the agonists, NMA and quinolinate, additionally caused the appearance of up to 500 ms long depolarizations (plateaus) on the falling phase of action potentials. These plateaus were seen in about two-thirds of the cells in this sample while in the other third the excitatory effects of NMA and quinolinate were indistinguishable from those of glu and quisqualate.3. The N-methyl-D-aspartate (NMDA) receptor antagonist D-a-aminoadipate (DAA) reversibly inhibited the effects of NMA and quinolinate but only on those cells where these two agents evoked action potential plateaus while on the same cells the effects of asp, glu and quisqualate were either only weakly antagonized or not affected. On cells not displaying plateaus to NMA or quinolinate none of the effects of the agonists could be antagonized by DAA. DAA applications that completely antagonized the effects of NMA never reduced the amplitudes of cortically evoked e.p.s.p.s.4. Cis-2,3-piperidine dicarboxylate also blocked the effects of NMA and asp at low application currents while at higher currents it enhanced the effects of glu or asp although still retaining its NMA antagonistic activity.5. High-frequency stimulation of the cortico-caudate pathway resulted in longlasting depolarizations and repetitive firing, but plateaus of the type caused by NMA or quinolinate were not seen.

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Effect of frontal cortex ablation on striatal glutamic acid level in rat

Cited by 303 publications

References 17 publications

Non‐cholinergic synaptic excitation in neostriatum: pharmacological evidence for mediation by a glutamate‐like transmitter

Non‐cholinergic synaptic excitation in neostriatum: pharmacological evidence for mediation by a glutamate‐like transmitter

Control of the Activity of the Two Dopaminergic Systems by Cortical, Cerebellar and Sensory Afferents in the Cat

Effects of excitatory amino acids and their antagonists on membrane and action potentials of cat caudate neurones.

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