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  • 1
    Electronic Resource
    Electronic Resource
    Bimodal effects of dopamine D2 receptor agonists on zero Mg2+-induced epileptiform activity in the rat cingulate cortex slice (1994)
    Springer
    Experimental brain research 102 (1994), S. 75-83 
    Details
    ISSN: 1432-1106
    Keywords: Cortex slice ; Zero magnesium ; Epileptiform activity ; Dopamine ; D2 agonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A previous study demonstrated a dopamine D1 receptor-dependent inhibition of zero Mg2+-induced epileptiform discharges in the rat cingulate cortex slice suspended in a grease-gap bath. This investigation considers the role of dopamine D2 receptors in the modulation of paroxysmal activity in this in vitro model. Some 123 of 143 slices exhibited spontaneous paroxysmal depolarizations, which in 105 cases were accompanied by secondary depolarizing after-potentials (SDAPs). In 43.5% of slices tested, dopamine preferentially and irreversibly facilitated SDAP production at low bath concentrations (1–100 μM), but at concentrations 〉 100 μM suppressed all components of the epileptiform responses. Similar dose-related bimodal responses were obtained with the D2 agonists LY 171555, PHNO and 7-OH-DPAT, but not with lisuride or RU 24213, which were exclusively inhibitory. The excitatory response to LY 171555 was attenuated by the D2 antagonist raclopride (2 μM), but not by the D1 antagonist SCH 39166 (0.5 μM). On the other occasions, the sole effect of dopamine (56.5% of slices) and the other D2 agonists, was to preferentially suppress SDAP number at low concentrations (1–100 μM) and to suppress all parameters of the epileptiform response at higher concentrations. The inhibitory effect of the D2 agonist LY 171555 on SDAP formation was paradoxically attenuated by the D1 antagonist SCH 39166, but not by the D2 antagonist raclopride. These results support the notion that dopamine can modulate epileptiform activity differentially, through its actions at D1 and D2 receptors. The possibility that these effects of dopamine may be mediated indirectly is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00232440
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  • 2
    Electronic Resource
    Electronic Resource
    Evidence for a GABAergic nigrothalamic pathway in the rat (1980)
    Springer
    Experimental brain research 40 (1980), S. 45-54 
    Details
    ISSN: 1432-1106
    Keywords: Substantia nigra ; Thalamus ; GABA ; Lesions ; Muscimol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Unilateral stereotaxic microinjection of muscimol into the caudal region of the substantia nigra (SN) evoked tight, dose-related contralateral locomotor asymmetry and stereotypy. These behaviours were partially attenuated by various pre-treatments, including 6-hydroxydopamine lesions of the nigrostriatal dopamine pathway, intraperitoneal (i.p.) haloperidol, and inhibition of thalamic GABA-transaminase activity by local intrathalamic injection of ethanolamine-O-sulphate. Electrolytic or kainic acid lesions of the medial thalamic nuclei (MTN) partially reduced the contraversive rotation to intranigral muscimol, and completely abolished the similar behaviour elicited by apomorphine (25 μg) injected into the ipsilateral caudate nucleus. Contraversive turning to intranigral muscimol was completely inhibited by kainic acid lesions of the ipsilateral SN, but potentiated by intrathalamic injection of picrotoxin. Muscimol (40 ng-4 μg) administered to the MTN complex in one hemisphere stimulated rats to move in ipsilateral circles that were unaffected by haloperidol. The results of these behavioural experiments suggest that the nigrostriatal dopamine pathway, the nigrothalamic projection and possibly other non-dopaminergic SN efferents all play important roles in mediating the influences of the SN on motor and stereotyped behaviours. Disruption of the nigrothalamic pathway following electrical or chemical injury to the SN was accompanied by falls in GABA and its synthesising enzyme in the corresponding MTN. These data, together with the findings of our electrophysiological study presented in the following paper, are consistent with the nigrothalamic system having a GABAergic inhibitory function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00236661
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  • 3
    Electronic Resource
    Electronic Resource
    Evidence for a GABAergic nigrothalamic pathway in the rat (1980)
    Springer
    Experimental brain research 40 (1980), S. 55-61 
    Details
    ISSN: 1432-1106
    Keywords: Substantia nigra ; Thalamus ; Inhibition ; GABA ; Electrophysiology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Extracellular recordings were made from neurones in the ventromedial and parafascicular nuclei of the rat thalamus, many of which had demonstrable capsular or caudate projections. These cells responded to electrical stimulation of the ipsilateral substantia nigra with a short latency (4 ms) inhibition presumed to be monosynaptic. This inhibitory response was often preceded by a brief period of increased excitability (latency ∼3 ms) attributed to activation of corticofugal collaterals. Longer latency, presumably oligosynaptic excitations (latency ∼8 ms) and inhibitions (∼18 ms) were also obtained, but were more commonly evoked in non-projection neurones. All units were inhibited by iontophoretically applied GABA, glycine or 5-HT. Short and long latency synaptic and GABA-induced inhibitions were selectively blocked by bicuculline. Strychnine only antagonised glycine, while 5-HT was not affected by either convulsant. Intranigral injection of muscimol greatly elevated the spontaneous discharge rate of thalamic neurones, particularly those with a striatal projection. These data are compatible with nigrothalamic neurones maintaining a tonically active, GABA-mediated inhibition of cells in the ventromedial and parafascicular nuclei of the thalamus. It is speculated that intranigral muscimol indirectly activates these thalamic cells and thereby initiates contraversive circling behaviour by suppressing this inhibitory system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00236662
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  • 4
    Electronic Resource
    Electronic Resource
    Muscarinic action of acetylcholine in the rat ventromedial thalamic nucleus (1984)
    Springer
    Experimental brain research 55 (1984), S. 553-561 
    Details
    ISSN: 1432-1106
    Keywords: Thalamus ; Electrophysiology ; Iontophoresis ; Acetylcholine ; Choline acetyltransferase ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Several lines of evidence suggest a role for ACh in the mediation of cerebello-thalamic transmission. The physiological, pharmacological and biochemical experiments described were designed to test this hypothesis for the rat cerebello-thalamic pathway. Unilateral electrolytic lesions of the superior cerebellar peduncle resulted in modest falls of CAT from both ventromedial thalamic nuclei (contralateral 35%, ipsilateral 15%). Iontophoretic application of ACh to relay cells evokes three types of response (i) excitation (ii) inhibition (iii) polyphasic combinations of (i) and (ii). The type of response evoked was directly related to the firing pattern of the cell. Thus, for example, excitatory responses were never recorded during high-frequency bursting but were easily evoked following a switch to tonic, single-spike activity. All responses to ACh and synaptic responses to cerebellar stimulation were sensitive to muscarinic but not to nicotinic cholinergic antagonists. The nicotinic antagonist mecamylamine was a potent blocker of excitant amino acid responses but had no effect on cerebellarevoked synaptic responses. Cholinergic and anticholinergic agents had a profound action on relay cell firing pattern. ACh promoted single-spike activity whereas atropine promoted high-frequency bursting. The actions of ACh are discussed with reference to recently discovered voltage-sensitive ionic conductances. Because of the modulatory action of ACh on relay cell firing pattern and excitability no firm conclusion can be reached concerning the hypothesis under test here. We tentatively suggest a dual role for ACh as both neurotransmitter and neuromodulator.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00235286
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  • 5
    Electronic Resource
    Electronic Resource
    Dysfunction of the midbrain angular complex can accentuate or attenuate circling behaviour in the rat (1985)
    Springer
    Experimental brain research 58 (1985), S. 45-55 
    Details
    ISSN: 1432-1106
    Keywords: Apomorphine ; Muscimol ; Electrolesion ; Circling ; Holeboard ; 6-hydroxydopamine ; γ-vinyl GABA ; Angular complex ; Stereotypy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The role of the midbrain angular complex (AC) in the execution of motor behaviours was investigated in the rat. In an automated holeboard apparatus bilateral AC electrolesions attenuated exploration and increased locomotor performance of drug-free rats on the first and second test occasions respectively; the latter result may signify a retarding of between-session habituation. Apomorphine also decreased locomotion and almost abolished head dipping and rearing in the holeboard; bilateral AC lesions reinstated locomotion to a normal level without modifying the other behavioural parameters. An electrolesion of one AC did not affect the animal's posture or spontaneous locomotion in the open field, but gave rise to pronounced ipsiversive circling when coupled with systemic administration of apomorphine. In unilaterally 6-hydroxydopamine (6-OHDA) treated rats subcutaneous injection of apomorphine evoked robust contraversive circling. A concomitant lesion of the ipsilateral AC introduced an additional ipsilateral bias to these animals' movements; contraversive circling was initially curtailed and posture reduced (or reversed), while stereotyped activities (particularly grooming) were suppressed. Contralateral orientation and circling were restored by subsequently lesioning the contralateral AC as well; bilateral AC lesions significantly potentiated circling to systemic apomorphine. Contralateral locomotor asymmetry was also produced by depositing apomorphine stereotaxically into the supersensitive caudate, or by microinjecting one substantia nigra zona reticulata with muscimol (in naive rats). Both rotational responses were facilitated by injury to the ipsilateral AC. The effects of electrocoagulating the AC were generally duplicated by discrete microinjection of muscimol or γ-vinyl GABA into this area, suggesting GABA-mediated synapses are normally operative in this part of the brain. These results do not support the claim that the AC is specifically engaged in mediating postural asymmetry in the unilaterally 6-OHDA denervated rat. Instead, we believe that impairment of neurotransmission through one AC imposes an independent and reciprocal tendency to move towards that side of the brain, as well as attenuating stereotypy and facilitating locomotion. The resultant behavioural response to systemic apomorphine shown by animals bearing these two types of lesion embodies these separate actions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00238952
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  • 6
    Electronic Resource
    Electronic Resource
    EFFECT OF METALLIC IONS ON COLOR AND PIGMENT CONTENT OF CRANBERRY JUICE COCKTAIL (1973)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of food science 38 (1973), S. 0 
    Details
    ISSN: 1750-3841
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2621.1973.tb02144.x
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  • 7
    Electronic Resource
    Electronic Resource
    Putative Neurotoxicity of SKF 38393 and Other D1 Dopaminergic Drugs Investigated in Rat Striatum (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The recently alleged neurotoxicity of the D1 receptor agonist, SKF 38393, was investigated in rat striatum by measuring the enzymes acetylcholinesterase (AChE) and glutamate decarboxylase (GAD). First, unilateral intrastriatal microinjection of the excitotoxin kainic acid (2 μg in 1 μ1) was shown to evoke vigorous contraversive circling, followed 1 or 2 weeks later by profound decreases in striatal AChE (24 and 54%), GAD (51 and 75%), and protein (36 and 47%), as well as loss of GAD (45% at 2 weeks) in the ipsilateral substantia nigra. Similar striatal treatments with SKF 38393 (30 μg in 0.5–1 μ), the related benzazepines SKF 82526 (D1 agonist, 30 μg in 1 μ1) and SCH 23390 (D1 antagonist, 5 μg in 1 μ1), or the phenanthridine D1 agonist CY 208-243 (5 μg in 1 μ1) failed to affect the rats' behaviour or their striatal levels of AChE, GAD, and protein. Intrastriatal SKF 38393 (30 μg in 0.5 μ1) also had no influence on these enzymes in the substantia nigra. It is concluded that none of the D1 dopaminergic compounds examined here was neurotoxic toward the many different cell groups that contain AChE and/or GAD in the striatum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11365.x
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  • 8
    Electronic Resource
    Electronic Resource
    ÈVIDENCE FOR THE COMPARTMENTATION OF GLUTAMATE METABOLISM IN ISOLATED RAT RETINA (1974)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 23 (1974), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —Glucose is a major precursor of glutamate and related amino acids in the retina of adult rats. 14C from labelled glucose appears to gain access to a large glutamate pool, and the resulting specific activity of glutamate labelled from glucose is always higher than that of glutamine or the other amino acids.Radioactive acetate appeared to label a small glutamate pool. The specific activity of glutamine labelled from acetate relative to that of glutamate was always greater than 1.0. Other precursors of the small glutamate pool were found to include glutamate, aspartate, GABA, serine, leucine and sodium bicarbonate.The level of radioactivity present in retinae incubated with [U-14C]glucose or [1-14C]sodium acetate was reduced in the presence of 10−5m-ouabain. Under these conditions, the relative specific activity of glutamine labelled from [1-14C]sodium acetate was lowered, but it was raised when [U-14C]glucose was used as substrate. Ouabain also considerably reduced the synthesis of GABA from [1-14C]sodium acetate. In all cases ouabain caused a fall in the tissue levels of the amino acids.Aminooxyacetic acid (10−4m) almost completely abolished the labelling of GABA from both [U-14C]glucose and [1-14C]sodium acetate, while the RSA of glutamine labelled from the latter substrate was significantly increased. Aminooxyacetic acid raised the tissue concentration of glutamate, but caused a fall in the tissue concentrations of glutamine, aspartate and GABA.The results suggest that there are separate compartments for the metabolism of glutamate in retina and that these can be modified in different ways by different drugs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1974.tb04363.x
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  • 9
    Electronic Resource
    Electronic Resource
    EFFECTS OF AMINO-OXYACETIC ACID, ETHANOLAMINE-O-SULPHATE AND GABA ON THE CONTENTS OF GABA AND VARIOUS AMINES IN BRAIN SLICES (1975)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 25 (1975), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —The effects of amino-oxyacetic acid, ethanolamine-O-sulphate and γ-aminobutyric acid (GABA) on the contents of GABA, noradrenaline, dopamine and serotonin (5-HT) in slices of rat hypothalamus and midbrain were studied in vitro using a simultaneous fluorimetric assay procedure. Following control incubations the levels of 5-HT were raised, while the levels of the other substances remained steady. Amino-oxyacetic acid caused a reduction in the contents of noradrenaline and 5-HT, but had no effect on either GABA or dopamine. Ethanolamine-O-sulphate both raised the GABA content and lowered the noradrenaline content of slices, while the levels of dopamine and 5-HT were not altered. The presence of GABA in the incubation medium produced complex changes in these levels, depending both on the dose of GABA used and the brain area studied. In the hypothalamus, 0·07 mm-GABA caused an elevation in 5-HT, a drop in noradrenaline, and no change in either GABA or dopamine. With 5 mm-GABA, the noradrenaline level was raised slightly above control values and the endogenous GABA level doubled, while 5-HT and dopamine levels were not different from controls. Similar changes in 5-HT and GABA contents were observed with midbrain slices, but noradrenaline and dopamine were not affected. The possible modes of action of amino-oxyacetic acid and ethanolamine-O-sulphate on the amino acid and amine systems in the brain are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1975.tb04370.x
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  • 10
    Electronic Resource
    Electronic Resource
    Effects of glutamate antagonists on the activity of aromatic L-amino acid decarboxylase (1998)
    Springer
    Amino acids 14 (1998), S. 43-49 
    Details
    ISSN: 1438-2199
    Keywords: L-DOPA ; Aromatic L-amino acid decarboxylase ; Glutamate antagonists ; Substantia nigra ; Corpus striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study examines the hypothesis that glutamate tonically suppresses the activity of the enzyme aromatic L-amino acid decarboxylase (AADC), and hence the biosynthesis of dopamine, to explain how antagonists of glutamate receptors might potentiale the motor actions of L-DOPA in animal models of Parkinson's disease. A variety of glutamate antagonists were therefore administered acutely to normal rats, which were sacrificed 30–60 min later and AADC activity assayed in the substantia nigra pars reticulate (SNr) and corpus striatum (CS). The NMDA receptor-ion channel antagonists MK 801, budipine, amantadine, memantine and dextromethorphan all caused a pronounced in creased in AADC activity, more especially in the SNr than CS. The NMDA glycine site antagonist (R)-HA 966 produced a modest increase in AADC activity in the CS but not SNr, whilst the NMDA polyamine site antagonist eliprodil, the NMDA competitive antagonist CGP 40116 and the AMPA antagonist NBQX were without effect. The results suggest that an increase in dopamine synthesis might contribute to the L-DOPA-facilitating actions of some glutamate antagonists.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01345241
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