International Journal of Neuropharmacology (Int J Neuropharmacol )

Publisher: Elsevier

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  • Other titles
    International journal of neuropharmacology
  • ISSN
    0375-9458
  • OCLC
    1778040
  • Material type
    Periodical
  • Document type
    Journal / Magazine / Newspaper

Publisher details

Elsevier

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    • Pre-print can not be deposited for The Lancet
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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The evoked and spontaneous activity of Renshaw cells in unanesthetized spinal cats was studied with metal microelectrodes before and after pentylenetetrazol (40 mg/kg). The drug did not prolong the discharge of Renshaw cells following dorsal root or ventral root stimulation. In addition, several cells were examined for the effects of the drug on spontaneous activity. Pentylenetrazol did not produce consistent changes in the rate of discharge.
    International Journal of Neuropharmacology 01/1970; 8(6):627-30.
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    ABSTRACT: The amino acids tryptophan and methionine are known to be involved in behavioral alterations and their metabolites have been implicated in mental illness. To learn more about the metabolic interrelationships of these two amino acids, rats were placed on amino acid diets deficient in nicotinic acid and nicotinamide and pair-fed with and without intestinal-antibiotics. Excess methionine (4%) added to such diets resulted in rats showing a decrease in body weight and urinary N1-methylnicotinamide (MNA) and an increase in urinary xanthurenic acid (XA) and total indoleacetic acid (TIAA) in comparison with controls. Urinary creatinine (CR) was relatively unchanged. Intestinal-antibiotics did not affect the overall methionine effect. The overall results demonstrate that excess-dietary methionine alters the tissue metabolism of tryptophan, and gives rise to urinary excretion patterns of tryptophan metabolites claimed to occur in mental illness. The observed data point to a metabolic alteration involving vitamin B6. A natural competition may exist between methionine and tryptophan for vitamin B6 which is utilized in the metabolic pathways of both amino acids. Our work suggests that tolerance load tests of methionine and tryptophan in behavioral alteration studies must take into account the metabolic competition between these two amino acids for vitamin B6, as well as the formation of psychotogenic metabolites by N-methylation and O-methylation reactions.
    International Journal of Neuropharmacology 01/1970; 8(6):615-26.
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    ABSTRACT: It has been observed that (1) in chloralosed cats, centrally pretreated with either reserpine, imipramine or chlorpromazine, injection of phentolamine (3mg) or pronethalol (2mg) into the lateral cerebral ventricle, significantly reduces noradrenaline-induced pressor responses and heart rate increases, respectively; (2) equal intravenous doses of phentolamine or pronethalol lead to a less marked blockade of the cardiovascular effects of intraventricular noradrenaline in cats centrally pretreated with imipramine. These findings would suggest that sympathetic receptor mechanisms showing responses like those of “alpha” and “beta” types, as postulated at peripheral adrenergic sites, might also be involved in the central nervous system regulation of cardiovascular manifestations.
    International Journal of Neuropharmacology 01/1970; 8(6):587-92.
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    ABSTRACT: Noradrenaline, isoprenaline, 5-hydroxytryptamine, acetylcholine, glutamate and gaba have been applied iontophoretically onto spontaneously active cortical neurones in cats under different anaesthetic conditions. Neurones were predominantly excited by monoamines in halothane anaesthetised cats and encéphale isolé preparations, and excitation was still seen when careful controls for current, pH and anion effects were made.Noradrenaline excitations were blocked selectively by α-adrenergic antagonists (dibenamine, thymoxamine and phentolamine) and β-adrenergic antagonists (propranolol, d-INPEA and sotalol) when responses to acetylcholine, 5-hydroxytryptamine and glutamate were unaffected. However, noradrenaline depressions were relatively resistant to these antagonists. Cells tested with both noradrenaline and isoprenaline invariably responded in the same direction, in contrast to cells tested with either noradrenaline and 5-hydroxytryptamine, or noradrenaline and acetylcholine.The time-course of noradrenaline, isoprenaline and 5-hydroxytryptamine excitation was similar, though slower than that seen with acetylcholine. The time-course of depression was identical for all four substances. The latency of onset of noradrenaline and 5-hydroxytryptamine excitation, but not depression, was inversely related to the spontaneous neuronal discharge rate. Since most neurones discharged at a low rate, there was usually a long latency for monoamine excitation.
    International Journal of Neuropharmacology 01/1970; 8(6):549-66.
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    ABSTRACT: Microinjections of histamine, norepinephrine or several cholinergic substances into the posterior hypothalamus of rats resulted in various effects on arterial blood pressure. Centrally injected histamine and norepinephrine produced an immediate rise in blood pressure. Carbachol usually produced a hypotensive response but on occasion a delayed rise in blood pressure or an immediate fall followed by a rise was observed. Pronounced changes in respiratory rate accompanied the rise in arterial blood pressure. The hypotensive response, which was also produced by acetylcholine and oxotremorine (a muscarinic agent) but not by nicotine, was mediated both centrally and peripherally by muscarinic mechanisms. Eserine, which produces a rise in blood pressure following systemic administration, caused a similar effect upon injection into the hypothalamus.
    International Journal of Neuropharmacology 01/1970; 8(6):593-600.
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    ABSTRACT: Rats receiving haloperidol for three days showed a dose dependent decrease of brain catecholamines. The hypothermic effect of the drug did not cause this. Haloperidol counter-acts the monoamine depletion of reserpine in both the brain and the heart provided it is given shortly before reserpine.
    International Journal of Neuropharmacology 01/1970; 8(6):631-4.
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    ABSTRACT: The effect of reserpine and p-chlorophenylalanine (PCPA) on the integrated voltage of the electrocorticogram (ECoG) of unrestrained rats was examined during 15 min and 2½ hr recording sessions. As previously reported, reserpine caused an increase in the ECoG voltage during 15 min sessions. This effect was slightly enhanced by PCPA pretreatment. PCPA treatment alone produced an increase in the ECoG voltage and an increase in synchronized activity similar to that induced by reserpine. Thus, it appears that the ECoG effect of reserpine during 15 min recording sessions does not depend upon increased “free” 5-HT. During 2½ hr sessions, PCPA produced a decrease in voltage with decreased slow-wave activity. A consistent increase in ECoG voltage was observed 4 hr after reserpine injection using the long recording time. By 24 hr, the voltage had returned to the control levels and was lower than the control at 48 hr and later. α-Methyltyrosine restored the decreased voltage to the control levels. PCPA pretreatment antagonized the reserpine-induced increase in ECoG voltage and instead of a return to the control at 24 hr after reserpine, a marked decrease in voltage was seen in the PCPA-pretreated animals at this time period. These results are discussed in terms of reciprocally acting “catecholaminergic” and “serotoninergic” systems.
    International Journal of Neuropharmacology 01/1970; 8(6):535-48.
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    ABSTRACT: The spontaneous and hypothalamically evoked discharge patterns of the preganglionic cervical sympathetic, splanchnic and vagal nerves have been described and discussed as potential indicators of central “autonomic tone” in cat. Chlorpromazine and diazepam, in i.v. doses of 0·3-3 mg/kg, generally reduced slightly spontaneous evoked impulse traffic in cervical sympathetic fibers, but markedly attenuated the electrical activity in splanchnic nerves. Vagal efferent activity was more subtly affected by these two agents. Pentobarbital (3–10 mg/kg i.v.) depressed spontaneous and evoked potentials in the sympathetic and vagal nerves. In addition, it prevented the poststimulatory inhibition observed in sympathetic nerves.
    International Journal of Neuropharmacology 01/1970; 8(6):567-72.
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    ABSTRACT: l-Epinephrine administered via the lateral cerebral ventricle was found to decrease exploratory locomotor activity and potentiate hexobarbital sleeping time in rats. Both effects were dose-dependent and occurred with microgram quantities (3·3–125 μg) of epinephrine. Additional signs of a central depressant effect were noted in gross behavior. Although subcutaneous injections of l-epinephrine (0·025 and 1·0 mg/kg) also depressed locomotor activity, intraventricular injections proved much more effective. Lethality of l-epinephrine was enhanced by the intraventricular route, but the observed depressant effects occurred at doses well below the ld50 and were observed to be completely reversible. The importance of the catechol moiety for the central depressant effects of epinephrine was emphasized by the results obtained from studying the effect on locomotor activity of a series of sympathomimetic amines. The parent compound, phenylethylamine, which is devoid of hydroxyl groups on the benzene ring and aliphatic side chain, was found to be excitant rather than depressant. Rank order of potency studies indicated that the depressant effect of catecholamines on locomotor activity might be mediated through central adrenergic receptors of the β-type. Studies with adrenergic blocking agents did not support this idea, however, and suggested that the central receptors involved are not identical to either the classical α or β adrenergic receptor.
    International Journal of Neuropharmacology 01/1970; 8(6):573-86.
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    ABSTRACT: EEG analyses of amphetamine and its psychotomimetic methodoxy derivatives have been made in order to find their sites for evoking EEG alerting in rabbit brain. Four groups of animals were studied: controls with intact brain and others with transections of the brain at one of three different levels: above the midbrain, below the midbrain and through the first cervical segment.Both d-amphetamine and methamphetamine induced EEG alerting at the midbrain level. In contrast, relatively potent psychotomimetic congeners paramethoxyamphetamine, 2,4,5-trimethoxyamphetamine and 2,5-dimethoxy-4-methylamphetamine provoked EEG alerting caudal to the midbrain and cephalad to the first cervical segment at the medullary level. A weak psychotomimetic congener 3,4-dimethoxyamphetamine possessed both sites, midbrain and medullary regions, for evoking EEG alerting.
    International Journal of Neuropharmacology 01/1970; 8(6):601-13.
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    ABSTRACT: Nicotine, in low doses of 20–40 μg/kg i.v., blocked the monosynaptic reflex without influencing spindle afferent activity. In contrast, succinylcholine depressed the monosynaptic reflex only when it enhanced spindle discharge. Abolition of the spindle excitatory effect of succinylcholine by gallamine or deafferentation eliminated the monosynaptic reflex depressant action of succinylcholine but did not affect that of nicotine. Mecamylamine, on the other hand, which blocks the nicotinic synapse at the Renshaw cell, abolished the monosynaptic reflex blocking effect of nicotine but not that of succinylcholine. These results emphasize the basically different mechanisms underlying the blockade of the monosynaptic reflex by nicotine and succinylcholine.At intermediate doses of nicotine (40–80 μg/kg i.v.) spindle afferent activity was affected through changes in fusinotor activity consisting of a brief increase followed by prolonged depression. In still higher i.v. doses of nicotine, a direct excitatory effect on the spindle organ was observed. Depression of the monosynaptic reflex through this peripheral effect was revealed when the central action of nicotine was blocked by mecamylamine. Like the action of succinylcholine, it could be blocked by gallamine. Excitation of skin receptors and motor nerve terminals was excluded as a contributory cause of the monosynaptic reflex depression induced by nicotine in the dose range used.
    International Journal of Neuropharmacology 01/1970; 8(6):515-33.
  • Source
    International Journal of Neuropharmacology 12/1969; 8(6):493.
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    ABSTRACT: The rapid uptake of3HNE exhibitedin vitro by rabbit irises depends on the presence of sympathetic nerves and the NE concentration in the incubation medium. Pretreatment of the animals with reserpine and pargyline fails to inhibit the efficiency of this neuronal uptake process, thus confirming previous reports in the literature that the depletion of neuronal NE elicited by reserpine is not the result of the blockade of the uptake of NE by sympathetic neurons.
    International Journal of Neuropharmacology 10/1969; 8(5):463-9.
  • International Journal of Neuropharmacology 10/1969; 8(5):489-90.
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    ABSTRACT: Rats pretrained in ago-nogo avoidance discrimination were treated daily with 1mgkg of scopolamine HBr s.c. 40 min before testing sessions. EEG records were taken twice a week, before and after sessions. The drug caused initially a disruption in performance and EEG synchronization. Upon repeated exposure the behavioural deficit was progressively compensated for, while the EEG alteration persisted. The administration of physostigmine (1mgkg s.c.) to desensitized scopolamine-treated animals provoked a disruption in the performance and an EEG desynchronization. Repeated exposure to scopolamine and physostigmine led to a rapid behavioural desensitization to the combined treatment.
    International Journal of Neuropharmacology 10/1969; 8(5):405-11.
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    ABSTRACT: Adrenaline (10–200 μg) and noradrenaline (50 μg) when injected into the lateral cerebral ventricle of pentobarbital-anesthetized rabbits produced a fall in systemic blood pressure, a decrease in spontaneous heart rate and a stimulation of spontaneous respiration. Isoproterenol (50–200 μg) caused a fall in blood pressure and an acceleration of heart rate, whereas phenylephrine (200 μg) caused a slight rise in blood pressure in association with a decrease in heart rate. The hypotension and bradycardia induced by adrenaline were not significantly affected by bilateral vagotomy. Pretreatment of rabbits with intravenous reserpine reversed the adrenaline-induced hypotension to a hypertension and abolished the bradycardia induced, but did not affect the respiratory stimulation. The cardiovascular responses to intraventricular adrenaline were abolished by transection of the spinal cord. In unanesthetized rabbits adrenaline produced presser and cardio-stimulatory effects followed by depressor and cardio-inhibitory effects. These findings would suggest a centrally mediated hypotensive action of adrenaline in anesthetized rabbits but a hypertensive action in unanesthetized rabbits. Furthermore, changes in the cardiac function might be associated with changes in local blood flow, as postulated byKanekoet al. (1960).
    International Journal of Neuropharmacology 10/1969; 8(5):451-61.
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    ABSTRACT: Effects of 5-hydroxytryptamine (5-HT), lysergic acid diethylamide (LSD) and other psychotomimetics upon the potentials induced in thin sections from the superior colliculus of the guinea pig were studiedin vitro. The postsynaptic field potential (PSR) evoked by optic tract stimulation was suppressed by 5-HT in concentrations of 10−7–10−6M. Single neuron discharges induced by optic tract stimulation were also suppressed by 5-HT but spontaneous cell firings were not affected. By higher concentrations of 5-HT (more than 10−4M) PSR was once suppressed but gradually recovered. LSD, lysergic acid ethylamide (LAE) and other related compounds potentiated the 5-HT suppressing action in relatively low concentrations but blocked it in higher ones. Morphine and 2-bromolysergic acid ethylamide (BOL) did not antagonize the 5-HT action. When two shocks were delivered to the optic tract at short intervals and the time course of suppression of the second PSR was studied, it was found that LSD and related compounds accelerated the recovery of the test PSR. Physiological roles of 5-HT in the superior colliculus are discussed.
    International Journal of Neuropharmacology 10/1969; 8(5):437-49.
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    ABSTRACT: Although considerable attention has been directed towards the effects of cerebral cortical damage on convulsive thresholds, few studies have involved subcortical structures. In the present report, the thresholds for flurothyl-induced myoclonic jerks and generalized seizures were determined in adult, male albino rats. Bilateral lesions of the lateral geniculate nucleus resulted in an almost 20% decrease in threshold to the convulsant. Although no sensitivity changes resulted from lesions of either the lateral thalamic posterior nucleus or the medial geniculate nucleus, lesions of these areas potentiated the effects seen with lesions of the lateral geniculate nucleus alone. In all cases, the increased sensitivity to the convulsant required more than 1 week after surgery for development. It was concluded that the visual system is intimately involved in at least some types of convulsive phenomena.
    International Journal of Neuropharmacology 10/1969; 8(5):393-8.
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    ABSTRACT: Biogenic amines and related compounds, and certain amino acids were applied by microelectrophoresis onto single red nucleus neurons. The cats were either lightly anesthetized or specially prepared in the unanesthetized state.l-Glutamic anddl-homoeysteic acids were potent excitants while gamma-aminobutyric acid was a strong depressant of neuronal activity. Acetylcholine and carbamylcholine, 5-hydroxytryptamine and lysergic acid diethylamide, noradrenaline and dopamine and other phenylethylamines stopped brachio-rubral synaptic transmission, reduced “spontaneous” firing and amino-acid evoked firing of RN neurons. Parenterally administered drugs which disturb motor coordination, such as lysergic acid diethylamide, bufotenine and mephenesin depress directly or indirectly rubral neuronal activity. 4-Methoxyphenylethylamine when applied locally did depress rubral neurons. However, when applied intravenously 4-methoxyphenylethylamine caused a hypokinetic rigid syndrome to develop; parallel to the increases in muscle tension and electromyogram activity were increases in rubral neuronal firing. The evidence presented and from a Preliminary Note (H. McLennan) indicates that the transmitter released from the brachium fibers to excite rubral neurons is not acetylcholine. The rubro-cerebellar fibers may be cholinergic.
    International Journal of Neuropharmacology 10/1969; 8(5):475-88.