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PubMed1987

Changeover from alternate to synchronous bilateral pattern of the phrenic bursts entrained by fictive locomotion in the spinal rabbit preparation.

Phrenic bursting resulting from locomotor entrainment during fictive locomotion was shown previously in high spinal preparation after nialamide-DOPA administration. The temporal evolution of the bilateral pattern of phrenic vs locomotor activity is considered here. At variance with the bilateral locomotor pattern which is always alternate (fictive stepping), the pattern on both phrenic nerves changes with time after DOPA injection: first alternate, left and right phrenic bursts become synchronous. A study of ipsilateral phrenic-locomotor phase relationships allowed to disclose the way the transition from alternate to synchronous phrenic coupling was achieved: synchronism appeared as resulting from a strong facilitation on the overlapping parts of the bilaterally alternating phrenic bursts; this phase shifting, vs the ipsilateral locomotor pattern, accounts for the transfer of phrenic bilateral coupling.

Action Potentials↗

PubMed1988

An attempt to localize the lumbar locomotor generator in the rabbit using 2-deoxy-[14C]glucose autoradiography.

An attempt was made to find the anatomical localization of the lumbar locomotion generators using 2-deoxy-[14C]glucose (2-DG) uptake in acute low spinal preparation of rabbits unanaesthetized, curarized and injected with nialamide and dihydroxyphenylalanine (DOPA). In such conditions, the locomotor generators were forced to work in isolation for 45 min without interruption as attested by the rhythmic activity recorded in hindlimb muscle nerves. Compared to spinal control preparations not activated pharmacologically, the treated animals showed a specific labeling in the intermediate part of the grey matter, extending from L6 to S1.

Action Potentials↗

PubMed1995

5-Hydroxytryptamine-immunoreactive nerve fibers in the rat and porcine prevertebral sympathetic ganglia: effect of precursor loading and relation to catecholaminergic neurons.

Localization of 5-hydroxytryptamine immunoreactivity was studied in the rat coeliac-superior mesenteric ganglion complex and in the porcine superior and inferior mesenteric ganglia by the indirect immunofluorescence technique. In normal rats, only 5-hydroxytryptamine immunoreactive SIF cells were seen in the coeliac-superior mesenteric ganglion complex. In the rats, pretreated with a 5-hydroxytryptamine precursor, L-tryptophan, and with a monoamine oxidase inhibitor, nialamide, a large number of 5-hydroxytryptamine-immunoreactive nerve fiber terminals were detected. In normal porcine superior and inferior mesenteric ganglia, intense 5-hydroxytryptamine immunoreactivity was found in numerous nerve fibers which were located around tyrosine hydroxylase-immunoreactive principal neurons. The origin and function of these fibers are discussed.

Animals↗

PubMed1993

Differential expression of serotonin and [Met]enkephalin-Arg6-Gly7-Leu8 in neurons of the rat brain stem.

The hypothesis that serotonin (5-HT) and [Met]enkephalin-Arg6-Gly7-Leu8 (MEAGL) coexist in the rat brain stem raphe nuclei was tested by a technique combining histofluorescence with immunocytochemistry, after treatment with colchicine and nialamide. In midbrain and pons serotonergic cell groups (B5-B9), no coexistence of 5-HT and MEAGL was detected. In serotonergic cell groups of the medulla oblongata (B1-B3), only 0.3-1.5% of 5-HT-fluorescent cells were MEAGL-immunoreactive. These findings suggest that putative 5-HT and MEAGL are mostly expressed in different populations of neurons in the rat raphe nuclei.

Animals↗

PubMed1984

Repeated treatment with antidepressant drugs prevents salbutamol-induced hypoactivity in rats.

We have found earlier that a number of antidepressant drugs, administered repeatedly, prevent the salbutamol-induced hypoactivity in rats. Our further experiments show that a similar effect is produced by repeated, but not acute, treatment with other antidepressants: clomipramine, mianserin and nialamide. Two non-antidepressant psychotropic drugs, haloperidol and diazepam, were inactive after repeated administration. These results seem to support our earlier hypothesis that prevention of the salbutamol-induced hypoactivity may be regarded as functional evidence at the behavioral level for the subsitivity of beta-adrenoceptors.

Albuterol↗

PubMed1997

Effects of tetrabenazine on methamphetamine-induced hyperactivity in mice are dependent on order and time-course of administration.

The ambulation-increasing effect of methamphetamine (MAP: 2 mg/kg s.c.) in mice persisted for about 3 h. Tetrabenazine (TBZ: 4 mg/kg s.c.), a depleter of monoamines from the cytoplasmic pool did not increase ambulation on its own. Pretreatment with TBZ at 1.5 h before administration of MAP inhibited the stimulant effect of MAP. In contrast, combined administration of two drugs resulted in a transient but considerable enhancement of MAPs stimulant effect. Post-MAP treatment with TBZ at 0.5-2 h hardly modified MAPs behavioral effects. In contrast, 3-6 h post-MAP treatment with TBZ induced a transient increase in activity, although the stimulant effect of MAP had already disappeared. The maximum increase in ambulatory stimulation was produced by 4-h post-MAP treatment with TBZ. The inhibitory effect of TBZ pretreatment on MAP-induced hyperactivity, as well as the transient hyperactivity elicited by TBZ when administered along with MAP, or 4 h after MAP, was dose-dependent. Preliminary studies revealed that transient hyperactivity was never produced by combination of GBR-12909 (a selective dopamine reuptake inhibitor) with TBZ or MAP with oxypertine (a selective norepinephrine releaser/depleter), but produced by combination of nialamide (a monoamine oxidase inhibitor) with TBZ. Inhibition of MAPs effects by TBZ pretreatment suggests that enhancement of dopamine release from cytoplasmic pool, and inhibition of dopamine reuptake by MAP, are involved in MAPs acute behavioral effects. Further, the fact that neither TBZ administration following GBR-12909 pretreatment, nor oxypertine treatment following MAP pretreatment, elicited transient hyperactivity suggests that dopamine is involved in hyperactivity elicited by post-MAP treatment with TBZ. It is also suggested that inhibition of monoamine oxidase (MAO) by MAP and dopamine displacement by TBZ may be responsible for the transient stimulation produced by 3-6 h post-MAP treatment with TBZ. It is hypothesized that the MAO inhibitory action of MAP persists after cessation of its acute stimulant effect, possibly up to 6 h after administration.

Adrenergic Uptake Inhibitors↗

PubMed1979

Studies on the tissue-disposition and fate of N-[14C]ethyl-N-nitrosourea in mice.

The tissue-disposition and fate of N-[14C]ethyl-N-nitrosourea has been studied in mice. A large part of the injected N-[14C]ethyl-N-nitrosourea radioactivity was found to be exhaled as 14CO2. Whole-body autoradiography showed evenly distributed radioactivity in most tissues shortly after the administration of N-[14C]ethyl-N-nitrosourea which probably is due to the homogeneously distributed substance and the non-enzymatically formed ethyl-carbonium ions which have reacted with the tissues. The blood-brain barrier seemed to have a capacity to partially prevent the uptake of the substance in the central nervous system. A high radioactivity was observed in the liver, which may imply that N-[14C]ethyl-N-nitrosourea is enzymatically decomposed in this tissue. An observed labelling of kidneys may be connected with urinary excretion of radioactivity. The radioactivity in the liver and kidney decreased at later survival intervals and a distribution pattern appeared, which was characterized by a labelling of tissues with a high protein or steroid synthesis and of fat containing tissues. The distribution pattern corresponded to the one seen after the administration of [14C]acetaldehyde and is probably due to normal biosynthetic incorporation of radioactivity in the 2-carbon pool. Pretreatments with pyrazole, nialamide and diethyldithiocarbamate caused a marked inhibition of the exhalation of 14CO2 and of the incorporation of radioactivity in the liver. This effect may be directed towards the decomposition of N-[14C]ethyl-N-nitrosourea itself, but an effect on the metabolism of formed 2-carbon fragments is also possible. The incorporation of radioactivity in other tissues was not influenced by the pretreatments.

Acetaldehyde↗

PubMed1977

Vitiligo: a new classification and therapy.

Local injection of physostigmine revealed that dermatomally distributed vitiligo was associated with a dysfunction of the sympathetic nerves in the affected skin and that non-dermatomally distributed vitiligo was not. These observations led to the hypothesis that the primary disturbance of dermatomally distributed vitiligo lies in the sympathetic nerves of the affected area and that non-dermatomally distributed vitiligo has its primary disturbance in the melanocyte itself, where an autoimmune mechanism is suspect. Results of therapy supported this hypothesis by showing that topical cortisteroid is effective only in the latter, while the former reacts to oral nialamide. It is proposed that non-dermatomally distributed vitiligo be referred to as Type A and dermatomally distributed vitiligo as Type B.

Adolescent↗

PubMed2000

Bulbospinal control of spinal cord pathways generating locomotor extensor activities in the cat.

Intracellular recording of lumbosacral motoneurones in the decerebrate and partially spinalized cat injected with nialamide and L-dihydroxyphenylalanine (l-DOPA) was used to investigate the interneuronal convergence of two bulbospinal pathways and of the segmental pathways involved with the generation of extensor activities during locomotion. Deiter's nucleus (DN) or the medial longitudinal fasciculus (MLF) was stimulated in alternation with, and in combination with, stimulation of group I afferents from extensor muscles or of contralateral flexor reflex afferents (coFRA). The evoked polysynaptic EPSPs were recorded in extensor motoneurones when long-latency, long-lasting discharges were evoked by the stimulation of coFRA and when the group I autogenetic inhibition in extensors was reversed to polysynaptic excitation. Spatial facilitation was inferred when the amplitude of the EPSPs evoked by the combined stimuli was notably larger than the algebraic sum of the EPSPs evoked by individual stimulation. Both DN (16 motoneurones) and MLF inputs (8 motoneurones) showed spatial facilitation when preceded by coFRA stimuli and both could reset the rhythm of fictive stepping by triggering a precocious extensor phase. MLF showed spatial facilitation with extensor group I inputs in 69% of trials but DN failed to show spatial facilitation in any cells. These results indicate that DN and MLF project to the coFRA pathways of the extensor half-centre for locomotion and MLF, but not DN, converge on segmental interneurones of the extensor group I pathways. The implications of such convergence patterns on the functional organization of the extensor half-centre are discussed.

Animals↗

PubMed1961

Relative activity of some inhibitors of mono-amine oxidase in potentiating the action of tryptamine in vitro and in vivo.

Several known inhibitors of mono-amine oxidase (iproniazid, isocarboxazid, nialamide, phenelzine, pheniprazine and tranylcypromine) were tested for their ability to (i) inhibit the mono-amine oxidase activity of a rat brain mitochondrial preparation in vitro; (ii) potentiate the action of tryptamine on the isolated rat fundal strip preparation; and (iii) potentiate the acute toxicity of tryptamine in mice. There was some correlation between the order of potency of the drugs in the three tests, particularly in inhibiting the enzyme activity in the Warburg and in the tryptamine toxicity test in mice. Exceptions to this were isocarboxazid which had unexpectedly high activity on the rat fundal strip preparation, and tranylcypromine which was devoid of tryptamine-potentiation action on the rat fundus preparation although it inhibited rat brain mono-amine oxidase in vitro and potentiated the action of tryptamine in vivo. Tranylcypromine was considerably less active in inhibiting the mono-amine oxidase of rat fundus than rat brain tissue in vitro, while iproniazid and isocarboxazid had about the same potency on the enzyme from the two tissues.

Animals↗

PubMed1961

Effects of cocaine and antidepressant drugs on the nictitating membrane of the cat.

Cocaine, imipramine and pipradol potentiated the contractions to adrenaline and noradrenaline, but not to tyramine, on the nictitating membrane of the spinal cat. Pheniprazine and dexamphetamine potentiated the responses to adrenaline, noradrenaline and tyramine, whereas nialamide only potentiated the response to tyramine. Potentiation of the response to stimulation of either the preganglionic or the postganglionic sympathetic nerve trunks was observed with imipramine, pipradol, pheniprazine and dexamphetamine. Only dexamphetamine and pheniprazine caused substantial contractions of the membrane when the preganglionic nerve was cut (acutely decentralized), or when the superior cervical ganglion was removed (acutely denervated). Cocaine produced contractions of the innervated but not of the acutely decentralized membrane. The significance of the peripheral effects of these antidepressant drugs in relation to their central actions is discussed.

Animals↗

PubMed1963

TACHYPHYLAXIS TO SOME SYMPATHOMIMETIC AMINES IN RELATION TO MONOAMINE OXIDASE.

Tachyphylaxis to the effects of indirectly acting sympathomimetic amines has been studied on the blood pressure of the cat, rabbit and rat, on the cat spleen and nictitating membrane and on the rabbit heart. The pressor responses to tyramine and to phenethylamine declined slowly with repeated injection; the extent of tachyphylaxis induced by these amines depended on the dosage and on the frequency of injection. The pressor responses to alpha-methyltyramine and to dexamphetamine (alpha-methylphenethylamine) declined rapidly with successive injections. The tachyphylaxis induced by one indirectly acting sympathomimetic amine is crossed to others, but not to directly acting amines, such as noradrenaline. In animals treated with nialamide, a drug which inhibits monoamine oxidase, the tachyphylaxis induced by tyramine and by phenethylamine was similar to that produced by their alpha-methyl derivatives in normal animals. Similar results were obtained when the responses to indirectly acting sympathomimetic amines were studied on the cat spleen in situ and on the rabbit heart in vitro. Indirectly acting sympathomimetic amines impaired the responses of the cat nictitating membrane to sympathetic nerve stimulation; this effect was most evident with alpha-methylated amines.

Animals↗

PubMed1969

Brain monoamines and adrenocortical activation.

1. The effect of a pharmacologically induced increase or depletion of brain monoamines (5-hydroxytryptamine, noradrenaline, dopamine) was investigated with respect to adrenocortical function.2. No strict correlation was found between the depletion of brain amine stores induced by prenylamine or p-chlorophenylalanine and adrenocortical activation, even at times in which the peak effect of brain amine depletion occurs.3. Restraint stress causes a manifest increase in brain 5-hydroxytryptamine while decreasing the cerebral noradrenaline and dopamine content. This stress strongly stimulates corticosterone secretion by the adrenals.4. A monoamine oxidase inhibitor, nialamide, at a dose which causes an evident increase in brain amine concentrations, does not modify plasma corticosterone. At the same dose it was, furthermore, unable to prevent the adrenocortical stimulation induced by restraint stress.5. Brain amine content does not seem to play an important part in the control of corticotrophin releasing factor in corticotrophin secretion by the pituitary gland. The relationship between hypothalamic monoamines and other neurohumours is discussed.

Adrenal Glands↗

PubMed1969

Effect of monoamineoxidase inhibitors on 5-hydroxytryptamine output from perfused cerebral ventricles of anaesthetized cats.

1. In cats anaesthetized with pentobarbitone sodium, intraperitoneal injections of four inhibitors of monoamine oxidase (MAO) were shown to increase the 5-hydroxytryptamine (5-HT) in the effluent from the perfused cerebral ventricles.2. Weight for weight, tranylcypromine was found to be about twice as potent as pheniprazine, eight times as potent as nialamide and sixty times as potent as pargyline.3. The effect of tranylcypromine was also examined after reserpine had been injected into the cerebral ventricles or after p-chlorophenylalanine, given intraperitoneally. In both conditions tranylcypromine retained its ability to increase the 5-HT output from the perfused cerebral ventricle, but the effect was attenuated, more after p-chlorophenylalanine than after reserpine.4. Evidence is put forward that in both conditions the brain is not completely depleted of its 5-HT, but that the 5-HT is only reduced, more after p-chlorophenylalanine than after reserpine.

Animals↗

PubMed1970

Physiological and drug-induced changes in the glycogen content of mouse brain.

1. The effect of the method of killing on the concentration of glycogen in mouse brain was determined. The cerebral glycogen content of mice killed by immersion in liquid nitrogen did not differe significantly from that of animals decapitated and the heads immediately frozen. A delay before freezing led to the rapid loss of brain glycogen, with a 17% fall at 10 s and an 82% loss after 5 min.2. Hyperglycaemia, induced by the administration of D-glucose, resulted in an 8.3% loss of brain glycogen after 120 min. Insulin hypoglycaemia produced a 10.7% fall in glycogen at 60 min followed by an 11.2% increase at 120 min.3. Exposure to either high (32 degrees C) or low (10 degrees C) ambient temperatures caused a depletion of brain glycogen.4. A circadian rhythm of brain glycogen concentration was found, with a nadir which was coincident with the peak of locomotor activity and body temperature.5. Drugs from several pharmacological classes were studied for their in vivo effect on the concentration of glycogen in mouse brain.6. Brain glycogen was increased by all the depressant drugs tested, and by some drugs which had little effect on behaviour (diphenhydramine, phenytoin and propranolol), or which caused excitation (caffeine and nialamide).7. Glycogen was depleted only by amphetamine-like compounds or by bemegride-induced convulsions.8. The results are discussed with particular reference to the possible relation between catecholamines and glycogen metabolism in the brain.

Amphetamine↗

PubMed1970

The role of monoamine oxidase in the response of the isolated central artery of the rabbit ear to tyramine.

1. Monoamine oxidase activity was demonstrated histochemically throughout the media of the rabbit ear artery but not in the adventitia at its border with the media where the sympathetic nerve terminals are concentrated. Neither intensity nor distribution of enzyme activity was perceptibly altered up to 60 days after sympathetic denervation.2. Iproniazid and nialamide increased the sensitivity of the artery to intraluminal tyramine much more than that to extraluminal tyramine, so that the difference between the potencies for the two routes of administration became less marked.3. The results indicate that inactivation by monoamine oxidase in the media is a factor contributing to the relatively low potency of intraluminal tyramine on the artery.

Animals↗

PubMed1970

A method for investigating the effects of drugs on the exploratory behaviour of mice.

1. Exploratory behaviour in mice was observed when they were put on a wooden board to which twelve tunnels were fixed. The number of different tunnels entered (indicating exploration) and the total entries into tunnels were recorded over 5 min on 2 successive days.2. Untreated mice entered more different tunnels in the first minute on the second day on the tunnel board, and this difference in behaviour was taken as an indication that exploration had occurred on the first day. When the behaviour of the treated mice on the second day was similar to that of inexperienced mice on the first day it was inferred that drug treatment had adversely affected exploration.3. Haloperidol 4 mg/kg, chlorpromazine 8 mg/kg and thioridazine 16 mg/kg adversely affected exploration at doses which almost immobilized the mice.4. Amphetamine at 8 mg/kg disrupted exploratory behaviour in the mice, although the mice were observed to move round the board very quickly.5. With tranylcypromine 2 mg and nialamide 100 mg, increased exploratory behaviour by comparison with controls was recorded in the mice when they were tested 24 h after drug treatment.6. Imipramine at 20 mg/kg reduced the total number of tunnels entered by the mice on the first day, but on the second day the mice behaved in a similar way to mice treated with monoamine oxidase inhibitors.

Amphetamine↗

PubMed1971

Pharmacological properties of centrally administered ouabain and their modification by other drugs.

1. Ouabain given by intracerebroventricular injection to mice in small doses (0.1-0.4 mug) produced a dose related depression of central nervous activity, characterized by a reduction in spontaneous locomotor activity, hypothermia, catalepsy and ptosis, lowered body posture and lack of response to external stimuli. Doses above 0.4 mug were excitatory, convulsant and lethal.2. The depressant effects could be antagonized by (+)-amphetamine, desmethylimipramine, dibutyryl cyclic 3'5'-adenosine monophosphate and caffeine.3. The MAO inhibitor nialamide produced only a small antagonism of ouabain, resulting in a greater rate of recovery from the depressant effects of ouabain.4. The depressant effects were associated with a marked elevation of whole-brain dopamine levels with little change in noradrenaline or 5-hydroxytryptamine.5. The dopamine-beta-hydroxylase inhibitor sodium diethyldithiocarbamate, administered by intracerebroventricular injection, produced effects qualitatively similar to those seen after ouabain.6. An interference with central transmitter function is postulated as a possible mode of action of intracerebroventricularly injected ouabain.

Adenine Nucleotides↗