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PubMed1980

Biphasic effects of thyrotropin-releasing hormone on exploratory behavior in mice.

The neurological mechanism involved in biphasic effects of thyrotropin-releasing hormone (TRH) on exploratory behavior was studied in mice. Intraperitoneal injection of TRH (2.5 mg/kg) induced an increase of ambulation which was followed by subsequent decrease. Pretreatment with nialamide (20 mg/kg i.p.) potentiated the hyperactivity elicited by TRH but failed to affect the subsequent hypoactivity. Tetrabenazine (3 mg/kg i.p.) administered after nialamide markedly increased and sequentially decreased the ambulation, whereas tetrabenazine injected after TRH decreased ambulation as did tetrabenazine alone. TRH administered in combination with and tetrabenazine elicited a pronounced excitation followed by depression, as compared with those elicited by TRH alone or nialamide plus tetrabenazine. The results suggest that TRH induces a biphasic action in exploratory behavior and that this action may involve facilitation of dopamine release which results in an activation of post- and presynaptic dopamine receptors.

Animals↗

PubMed1994

Effect of various serotoninergically induced manipulations on audiogenic seizures in magnesium-deficient mice.

The aim of our study was to analyse the possible implication of the serotoninergic system in the pathophysiology and the lethality of audiogenic seizures induced by magnesium deficiency, either by decreasing cerebral serotonin (5-HT) levels (p-chlorophenylalanine) or by increasing 5-HT levels in the brain (5-hydroxytryptophan, L-tryptophan, nialamide, fluoxetine). In magnesium-deficient mice, the percentages of audiogenic seizures and of fatal seizures were dependent on the time lapse between the p-chlorophenylalanine (PCPA) injection and the audiogenic test. The percentage was at least 24 h after the injection: in OF1 and C57BL/6 strains, PCPA fully protected the mice from seizure occurrence, whereas it only partially protected the animals of the other strains. 5-Hydroxytryptophan caused a decrease in the audiogenic seizures in magnesium-deficient OF1 mice as well as in control DBA/2 mice. In contrast L-tryptophan did not reduce the number of wild courses or of clonic and tonic seizures in either the magnesium-deficient OF1 strain or control DBA/2 mice. Nialamide and fluoxetine were only effective in decreasing the numbers of clonic and tonic convulsions of the audiogenic seizure without affecting the wild courses. The combination of nialamide and tryptophan caused a cessation of the audiogenic seizure phases in both magnesium-deficient OF1 and control DBA/2 mice. In contrast, the fluoxetine-tryptophan combination did not have the same effect on magnesium-deficient and non-magnesium-deficient mice. This work showed that the serotoninergic system plays a secondary role in the pathophysiology of audiogenic seizures in magnesium-deficient mice rather than in that of genetically audiosusceptible mice.

5-Hydroxytryptophan↗

PubMed1996

Neuropharmacological studies on Fusarium toxins--I: Total toxin extract from Fusarium moniliforme.

The neuropharmacological profile of the total fungal extract of F. moniliforme (FM) has been investigated. FM produced dose related decrease in spontaneous motor activity (SMA) and exploratory activity, potentiated pentobarbitone hypnosis and the anticonvulsant actions of phenobarbitone and phenytoin against MES seizures, potentiated PTZ and tryptamine seizures, antagonised reserpine induced syndrome, attenuated tetrabenazine and morphine induced catalepsy and potentiated haloperidol catalepsy. FM showed per se antinociceptive activity and potentiated morphine analgesia. It increased rectal temperature, antagonised reserpine and apomorphine hypothermia and potentiated the hyperthermic response of haloperidol and 5-hydroxytryptophan (5-HTP) and hypothermic response of betaphenylethylamine (PEA) and L-dopa. FM had no per se effect on amphetamine lethality, but enhanced the lethality induced by morphine in aggregated animals. Stereotypy by amphetamine was potentiated while that of apomorphine was not affected. The behavioural response of 5-HTP and L-dopa was potentiated. FM had no effect on swim induced behavioural despair. The effect on aggressive behavior was complex, and while the cumulative aggressive score was reduced, the onset of fighting behaviour and contact period was increased. It also inhibited clonidine induced auto mutilation. Since earlier investigation had shown that FM, like nialamide, induced non-selective inhibition of monoamine oxidase (MAO), the results were compared with those induced by nialamide. A comparative profile of action reveals that the neuropharmacological action of FM are qualitatively similar to those induced by nialamide, and likely to be due to inhibition of MAO. The investigation has practical implications because F. moniliforme is a common contaminant of cereals and fruits.

Analgesics↗

PubMed1991

Effect of catechol oestrogens on extraneuronal metabolism of noradrenaline by rabbit uterine endometrium and myometrium.

The effects of 2-hydroxy and 2-methoxy oestrogens on the extraneuronal O-methylation of 3H-(-)-noradrenaline were examined in progesterone-dominated, monoamine oxidase (MAO)-inhibited, rabbit uterine tissues in vitro. Both the corticosteroid-sensitive system in myometrium and the cocaine-sensitive system in endometrium were examined. In myometrial slices preincubated with nialamide to inhibit MAO and incubated with cocaine to inhibit neuronal uptake, 3H-normetanephrine (3H-NMN) formation was inhibited in the order of potency 2-hydroxy oestrone greater than or equal to 2-hydroxy oestradiol = 2-methoxy oestradiol greater than or equal to 2-methoxy oestrone. In myometrial slices not exposed to cocaine and nialamide, inhibition of 3H-NMN formation by both 2-hydroxy and 2-methoxy oestradiol did not affect the formation of deaminated metabolites of 3H-(-)-noradrenaline by the alternative metabolising pathway. In endometrial slices preincubated with nialamide to inhibit MAO, only 2-hydroxy oestrogens inhibited 3H-NMN formation, but they were one to two orders of magnitude less potent in this regard than in the myometrium. The uptake of 3H-(-)-noradrenaline by MAO- and COMT-inhibited myometrial slices was inhibited by 2-hydroxy and 2-methoxy oestrogens in the order of potency 2-methoxy oestradiol greater than or equal to 2-methoxy oestrone greater than or equal to 2-hydroxy oestrone greater than 2-hydroxy oestradiol. Uptake of 3H-(-)-noradrenaline by endometrial slices was not affected by either 2-hydroxy or 2-methoxy oestrogens.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Methoxyestradiol↗

PubMed1980

Further studies on the effects of 5-hydroxytryptophan on plasma glucose and insulin in the mouse.

The effects of 5-hydroxytryptophan on plasma concentrations of glucose and immunoreactive insulin were examined in conscious mice. Blood samples were obtained after anaesthetizing the mice lightly with ether at the desired time. Large doses of L-5-hydroxytryptophan (5HTP) (200-400 mg/kg IV) produced a dose-dependent hypoglycaemic response in fasted mice (e.g. control 5.7 +/- 0.2 mmol/l, 5HTP 400 mg/kg 2.6 +/- 0.3 mmol/l). This response was preceded by a significant elevation in the plasma immunoreactive insulin concentration (e.g. control 6 +/- 2 mU/l; 5HTP 400 mg/kg 53 +/- 7 mU/l). Induction of diabetes with alloxan (80 mg/kg IV 72 h previously) prevented the hypoglycaemic effect of 5HTP. Alloxan diabetes abolished the hyperinsulinaemic response to 100 mg/kg of 5HTP and reduced by 66% the response to 400 mg/kg of 5HTP. In alloxan diabetic mice 5HTP produced a marked hyperglycaemic response (control 17.9 +/- 2.0 mmol/l; 5HTP 100 mg/kg 36.1 +/- 2.3 mmol/l). In normal mice pre-treated with nialamide, a monoamine oxidase inhibitor, much lower doses of 5 HTP (5-10 mg/kg) were required to produce hypoglycaemia. There was no detectable elevation in the plasma insulin concentration accompanying the hypoglycaemic response to smaller doses of 5HTP in nialamide treated mice. The hyperinsulinaemic and hypoglycaemic actions of 5HTP in normal mice were prevented completely by pretreatment with benserazide, an inhibitor of aromatic amino acid decarboxylase. 5-hydroxytryptamine did not modify the plasma glucose concentration in either normal or nialamide-treated animals. It is concluded that the hypoglycaemic response to 5HTP in normal mice is mediated at least partly through an elevation in the plasma insulin concentration, although it is likely that additional mechanisms are involved.

5-Hydroxytryptophan↗

PubMed1989

Serotonin uptake into cerebrovascular nerve fibers of rat, visualization by immunohistochemistry, disappearance following sympathectomy, and release during electrical stimulation.

Immunohistochemistry as well as in vitro uptake and release of [3H]5-HT were performed on pial arteries of rat to investigate the nature of 5-HT containing nerve fibers. Immunoreactive fibers were constantly found only in the basilar, vertebral and superior cerebellar arteries, while in the other parts of the circle of Willis, 5-HT immunofluorescent fibers were absent. After systemic treatment with tryptophan following inhibition of monoamine oxidase with nialamide the immunofluorescence intensity was markedly enhanced. The 5-HT immunoreactive fibers disappeared after superior cervical ganglionectomy or intraventricular administration of 6-hydroxydopamine, but persisted after administration of 5,6-dihydroxytryptamine. When isolated vessels were incubated in low concentration of 5-HT (1 nM) together with nialamide, a very dense plexus of 5-HT immunoreactive fibers appeared in all branches of the circle of Willis. Uptake and release experiments were carried out by incubation of arterial preparations with 3 nM [3H]5-HT (together with nialamide), followed by electrical field stimulation, or by exposure to tyramine or 124 mM potassium, all of which induced a 100%-350% increase in the tritium release over prestimulation values. Preincubation with cocaine and bilateral superior cervical ganglionectomy abolished or markedly attenuated the release upon all modes of stimulation. The results suggested that the 5-HT observed by immunohistochemistry in pial arteries is located in sympathetic nerve terminals where it may serve as a neuromodulator that is released during nerve activation.

Adrenergic Fibers↗

PubMed1987

The effect of monoamine oxidase inhibitors compared with classical tricyclic antidepressants on learned helplessness paradigm.

The present study investigated the effect of monoamine oxidase inhibitors, nialamide which is a non specific monoamine oxidase inhibitor (MAOI), toloxatone which is a A type MAOI and L-deprenyl which is a B type MAOI compared with classical tricyclic antidepressants (clomipramine, desipramine and imipramine), on the escape deficit induced by inescapable shocks (learned helplessness paradigm). Rats were first exposed to inescapable shock pretreatment (60 shocks, 15 sec duration, 0.8 mA, every minute + 15 sec) and 48 h later, shuttle box training (30 trials/day, 15 min.) was initiated in order to evaluate interference effect. Rats with inescapable shocks exhibited escape and avoidance deficits when tested for subsequent responding in a shuttle-box. Daily i.p. injections of nialamide (8 and 16 mg/kg), toloxatone (16 and 32 mg/kg), L-deprenyl (32 and 64 mg/kg) and tricyclic antidepressants (clomipramine: 16 and 32 mg/kg, desipramine: 16 and 24 mg/kg, imipramine: 16 and 32 mg/kg) eliminated escape deficits. In rat exposed to inescapable shocks and treated with L-deprenyl (16 mg/kg/day), nialamide (32 mg/kg/day) or toloxatone (64 mg/kg/day), avoidance responses are significantly increased as compared with non drugged rats preexposed to inescapable shocks. These data extend previous results bearing on the similarity of action of MAOI and tricyclic antidepressants in learned helplessness paradigm (Sherman et al., 1982) and are in agreement with data obtained in other animal models of depression.

Animals↗

PubMed1980

Rotational behaviour elicited by 5-HT in the rat: evidence for an inhibitory role of 5-HT in the substantia nigra and corpus striatum.

Unilateral intranigral microinjection of 5-HT or Wy 25093, a selective inhibitor of 5-HT uptake, elicited ipsiversive circling and a fall in striatal dopamine (DA) turnover. Conversely intranigral methysergide or unilateral lesions of the raphé-nigral 5-HT pathway produced contraversive turning and/or increased DA turnover. Both types of behaviour were accentuated by nialamide and attenuated by haloperidol. Caudate injections of 5-HT or Wy 25093 provoked contraversive turning which was increased by nialamide and hyoscine, partially diminished by haloperidol and antagonized by eserine. Ipsiversive circling was induced by intracaudate methysergide, which was potentiated by nialamide and eserine, unaffected by haloperidol and depressed by hyoscine. It is proposed that 5-HT normally subserves an inhibitory function both in the substantia nigra and corpus striatum.

Animals↗

PubMedDate not supplied

[The effect of pyrazidol and inkazan on the rotation behavior of rats].

Effect of some MAO inhibitors on rotational behavior induced by d-amphetamine in unilaterally 6-OHDA-lesioned rats was studied. Among all MAO inhibitors tested only 1-deprenyl induced rotational behavior. Nialamide, chlorgiline, pyrazidol and inkazan dose-dependently enhanced rotational behavior induced by 2 mg/kg i. p. d-amphetamine and pargiline depressed it. Nialamide and inkazan greatly enhanced rotational behavior induced by 0.5 mg/kg i. p. d-amphetamine. It is suggested that nialamide and inkazan may have similar effects on DA-ergic neurotransmission.

Animals↗

PubMed1992

Serotonin promotes region-specific glial influences on cultured serotonin and dopamine neurons.

To test the hypothesis that glia mediate interactions between embryonic serotonergic (5-HT) neurons and dopamine neurons, we studied the effects of 5-HT in co-cultures of E14 raphe neurons of mesencephalic dopamine neurons and radial glia/astrocytes derived from the same (homotypic) or opposite (heterotypic) brain region using a dose (10(-5) M) that would produce 5-HT uptake into glial cells as well as activate 5-HT receptors. Morphometric analysis of 5-HT and tyrosine hydroxylase (TH) immunoreactive neurons revealed regional differences in the effects of 5-HT (and nialamide) on survival, cell soma size, and dendrite-like neurite outgrowth in neuronal-glial co-cultures. In general, 5-HT had more significant effects on both types of monoamine neuron when they were cultured with mesencephalic glia (GSN). Stimulatory effects of 5-HT on growth of TH neurons in GSN cultures suggest that developing raphe axons, which reach the mesencephalon during the early differentiation of these neurons, may enhance the influence of local glial-derived trophic factors. Likewise, the promotion of 5-HT neuronal survival in these cultures suggests that glial factors in the mesencephalon may contribute to the support of 5-HT neurons in addition to the influences of raphe glia. The inhibitory effects of 5-HT on neurite outgrowth by raphe neurons in GSN co-cultures indicates enhanced sensitivity of these neurons to the inhibitory effects of 5-HT in the presence of mesencephalic glia. The region-specific effects of 5-HT and nialamide in glial co-cultures suggest that raphe and mesencephalic glia may express different capacities for 5-HT uptake, receptors, and/or monoamine oxidase (MAO) activities. These characteristics could be important for the specificity of growth-regulatory influences of glial cells on the development of brain monoamine neurons.

Animals↗

PubMed1999

Sources of reactive oxygen species production in excitotoxin- stimulated cerebellar granule cells.

Reactive oxygen species (ROS) production in rat cerebellar granule cells in the presence of the excitotoxins N-methyl-d-aspartate (NMDA) and kainic acid (KA) and by the protein kinase C activator phorbol myristate acetate (PMA) was Ca2+-dependent and resulted in decreased cell viability. Exposure of stimulated cells to rotenone (a respiratory chain inhibitor) did not decrease ROS levels and did not affect short-term cell viability. In cells stimulated by NMDA and KA, exposure to indomethacin (a cyclooxygenase inhibitor) and nialamide (a monoamine oxidase inhibitor) caused a decrease in ROS levels and increased cell viability occurred in NMDA-treated cells. In contrast, PMA-stimulated neurons did not show decreased ROS levels when exposed to indomethacin and nialamide. These studies suggest that there is a multiplicity of routes for Ca2+-dependent ROS production in neurons but that ROS generation by cyclooxygenase and monoamine oxidase is not controlled by protein kinase C.

Animals↗

PubMed1994

Effects of befloxatone, a new potent reversible MAO-A inhibitor, on cortex and striatum monoamines in freely moving rats.

Single administration of befloxatone (0.75 mg/kg, i.p.) in the rat increased extracellular levels of DA (+300%) in striatum. In frontal cortex, befloxatone (0.75 mg/kg, i.p.) and nialamide (100 mg/kg, i.p.) increased NA by +100% but did not modify 5HT, whereas pargyline (100 mg/kg i.p.) increased extracellular NA and 5HT by 400 and 600%, respectively. At these doses, befloxatone inhibited totally and selectively MAO-A, pargyline inhibited totally MAO-A and MAO-B. Increases of tissue and extracellular concentrations of NA and 5HT were highest after Pargyline suggesting that both monoamines may be metabolized by MAO-A and MAO-B. Befloxatone and nialamide potentiated the effects of idazoxan (20 mg/kg, i.p.) on extracellular NA in frontal cortex, which increased from 350% to 2,000 and 1,500% respectively. These results suggest that alpha 2-adrenoceptors play a major role in the regulation of extracellular NA in frontal cortex.

Animals↗

PubMed1975

5-HT nerve terminals in the fourth ventricle of the rat brain: their identification and distribution studied by fluorescence histochemistry and electron microscopy.

The occurrence and distribution of supra-ependymal nerve terminals storing serotonin (5-HT) are described for the fourth ventricle of the rat brain. The nerve terminals were identified as monoaminergic 1) fluorescence-histochemically, by the presence of a varicose, formaldehyde-induced fluorescence (FIF) on the free surface of the ependyma, 2) electron microscopically, by the presence of electron dense (chromaffin) cores in small (50nm) and large (100 nm) vesicles found within the varicose regions of supra-ependymal nerve fibres, and 3) by the absence of both the FIF and chromaffin dense cores after treatment with reserpine. Moreover, the serotonergic nature of these nerve fibres could be concluded from 1) the yellow colour of the FIF, 2) the increased FIF after treatment with nialamide or reserpine+nialamide, 3) the diminished FIF and absence of chromaffin dense cores after treatment with p-CPA, and finally 4) the persistence of the FIF anc chromafin dense cores after treatment with alpha-MPT. A high density of 5-HT nerve terminals occurred throughout the floor of the fourth ventricle and on the floor and roof of the lateral recess. Few 5-HT nerve terminals occurred only on the roof of the fourth ventricle (velum medullare, lamina epithelialis of the tela chorioidea), and the surface of the choroid plexus epithelia was devoid of such nerves. Virtually all nerve terminals in the fourth ventricle appear to be serotonergic.

Animals↗

PubMed1982

alpha-methyl-p-tyrosine inhibition of a conditioned avoidance response: reversal by dopamine applied to the nucleus accumbens.

These experiments sought to determine whether dopamine (DA) could reverse the depressive effects of alpha-methyl-p-tyrosine (AMPT) on a conditioned avoidance response (CAR). Rats were randomly allocated to shocked groups (CAR-trained) and non-shocked (CAR-naive) groups. The CAR-trained rats, conditioned to avoid an electric shock, were administered AMPT (150 mg/kg at -24 h and 50 mg/kg at -1 h, both IP), nialamide (80 mg/kg IP at -1 h) and saline (1 microliter) or DA (5 or 10 micrograms/microliters, dissolved in 1 microliter saline, at time 0) directly into the nucleus accumbens. The rats were then tested for CAR at 0.5, 1, 2, 3, 4, 8, 12, 24 an 48 h. The CAR-naive rats, conditioned to the behavioural environment without electric shock being presented, were administered AMPT, nialamide and DA or saline as above. Both doses of DA antagonised the AMPT-induced suppression of the CAR in the CAR-trained rats, reaching a maximum 2-4 h after its local application. In the CAR-naive rats, DA produced a "pseudo-CAR' that lasted about 4 h, but which completely disappeared at 8 h when the DA effect had worn off. These CAR-naive rats did not learn a CAR under the influence of DA. In a third group of rats, DA produced locomotor activation which, in its time course, resembled the effect of DA on CAR. It is concluded that the ability of DA to antagonise AMPT-induced depression of CAR is, in all likelihood, dependent upon DA-induced locomotor excitation, rather than upon an effect of DA on associative learning.

Animals↗

PubMed1982

Prevention of the serotonin syndrome in rats by repeated administration of monoamine oxidase inhibitors but not tricyclic antidepressants.

The serotonin syndrome, a behavioral response produced by the activation of serotonin receptors, and 3H-serotonin binding were examined after repeated treatment of rats with different types of antidepressant drugs. The serotonin syndrome was produced by the direct-acting serotonin receptor agonists 5-methoxy-N,N-dimethyltryptamine (5-MeDMT) or d-lysergic acid diethylamide (LSD). Repeated, but not acute treatment of rats with monoamine oxidase inhibitors (nialamide, pargyline, and phenelzine) prevented the serotonin syndrome in response to either 5-MeDMT or LSD and also reduced 3H-serotonin binding in the brain stem and spinal cord. Pretreatment of rats with p-chlorophenylalanine blocked the ability of nialamide treatment to inhibit the serotonin syndrome caused by 5-MeDMT. By contrast, neither the serotonin syndrome or 3H-serotonin binding was affected significantly by the repeated administration of tricyclic antidepressants (amitriptyline, desmethylimipramine, and chlorimipramine) or iprindole. Repeated monoamine oxidase inhibitor treatments may prevent the serotonin syndrome by causing a reduction of 3H-serotonin receptor binding sites in the brain stem and/or spinal cord.

Animals↗

PubMed1979

Selective stimulation of central alpha-autoreceptors following treatment with alpha-methyldopa and FLA 136.

1. The accumulation of normetanephrine in the rat brain induced by the monoamine oxidase inhibitor nialamide was inhibited following alpha-methyldopa and 4-amino-3-(2,6-dichlorobenzylidenehydrazino)-1,2,4-triazole (FLA 136). It was not changed following alpha-methylmetatyrosine despite a greater disappearance of noradrenaline than after alpha-methyldopa. The alpha-adrenoreceptor blocking agent yohimbine increased the nialamide-induced accumulation of normetanephrine and completely antagonized the actions of alpha-methyldopa and FLA 136, indicating that the effects of the two drugs are due to stimulation of alpha-adrenoreceptors. 2. The flexor reflex activity of spinalized rats was not influenced by alpha-methyldopa and alpha-methylmetatyrosine at the doses used in the biochemical experiments, as previously found for FLA 136, indicating no stimulation of classical, postsynaptic, central alpha-adrenoreceptors. 3. The biochemical effects of alpha-methyldopa and FLA 136 might be caused by stimulation of alpha-autoreceptors on the cell bodies and the nerve terminals of noradrenaline neurons. A similar mechanism might be involved in the hypotension reported by other investigators following these drugs.

Adrenergic alpha-Agonists↗

PubMed1979

Ultrastructural localization of monoamines in nerve fibers of the pineal gland in golden hamsters.

Nerve terminals in the pineal glands of control, parachlorophenylalanine (PCPA)-, reserpine- and nialamide-administered hamsters were studied with glutaraldehyde-dichromate (GD) and formaldehyde-glutaraldehyde-dichromate (FGD) techniques in the electron microscope. In control pineals treated with the FGD or GD technique, clusters of electron dense reactive particles with a diameter of 20-30 nm, and mainly located in the perivascular space, were identified as dense cores of the small granulated vesicles (SGVs) in the pineal nerve fibers. After the administration of PCPA, the reactive cores were greatly decreased in number in the FGD-treated pineal blocks, whereas a lot of clusters of reactive cores were observed in the perivascular space in GD-treated specimens. After reserpine treatment, no reactive structures were revealed by GD or FGD technique. Reactive cores appeared to be increased in number and in electron density in GD- or FGD-treated pineals of hamsters after administration of nialamide. From the observations, it is concluded that the dense cores of SGVs in the pineal nerve fibers contain both primary catecholamines and 5-hydroxytryptamine although it was not determined whether both amines are located in the same or separate vesicles.

Animals↗

PubMed1980

Indoleamines in the pineal complex of Lampetra planeri (Petromyzontidae). A fluorescence microscopic and microspectrofluorimetric study.

Using the technique of Falck and Hillarp, the pineal and parapineal organs of Lampetra planeri were found to exhibit a labile yellow fluorescence characteristic of indoleamines. Microspectrofluorimetric analysis of the yellow fluorophores yielded emission and excitation spectra very similar to those of the melatonin precursors serotonin (5-HT) or 5-hydroxytryptophan (5-HTP). 5-HT/5-HTP fluorophores are concentrated essentially in the region of the atrium, along the pineal tract and in the rostral part of the parapineal organ. The fluorescence is strong in early autumn, decreases in winter and is weak or absent in spring, implying a seasonal variation in indoleamine metabolism. Fluorescence intensity increases after injections of nialamide or nialamide and 5-HTP and is lowered by injection of reserpine. Indoleamine fluorescence is localized in the recently identified sensory-type cells: the photoneuroendocrine cells (Meiniel, 1980). The ependymal-like cells, the sensory neurons and the classical photoreceptor cells (Collin, 1969 a) do not appear to be involved in indole metabolism. The absence of catecholamine fibres in the perivascular spaces suggests that indole biosynthesis is regulated via the direct photosensitivity of the pineal complex.

5-Hydroxytryptophan↗