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PubMed1991

Effects of an NMDA-receptor antagonist, MK-801, on central locomotor programming in the rabbit.

NMDA has been shown to disclose spinal fictive locomotor activity in various in vitro preparations. In the present work the NMDA-mediated effects of endogenously released excitatory aminoacids (EAA) on fictive locomotion in the adult rabbit preparation were assessed in vivo using systemic injections of a non competitive NMDA-antagonist, MK-801. In acute low spinal and curarized preparations, the amplitude of the "spontaneous" fictive locomotor activities recorded from hindlimb muscle nerves after nialamide-DOPA pretreatment was much decreased in flexor and extensor nerves after MK-801 administration (0.25 mg/kg i.v.) whereas the locomotor period increased slightly. The more potent locomotor bursts, evoked by repetitive sural nerve stimulation at 10 Hz during 10 s, were differently affected after MK-801: the main effect was a lengthening of the locomotor period and a less drastic drop in the burst amplitude. These changes in the burst period were maximal for activities evoked by A fibre group stimulation (+100%) and less when C fibres were recruited (+70%). In decerebrate curarized preparations where the locomotor sequences were evoked either by sural nerve stimulation or by stimulation of the mesencephalic locomotor region, MK-801 (0.25 mg/kg i.v.) caused the same drop in burst amplitude (by at least 50%) as in the spinal preparation but, in contrast, it reinforced rhythmic bursting: this was revealed by a clear shortening (up to -65%) of the locomotor period and by the prolongation of rhythmic bursting after stimulation. All these effects obtained in decerebrate preparations were maximal 20-30 min after MK-801 injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗

PubMed1993

Characterization of hindlimb muscle afferents involved in ventilatory effects observed in decerebrate and spinal preparations.

Neurogenic changes of phrenic activity have previously been observed during periodic passive motions of one hindlimb in decorticate, unanaesthetized and curarized rabbit preparations before and after high spinal transection (Palisses et al. 1988). In decerebrate and spinal preparations, we aimed to determine, through rhythmic electrical stimulation of hindlimb muscle nerves, which muscle afferents are involved in these effects. In decerebrate preparations, these electrical stimulations (trains of shocks at 80 Hz for 300 ms every second for 20 s) produced ventilatory effects when group I + II afferent fibres of either flexor or extensor nerves were stimulated together and more powerful changes as soon as group III fibres were recruited. Stimulation of group I fibres alone induced no such effects. When present, these changes in respiratory activity consisted of a maintained decrease of the respiratory period due to both inspiratory and expiratory time shortening; in addition, the amplitude of the phrenic bursts greatly increased at the onset of electrical stimulation. After spinal transection at C2 level and pharmacological activation by nialamide and DOPA, only short-lasting phrenic bursts developed spontaneously; the electrical stimulation of group II and mainly group III flexor afferent fibres induced large amplitude phrenic activity whereas the stimulation of the same extensor afferents was relatively ineffective. The activation of phrenic motoneurones during group III flexor afferent stimulation was closely linked to each 300 ms period of stimulation. While the phrenic effects obtained in the spinal preparations by natural and by electrical periodic stimulation are quite similar to each other, those produced in decerebrate preparations differ substantially.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1979

On the central generation of locomotion in the low spinal cat.

A central network of neurones in the spinal cord has been shown to produce a rhythmic motor output similar to locomotion after suppression of all afferent inflow. The experiments were performed mainly in acute spinal cats (th. 12), which had received DOPA i.v. and the monoamine oxidase inhibitor Nialamide. In some preparations all dorsal roots supplying the spinal cord were transected, in others phasic afferent activity was suppressed by curarization. The activity was recorded as neurograms from nerve filaments or as electromyograms. It is concluded that: 1. alternating activity between flexors and extensors of foot, ankel, knee, and hip of one limb can still occur 2. the duration of the flexor discharges vary less with the cycle duration than the extensor discharges 3. different flexor muscles may retain individual patterns 4. the activity at different joints can be dissociated 5. there is at least one network for each limb. 6. the coordination between the two hindlimbs can be alternating as in walking or be more closely spaced as in galloping 7. alternating activity in the ankle remains even when only segments L6, L7 and S1 are intact.

Afferent Pathways↗

PubMed1984

Peripheral and central control of flexor digitorum longus and flexor hallucis longus motoneurons: the synaptic basis of functional diversity.

The two long toe flexor muscles in the cat, flexor digitorum longus (FDL) and flexor hallucis longus (FHL), have essentially identical mechanical actions, yet are used very differently during locomotion (O'Donovan et al. 1982). We attempted to identify the origin of the synaptic drive responsible for this functional differentiation. The organization of peripheral and central synaptic drive to FDL and FHL motoneurons was examined using two basic paradigms. (1) In animals anesthetized with chloralose or after ischemic destruction of the brain, peripheral reflex circuits were studied by recording intracellular responses from alpha-motoneurons produced by electrical stimulation of muscular and cutaneous nerves. (2) "Fictive locomotion", the centrally generated rhythmic synaptic drive produced in paralyzed, decerebrate animals by stimulation of the mesencephalic locomotor region or intravenous injection of L-DOPA and Nialamide, was monitored by recording electroneurograms from the central end of cut motor nerves. Despite their functional dissimilarity, FDL and FHL motoneurons received monosynaptic EPSPs from both FDL and FHL la afferents. Ipsilateral cutaneous afferents in the sural nerve and from the central plantar pad produced multiphasic PSPs which were not different in FDL and FHL cells. However afferents from the saphenous and superficial peroneal nerves did exert differential effects: the first component of the multiphasic PSP in most FDL cells was an EPSP, which was not present in most FHL cells. The central latency of this early EPSP in FDL motoneurons (0.8-1.5 ms) strongly suggests a disynaptic linkage. Cutaneous afferents from the ipsilateral forelimb produced IPSPs in most FHL cells but in only one of 18 FDL cells. Since some peripheral reflex circuits exerted differential effects on FDL and FHL cells, but others did not, the intracellular data did not demonstrate that the functional differences between FDL and FHL could be explained by differences in reflex organization. During fictive locomotion elicited by electrical or pharmacological stimulation, FHL motoneurons were coactive with ankle extensors during the extension phase of the fictive step cycle. In contrast, FDL motoneurons were most consistently activated in a brief burst at the onset of the flexion phase, showing much weaker and more variable coactivity with ankle extensors. These patients were essentially identical to those reported for FDL and FHL motor pools during treadmill locomotion by O'Donovan et al. (1982). We conclude that the central pattern generator (CPG) for locomotion produces distinct and highly differentiated sets of instructions for FDL and FHL motoneurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗

PubMed1976

The avian pineal organ. Distribution of exogenous indoleamines: a qualitative study of the rudimentary photoreceptor cells by electron microscopic radioautography.

The uptake of 5-hydroxytryptophan (3H-5-HTP) and serotonin (3H-5-HT) and their distribution have been demonstrated, at the ultrastructural level, in the secretory rudimentary photoreceptor cells (SRP cells), in the pineal organ of the parakeet and the duck. In vivo experiments. When the parakeets were injected with 3H-5-HTP alone or pretreated with drugs interfering with monoamine metabolism (e.g. R04-4602, nialamide) prior to injection of the label, the SRP cells always exhibited specific radioautographic reactions, in the regions of the dense secretory granules of the cell body and asynaptic pedicles. The labeling concentration avried quantitatively with time (interval between injection of the label and sacrifice) and drugs used. In vitro experiments. The uptake of 3H-5-HTP and 3H-5-HT in the pineal organ of the duck has also been studied, using an incubation procedure. The results with the two precursors confirmed those obtained "in vivo" with the parakeet. From these results it is suggested that the uptake of precursors in some compartments of SRP cells is qualitatively independent of: a) the experimental period (experiments performed in winter, spring, and summer; uptake of precursors between 11.00 a.m. and 12.00) b) the precursor (3H-5-HTP or 3H-5-HT) c) the observation times. It is concluded that the SRP cell, an important step in the cytological and functional evolution of the pineal organ (Collin, 1969, 1971), is responsible for the synthesis of 5-HT. The metabolism of 5-HT seems also possible in such cells.

5-Hydroxytryptophan↗

PubMed1983

Evidence for respiratory and locomotor pattern generators in the rabbit cervico-thoracic cord and for their interactions.

In addition to the wellknown fictive locomotion, a fictive respiration can also be obtained in decorticate, unanaesthetized rabbit preparations after curarization and vagotomy. Both patterns were abolished after high spinal (C2 or C3) transection. Spinal rhythmic capabilities could be disclosed after administration of nialamide and DOPA: together with the earlier demonstrated locomotor-like bursting in hindlimb and forelimb muscle nerves, two different types of phrenic bursting patterns could be observed, depending on endtidal CO2 levels: (1) short lasting phrenic bursts (SLPBs), coordinated with locomotor bursts, result of a locomotor driving process; (2) when end-tidal CO2 was slightly increased (4.5 instead of 4.0%), long lasting phrenic bursts (LLPBs) developed: they have no causal link with the locomotor bursts. Intraspinal interactions were shown to operate between these rhythmic patterns: (1) the already mentioned caudo-rostral driving from hindlimb or posterior locomotion generators (pLGs) onto forelimb bursting and onto phrenic activity too (providing SLPBs in the latter case); (2) the rostro-caudal inhibition of fore- and hindlimb locomotor activity throughout each LLPB. Since forelimb locomotor-like bursting and LLPBs could still be obtained after functional isolation of the cervico-thoracic cord (through C2 and Th12 spinal transections) with comparable interactions as before Th12 transection, it is concluded that: two categories of generators, forelimb or anterior locomotion generators (aLGs), and chemosensitive respiration generators (RGs) are both present in this part of the cord, on the one hand; interactions between RGs and pLGs are likely to be achieved via aLGs on the other.

Animals↗

PubMed1988

Phasic modulation of short latency cutaneous excitation in flexor digitorum longus motoneurons during fictive locomotion.

We examined modulation of transmission of short-latency excitation produced by distal hindlimb cutaneous input, as well as fluctuations in motoneuron membrane potential and input resistance, in flexor digitorum longus (FDL) motoneurons during fictive locomotion. Fictive stepping was induced in unaesthetized, decerebrate cats either by repetitive stimulation of the mesencephalic locomotor region (MLR) or by administration of Nialamide and 1-DOPA after low spinal section. In the MLR preparations, brief depolarizing waves occurred in FDL cells during the early flexion phase of fictive stepping, immediately after cessation of activity in extensor muscles. In some FDL cells, plateau-like depolarizations also occurred during the extensor phase. Fictive stepping induced in acutely spinalized cats by administration of 1-DOPA was slower and more variable; peak polarization in FDL motoneurons always occurred during the early flexion phase but there was usually no distinct depolarization during extension. In both types of preparation, the initial EPSP components in synaptic potentials (SP-EPSPs) produced by electrical stimulation of the cutaneous division of the superficial peroneal nerve (SP) were maximally facilitated during early flexion, coincident with the peak of background depolarization. This enhancement was manifested by an increase in the amplitude of initial SP-EPSP components or by decreased central latency of the initial EPSP components, or both. In most FDL motoneurons, input resistance decreased systematically during late flexion, coincident with relative membrane hyperpolarization. Correction of SP-EPSP amplitudes for changes in input resistance suggested that SP-EPSP facilitation persisted throughout the flexion phase. These findings are discussed with reference to modulation of cutaneous reflexes during locomotion and the possibility that excitatory last-order interneurons in particular cutaneous reflex pathways may distribute excitatory drive from the central pattern generator for locomotion to FDL alpha-motoneurons.

Action Potentials↗

PubMed1987

Proprioceptive input resets central locomotor rhythm in the spinal cat.

The reflex regulation of stepping is an important factor in adapting the step cycle to changes in the environment. The present experiments have examined the influence of muscle proprioceptors on centrally generated rhythmic locomotor activity in decerebrate unanesthetized cats with a spinal transection at Th12. Fictive locomotion, recorded as alternating activity in hindlimb flexor and extensor nerves, was induced by administration of nialamide (a monoamine oxidase inhibitor) and L-DOPA. Brief electrical stimulation of group I afferents from knee and ankle extensors were effective in resetting fictive locomotion in a coordinated fashion. An extensor group I volley delivered during a flexor burst would abruptly terminate the flexor activity and initiate an extensor burst. The same stimulus given during an extensor burst prolonged the extensor activity while delaying the appearance of the following flexor burst. Intracellular recordings from motoneurones revealed that these actions were mediated at premotoneuronal levels resulting from a distribution of inhibition to centres generating flexor bursts and excitation of centres generating extensor bursts. These results indicate that extensor group I afferents have access to central rhythm generators and suggest that this may be of importance in the reflex regulation of stepping. Experiments utilizing natural stimulation of muscle receptors demonstrate that the group I input to the rhythm generators arises mainly from Golgi tendon organ Ib afferents. Thus an increased load of limb extensors during the stance phase would enhance and prolong extensor activity while simultaneously delaying the transition to the swing phase of the step cycle.

Afferent Pathways↗

PubMed1989

Modulation of short latency cutaneous excitation in flexor and extensor motoneurons during fictive locomotion in the cat.

We examined modulation of transmission in short-latency, distal hindlimb cutaneous reflex pathways during fictive locomotion in 19 decerebrate cats. Fictive stepping was produced either by electrical stimulation of the mesencephalic locomotor region (MLR) or by administration of Nialamide and 1-DOPA to acutely spinalized animals. Postsynaptic potentials (PSPs) produced by electrical stimulation of low threshold afferents (less than 2.5 times threshold) in the superficial peroneal (SP), sural, saphenous or medial plantar nerves were recorded intracellularly from various extensor (n = 28) and flexor (n = 24) motoneurons and averaged throughout the step cycle, together with voltage responses to intrasomatic constant current pulses (in order to monitor relative cell input resistance). Each motoneuron studied displayed rhythmic background oscillations in membrane potential and correlated variations in input resistance. The average input resistance of extensor motoneurons was lowest during mid-flexion, when the cells were relatively hyperpolarized and silent. Conversely, average input resistance of flexor motoneurons was highest during mid-flexion, when they were depolarized and active. The amplitude of the minimum-latency excitatory components of PSPs produced by cutaneous nerve stimulation were measured from computer averaged records representing six subdivisions of the fictive step cycle. Oligosynaptic EPSP components were consistently modulated only in the superficial peroneal responses in flexor motoneurons, which exhibited enhanced amplitude during the flexion phase. With the other skin nerves tested (sural, saphenous, and plantar), no consistent patterns of modulation were observed during fictive locomotion. We conclude that transmission through some, but not all, oligosynaptic excitatory cutaneous pathways is enhanced by premotoneuronal mechanisms during the flexion phase of fictive stepping in several cat hindlimb motor nuclei. The present results suggest that the patterns of interaction between the locomotor central pattern generator and excitatory cutaneous reflex pathways depend on the source of afferent input and on the identity of the target motoneuron population.

Action Potentials↗

PubMed1976

Characterisation of the mechanisms for hyperactivity induction from the nucleus accumbens by phenylethylamine derivatives.

A wide variety of phenylethylamine derivatives were injected bilaterally into the nucleus accumbens of rat following a nialamide pretreatment and hyperactivity was recorded. 2-Phenylethylamine was shown to induce a low intensity hyperactivity but the introduction of hydroxyl functions on to the phenyl ring at the 3- and/or 4-positions enhanced activity and m- and p-tyramine and dopamine each caused marked hyperactivity in the 3.4-25 mug dosage range. Methylation of one hydroxyl function reduced activity (3-methoxy-4-hydroxy- and 3-hydroxy-4-methoxy-phenylethylamine); 2(3,4-methylenedioxyphenyl) ethylamine was inactive. Agents with substitution of the side chain, such as noradreline, d-amphetamine and alpha-methyldopamine, were all shown to induce marked hyperactivity at doses of 1.6-25 mug. Alterations in the chain length markedly reduced activity (4-(3,4-dihydroxyphenyl) butylamine, 3,4-dihydroxybenzylamine). A variety of N-substituted compounds were shown to be potent inducers of hyperactivity from the nucleus accumbens (adrenaline, epinine, N-ethyldopamine, N-isopropyl-dopamine, isoprenaline) (0.2-25 mug). However, N-methyl-N-isopropyldopamine showed only weak activity and N,N-dimethyldopamine was inactive. All hyperactivity effects were shown to be dose-dependent. The hyperactivities induced by dopamine, noradrenaline and isoprenaline were each inhibited in a dose-dependent manner by subsequent injections of fluphenazine (1.25-25 mug) into the nucleus accumbens, although no reductions were recorded following similar injections of saline, solvent, 2% procaine, 50 mug propranolol or 50 mug piperoxan.

Animals↗

PubMed1977

Locomotor stimulation by L-dopa: relative importance of noradrenaline receptor activation.

The importance of brain noradrenaline synthesis and receptor activation for the hyperkinesia induced by carbidopa plus L-Dopa in reserpine-treated or normal mice was analyzed in four different models. After pretreatment with reserpine and the monoamine oxidase inhibitor nialamide, the hyperkinesia induced by L-Dopa (25 mg/kg i.p.) was partly mediated via stimulation of noradrenaline receptors since it was significantly antagonized by the noradrenaline receptor-blocking agent phenoxybenzamine. Treatment with reserpine plus L-Dopa (125 mg/kg i.p.) produced an increase in motor activity probably due to stimulation of dopamine receptors since it was not accompanied by an accumulation of noradrenaline and it was not inhibited by phenoxybenzamine. The hyperkinesia following treatment with reserpine and a higher dose of L-Dopa (250 mg/kg i.p.) was probably due to stimulation of both dopamine and noradrenaline receptors since the dopamine-beta-hydroxylase inhibitor FLA-63 partly reduced the effect of L-Dopa. Phenoxybenzamine potentiated the motor stimulation by L-Dopa (125 mg/kg i.p.) in mice not pretreated with reserpine, perhaps depending on a slight enhancement of the net accumulation of brain dopamine. Thus, noradrenaline receptor activation is of importance for the L-Dopa-induced hyperkinesia, at least after high doses or after monoamine oxidase inhibition.

Animals↗

PubMed1984

Passive avoidance in rats: disruption by dopamine applied to the nucleus accumbens.

The acquisition of a one-trial step-through passive avoidance task was examined in rats following the administration of nialamide IP and dopamine (DA) or saline into the nucleus accumbens. DA-treated rats displayed impaired learning of the task as evidenced by their lower step-through latencies on a retest trial 7 days later. The specificity of this impairment was studied in a 2 x 2 design involving intracerebral injections prior to both training and testing trials. It was found that DA treatment prior to the training trial disrupted learning or memorization of the task but that DA did not affect performance or retrieval and did not induce state-dependent learning. These findings suggest that DA applied to the nucleus accumbens does not facilitate learning per se.

Animals↗

PubMed1975

A functional effect of dopamine in the nucleus accumbens and in some other dopamine-rich parts of the rat brain.

Dopamine (5 to 50 mug) applied bilaterally to the nucleus accumbens of reserpine-nialamide pretreated rats produced a marked dose-dependent rise in coordinated locomotor activity, devoid of stereotypies such as gnawing, rearing and licking seen after dopamine application (50 mug) to the neostriatum. The locomotor activity was completely blocked by pimozide, but not by phenoxybenzamine. The effects of apomorphine or d-noradrenaline was similar to those of dopamine. In contrast, l-noradrenaline produced a "convulsive" syndrome devoid of coordinated locomotor activity, and this convulsive syndrome could be completely blocked by phenoxybenzamine but not by pimozide. Release of endogenous dopamine by d- or l-amphetamine (10 and 50 mug) in the nucleus accumbens produced a rise in coordinated activity, the d-isomer was about 4 times as potent as the l-isomer, and the effect of the d-isomer was blocked completely by alpha-methyltyrosine. Bilateral application of trifluoperazine (2.5 mug) to the nucleus accumbens completely blocked the effect of systemically administered d-amphetamine (1.5 and 3.0 mg/kg), but similar application to the area of the central nucleus of the amygdala or the neostriatum was much less effective. Partial protection of the endogenous dopamine stores against the depleting action of reserpine by local application of metatyramine to the nucleus accumbens resulted in a higher level of basal activity than in control animals. Application of dopamine or noradrenaline to the area of the central nucleus of the amygdala or to the olfactory tubercles did not lead to any consistent changes in locomotor activity. The nucleus accumbens and olfactory tubercles contained most of the dopamine in the limbic forebrain, with noradrenaline more evenly distributed. These data suggest that the nucleus accumbens plays an important role in the locomotor activity in rats.

Amphetamine↗

PubMed1976

Role of catecholamines in the hypothermic activity of cannabis in albino rats.

Role of brain monoamines in the hyprothermic activity of cannabis resin (CI) in albino rats was studied using agents which influence monoamine synthesis, storage, release, reuptake, metabolism and receptor activity and monoaminergic neuronal activity. Delta-9-tetrahydrocannabinol content of resin was estimated to be 17%. Reserpine was used for comparison. CI was given orally in the dose of 50 mg/kg. Nialamide (NM) and alpha-methyl-metatyrosine (MMT) caused slight hyperthermia. p-Chlorophenylalanine (PCPA), alpha-methol-p-tyrosine (MPT), 5,6-dihydroxytryptamine (DHT, icv) and 6-hydroxydopamine (6-HD, icv) had no effect on body temperature. alpha-Methyl-dopa (m-Dopa), diethyldithiocarbamate (DDC), DDC with l-Dopa, gammabutyrolactone (GBL), phentolamine (PHENT), phenoxybenzamine (PBZ), propranolol (PROP) and imipramine (IMP) produced hypothermia. Hyprothermic activity of CI was potentiated by NM and PCPA, unaffected by DHT and m-Dopa, blocked by MMT, MPT, 6-HD, GBL, PHENT, PROP and chlorpromazine (CPZ), inhibited by DDC, DDC and l-Dopa and PBZ. CI induced hyperthermia in tolerant rats could be reversed to hypothermia by IMP. Reserpine hypothermia was blocked by NM, MPT, 6-HD and CPZ. There was a partial cross tolerance between cannabis and reserpine. Studies indicate that the hypothermic activity of CI similar to that of reserpine is mediated through central catecholamines and not 5-HT, and that noradrenaline is involved and not dopamine. However, the mechanism of action of cannabis and reserpine on noradrenergic neurone seems to be different.

Animals↗

PubMed1975

Neuropharmacological studies on D145 (1,3-dimethyl-5-aminoadamantan).

The effects of D145 (1,3-dimethyl-5-aminoadamantan) and amantadine on dopaminergic mechanisms in the rat were investigated by use of pharmacological agents known to disrupt dopamine function, by placing electrolytic lesions in the dopamine-containing areas of the extrapyrimidal and mesolimbic systems and by the direct application to dopamine sensitive areas. Stereotypy and circling behaviour were used as behavioural indices of dopaminergic stimulation and apomorphine and d-amphetamine were used as standard dopaminergic agonists. In addition, the possible importance of 5-hydroxytryptamine to the dopamine effects was investigated using electrolytic lesions of the midbrain raphé nuclei. Both D145 and amantadine caused a stereotyped behaviour characterized by periodic sniffing, repetitive limb movements and biting, but the effect of amantadine was far more periodic. In addition D145, but not amantadine, caused marked hyperactivity. These behavioural effects were resistant to pretreatment with alpha-methylparatyrosine but not to combined alpha-methylparatyrosine/reserpine or low doses of haloperidol. Also, the prior administration of D145 or amantadine inhibited the development of the biting components of apomorphine and d-amphetamine stereotypy. Both D145 and amantadine caused circling behaviour in animals with asymmetric lesions of the medial raphé nucleus or unilateral lesions of the substantia nigra but the action of D145 was more intense. Bilateral electrolytic lesions placed in the extrapyrimidal (caudate-putamen, globus pallidus, substantia nigra), mesolimbic (nucleus accumbens septi, tuberculum olfactorium, nucleus interstitialis stria terminalis, nucleus amygdaloideus centralis) nuclei or the neuronal pathways supplying them showed D145 and amantadine to act in both areas although their action on the extrapyrimidal system was most marked. However, of particular note was the significantly greater involvement of the substantia nigra with the D145 effect, and the greater involvement of the D145 effect with mesolimbic function. Lesions placed in the medial and/or dorsal raphé nucleus indicated some involvement of 5-hydroxytryptamine with the actions of both D145 and amantadine. The bilateral intrastriatal application of D145 or amantadine in nialamide pretreated animals failed to induce stereotyped or hyperactive behaviour although contralateral asymmetries, which were abolished by lesions of the substantia nigra, were recorded following the unilateral intrastriatal application of D145 or amantadine in haloperidol pretreated animals.

Amantadine↗

PubMed1984

Biochemical and immunohistochemical determination of 5-hydroxytryptamine located in mast cells in the trigeminal ganglion of the rat and guinea pig.

The presence of 5-hydroxytryptamine (5-HT), as well as its precursor (5-HTP) and metabolite (5-HIAA), were biochemically determinated in the trigeminal ganglion of the guinea pig and rat. The distribution of 5-HT in the ganglion and in its posterior root was studied using both indirect immunofluorescence and the peroxidase-antiperoxidase method. In order to increase the possible 5-HT content of primary sensory neurons for subsequent immunohistochemical visualization, animals were first treated with nialamide, an inhibitor of monoamine oxidase, and then loaded with L-tryptophan. Another group of animals received colchicine to inhibit intra-axonal transport of transmitter substances. However, even combined use of loading and colchicine treatment did not reveal 5-HT immunoreactivity in ganglion cells. The only source of 5-HT immunoreactivity in the trigeminal ganglion and its posterior root was mast cells. These cells were located around the ganglion in adjacent leptomeningeal and connective tissues, as well as between the ganglion cells and nerve fibers. Only occasionally were mast cells found in the posterior root of the ganglion.

5-Hydroxytryptophan↗

PubMed1976

Noradrenaline synthesis and utilization: control by nerve impulse flow under normal conditions and after treatment with alpha-adrenoreceptor blocking agents.

The changes in the synthesis and utilization or noradrenaline cranial and caudal to an acute section of the rat spinal cord have been used to investigate the importance of nerve impulses for these processes. 1. Cranial to a lesion of the spinal cord, the alpha-methyltyrosine-induced disappearance of noradrenaline was accelerated by the alpha-adrenoreceptor blocking agents yohimbine (10 mg/kg), piperoxan (60 mg/kg) and tolazoline (50 mg/kg). In the absence of nerve impulses caudal to a lesion of the spinal cord, this disappearance was decelerated as compared to that cranial to the lesion and it was not influenced by the three alpha-adrenoreceptor blocking agents. 2. The nialamide-induced accumulation of normetanephrine in the whole brain was increased by phenoxybenzamine (20 mg/kg) and yohimbine whereas it was decreased by the alpha-adrenoreceptor stimulating agent clonidine (0.1 mg/kg). The effect of clonidine was completely antagonized by yohimbine, but not by phenoxybenzamine, giving further evidence for the view that clonidine and yohimbine have a stronger effect than phenoxybenzamine on the alpha-adrenoreceptors regulating the release of noradrenaline induced by nerve impluses. 3. The accumulation of Dopa after decarboxylase inhibition cranial to a lesion of the spinal cord was accelerated by yohimbine, piperoxan and tolazoline, but not significantly affected by phenoxybenzamine and haloperidol (10 mg/kg). In the absence of nerve impulses caudal to a lesion of the spinal cord, the popa accumulation was decelerated as compared to that cranial to the lesion and it was not influenced by the former three alpha--adrenoreceptor blocking agents as well as by clonidine. 4. The results show that the synthesis and the utilization noradrenaline normally, as well as the accelerations of these processes by alpha-adrenoreceptor blocking agents, are dependent on nerve impulses. The stimulation of the synthesis and utilization of noradrenaline by nerve impulses might by influenced via the activity of teh alpha-adrenoreceptors located either on the nerve terminals or on the cell bodies or on both parts of the noradrenergic neurones. In the absence of nerve impulses, a receptor-mediated feedback mechanism similar to that described for the synthesis of dopamine does not appear to regulate the synthesis of noradrenaline.

Adrenergic alpha-Antagonists↗

PubMed1977

Consecutive demonstration of nerves containing catecholamine and acetylcholinesterase in the rat cornea.

The innervation of the cornea of newborn (two day old) and adult rats was investigated using glyoxylic-acid-induced fluorescence (GIF) for catacholamines and subsequent acetylcholinesterase reaction. Fluorescent nerve were observed around the limbal vessels and in the pericorneal nerve plexus, from which they branched towards the central parts of the cornea. The fluorescent corneal nerves were either nonvaricose or had varicosities at intervals of 10 micra. When the animals had been pretreated with nialamide, noradrenaline and propranolol, some fluorescent branching nerve terminals with numerous varicosities also appeared. All fluorescent nerves disappeared two days after ipsilateral superior cervical sympathectomy. When the acetylcholinesterase (AChE) reaction was performed subsequently to the GIF reaction the following nerve types could be identified: 1. nerves containing both catecholamine (CA) fluorescence and AChE, 2. Nerves containing only AChE.

Acetylcholinesterase↗