Showing papers in "Journal of Neural Transmission in 1974"
TL;DR: The failure of five putative antagonists to block 5-HT in any of the three areas tested that receive a heavy serotonergic input casts doubt on the assumption that any one of these compounds is a universal central 5- HT antagonist.
Abstract: It has been suggested that drugs block the effects of serotonin (5-HT) in the brain based on (1) the ability to block the effects of 5-HT on smooth muscle and on invertebrate neurons (e.g., cinanserin, cyproheptadine, methysergide [UML], and metergoline [MCE]) and (2) the ability to block certain gross electrophysiological effects of 5-hydroxytryptophan (e.g., methiothepin). Although these “antagonists” are often assumed to block all 5-HT receptors in the CNS, the ability of these drugs to block 5-HT at documented 5-HT synapses in the brain has not been thoroughly tested. Since 5-HT may produce either excitation or inhibition, these antagonists were evaluated with respect to both types of responses. Only inhibition is produced by 5-HT on cells in areas receiving a heavy serotonergic input (e.g., ventral lateral geniculate, optic tectum and amygdala) as determined by fluorescent histochemistry. Raphe cells, virtually the only 5-HT-containing neurons in the CNS, are also inhibited by 5-HT. Cells in the reticular formation, an area which receives little or no 5-HT input may be either excited or inhibited by 5-HT. The five putative antagonists do not block the inhibitory response to 5-HT in any of these areas. The excitatory response to 5-HT in the reticular formation can be blocked by the putative antagonists. However, the failure of these compounds to block 5-HT in any of the three areas tested that receive a heavy serotonergic input casts doubt on the assumption that any one of these compounds is a universal central 5-HT antagonist.
264 citations
TL;DR: The values of L-tyrosine in all investigated areas were increased in parkinsonian patients as well as in L-Dopa psychosis, and 5-hydroxyindoleacetic acid levels show a similar pattern as 5-HT.
Abstract: 1.
In various areas of the brainstem: nucleus caudatus, putamen, gyrus cinguli, oral and caudal part of substantia nigra, nucleus amygdalae, globus pallidus, raphe, and nucleus ruber L-tyrosine, dopamine, noradrenaline, L-tryptophan, serotonin and 5-hydroxyindoleacetic acid were investigated in eight cases of deceased L-Dopa psychosis, six cases of parkinsonian patients without psychotic symptoms, and in nine controls.
2.
The values of L-tyrosine in all investigated areas were increased in parkinsonian patients as well as in L-Dopa psychosis.
3.
The dopamine levels in all areas were decreased in both groups.
4.
Noradrenaline shows moderate slight increase in six out of nine regions in the psychotic group, when compared to parkinsonian patients without psychotic symptoms.
5.
L-tryptophan levels in the psychotic group are decreased in all areas, whereas levels in parkinsonian patients without psychotic symptoms are equal to those of the Controls.
6.
The 5-hydroxytryptamine levels in the psychotic group are increased in eight of nine regions, when compared to parkinsonian patients without psychotic symptoms, predominantly in the nucleus ruber, somewhat less in the raphe, and in the globus pallidus.
7.
5-hydroxyindoleacetic acid levels show a similar pattern as 5-HT.
8.
The loss of balance will be discussed as trigger of the psychotic symptoms.
68 citations
TL;DR: While hypoxia may in part influence monoamine metabolism directly, by reducing the availability of oxygen for oxidative processes, the biochemical consequences of changes in physiological neuronal activities probably contribute to the overall effect and especially to the complex interaction between Hypoxia and shock stress.
Abstract: Rats were exposed to 21, 8 or 6% O2 or to 8% O2 with 5% CO2. After 30 min equilibration, groups of normoxic and hypoxic rats received electrical foot shocks for 15 min through a grid floor. The initial, rate-limiting steps in brain monoamine synthesis were measuredin vivo by determining the accumulation in different brain regions of dopa and 5-hydroxytryptophan (5-HTP), induced by the inhibitor of the aromatic amino acid decarboxylase, NSD 1015 (3-hydroxybenzylhydrazine HCl 100 mg/kg i.p.). In other rat groups a different approach to measuring catecholamine turnover was used, i.e. the depletion of brain dopamine and noradrenaline, induced by the tyrosine hydroxylase inhibitorα-methyltyrosine (400 mg/kg of the methylester HCl i.p.).
63 citations
TL;DR: Changes in distribution of acetylcholine (ACh) along the length of the sciatic nerve of the rat have been studied up to 24 hours after axotomy, and it is suggested that the marked proximal increase in ACh was due to interruption of a proximo-distal transport of ACh and that the small decline in the more distal parts of the nerve wasdue to continued transport of axonal ACh out of that segment of the nerves following operation.
Abstract: 1.
Changes in distribution of acetylcholine (ACh) along the length of the sciatic nerve of the rat have been studied up to 24 hours after axotomy produced usually by crushing but sometimes by cutting or ligating the nerves. The ACh was extracted with trichloracetic acid from 5 mm lengths of nerve cut relative to the lesion and estimated by bio-assay techniques.
2.
Axotomy usually produced an increase in the ACh content in the 5 mm on either side of the lesion within 1–2 minutes of operation. Subsequently there was a continued marked increase in ACh content in the 5 mmproximal to the lesion up to nearly three times the control level by 12 hours, with no further increase by 24 hours. In the 5 mmdistal to the lesion there was a further slight increase up to 60% above control by 6 hours with a subsequent decline to about the control level by 24 hours. In the more distal parts of the nerve (i.e. 5–20 mm distal to the lesion) there was a decline in ACh content of about 20% by 6–12 hours after operation. The three types of axotomy produced similar changes.
3.
The initial small increase of ACh on both sides of the lesion was probably due to local synthesis of ACh, as previously described by other authors. It is suggested that the marked proximal increase in ACh was due to interruption of a proximo-distal transport of ACh and that the small decline in the more distal parts of the nerve was due to continued transport of ACh out of that segment of the nerve following operation; the size of this decline has been taken as an estimate of the proportion of axonal ACh which is rapidly transportable (20% of the total). The rate of transport of this fraction of the axonal ACh has been estimated as about 5 mm/hour. The rest of the axonal ACh is thought to be either stationary or moving slowly with bulk proximo-distal movement of the axoplasm.
48 citations
TL;DR: The data give support to the hypothesis that axotomy of dopaminergic neurons gives rise to an increase in tyrosine hydroxylation due to a receptor-mediated feedback mechanism and the rapid rise in DA after axotomy is caused by increased synthesis, while at the same time DA release and metabolisn are reduced.
Abstract: Axotomy was performed by means of a complete transverse cerebral hemisection in rats at the level of the caudal hypothalamus An inhibitor of the aromatic amino acid decarboxylase, NSD 1015 (3-hydroxybenzyl-hydrazine) was injected at the time of hemisection or 1 to 72 h post operation and the animals killed 30 min later DOPA, accumulating as a consequence of decarboxylase inhibition, tyrosine, noradrenaline (NA), and dopamine (DA) were measured DOPA accumulation on the lesioned side was increased four fold in the corpus striatum and 50% in the dopamine-rich part of the limbic forebrain when measured directly after hemisection When measured 1 1/2 h after hemisection DOPA synthesis had almost returned to control values and stayed constant up to 12 h, while DA levels had increased in c striatum and limbic forebrain to 90%, and 70% above the respective control value After 1–3 days the tyrosine hydroxylation rate on the lesioned side declined below control values, and was accompanied by a drastic fall in DA concentration There were only slight changes on the intact side In the predominantly NA-innervated hemisphere portion changes in DOPA synthesis were less marked
39 citations
TL;DR: DOPAC and 4-hydroxy-3-methoxyphenylacetic acid (HVA) could be determined concomitantly in the same sample, by using the described technique for derivative preparation and an AVA allowing simultaneous recording of 4 mass numbers.
Abstract: A massfragmentographic method for determination of 3, 4-dihydroxyphenylacetic acid (DOPAC) is described. Deuterium labelled DOPAC was used as internal standard. Derivatives suitable for GC-MS were prepared by reacting standard solutions and rat brain extracts with pentafluoropropanol and pentafluoropropionic anhydride. Fragments set into focus were m/e 592/597 (M+) and m/e 415/420 (M+ −177). The sensitivity was in the pmole range with high specificity as tested by multiple ion analysis. The DOPAC level in rat striatum was 6.0 ± 1.1 nmoles/g with an experimental error below 8.5%. The recovery of 575 pmoles DOPAC added to brain extracts was 91 %. Treatment of rats with pargyline (150 mg/kg i.p.) reduced the DOPAC level by about 95% whereas a slight elevation was obtained after administration of chlorpromazine (10 mg/kg i.p.). DOPAC and 4-hydroxy-3-methoxyphenylacetic acid (HVA) could be determined concomitantly in the same sample, by using the described technique for derivative preparation and an AVA allowing simultaneous recording of 4 mass numbers.
39 citations
TL;DR: It is shown that there is a permanent adrenergic control of acetylcholine output, and it is also shown that acetylCholine may regulate its own release by a negative feedback mechanism.
Abstract: Noradrenaline and adrenaline inhibit acetylcholine release due to nerve activity, through α-adrenoceptors. The inhibition of acetylcholine release by the adrenergic transmitters is, in fact, a rather economical way for the adrenergic (orthosympathetic) nervous system to counteract the parasympathetic nervous system. It is shown that there is a permanent adrenergic control of acetylcholine output. The increase in acetylcholine output after catecholamine depletion or α-blockade of nervous tissue only represents partial removal of an adrenergic restraint. The modulatory role of catecholamines on acetylcholine release mechanism seems to be of physiological importance. Furthermore, it is also shown that acetylcholine may regulate its own release by a negative feedback mechanism. Although this mechanism operates in brain cortex, no such phenomenon, however, was found in the Auerbach plexus.
36 citations
TL;DR: The daily rhythm of HVA, VMA, (VA) and 5-HIAA was studied in 21 depressed patients and was compared to the values of 13 healthy subjects, showing a good connexion to the clinical feature with the morning listlessness.
Abstract: The daily rhythm (8–14 h, 14–20 h, 20–2 h, 2–8 h) of HVA, VMA, (VA) and 5-HIAA was studied in 21 depressed patients and was compared to the values of 13 healthy subjects. In healthy subjects all compounds trend to high values during day-time and significant lower values in the nightphase (2–8 h). Depressed patients did not show a significant rhythm during the four fractions; the values of HVA and VMA were significant lowered in the morning-phase (8–14 h). This demonstrates a good connexion to the clinical feature with the morning listlessness. Normal concentrations were reached in the night-phase (2–8 h). 5-HIAA did not show any significance between healthy subjects and depressed patients during the circadian rhythm. The ratio VMA/HVA in healthy subjects fell significant from morning-phase (8–14 h) to night-phase (20–2 h, 22–8 h). In depressed patients the ratio was approximately equal in all fractions. Whereas the ratio 5-HIAA×100/ VMA>+HVA increased from the morning-phase to the night-phase in healthy persons, this ratio did not show any significance in the four fractions of depressed patients.
28 citations
TL;DR: A cobra neurotoxin acts by blocking acetylcholine receptors of mouse fast and slow muscles in an irreversible way and its blocking effect on neuromuscular transmission in an isolated phrenic nerve-hemidiaphragm preparation is dependent upon incubation time and toxin concentration.
Abstract: A cobra neurotoxin (Naja naja siamensis 3) acts by blocking acetylcholine receptors of mouse fast and slow muscles in an irreversible way.
25 citations
TL;DR: It is demonstrated that the same hypothalamic lesion and syndrome of neuroendocrine manifestations occurs following treatment of infant mice with either of two other neuroexcitatory amino acids (L-cysteic or L-aspartic acids) which destroy arcuate neurons but not from a structurally related amino acid (DL-α-aminoadipic acid) which lacks neuro excitatory properties and spares arcsuate neurons.
Abstract: Monosodium L-glutamate (MSG), a neuroexcitatory amino acid is known to destroy hypothalamic (arcuate nucleus) neurons and give rise to subsequent obesity, skeletal stunting and reduced mass of pituitaries, ovaries and testes when administered subcutaneously to infant rodents. Here it is demonstrated that the same hypothalamic lesion and syndrome of neuroendocrine manifestations occurs following treatment of infant mice with either of two other neuroexcitatory amino acids (L-cysteic or L-aspartic acids) which destroy arcuate neurons but not from a structurally related amino acid (DL-α-aminoadipic acid) which lacks neuroexcitatory properties and spares arcuate neurons.
25 citations
TL;DR: Administration of ethanol (2 g/kg, 20% w/v i.p.) to mice produced a significant increase in their locomotor activity and the possibility that this effect of nialamide is mediated by a feed-back mechanism is discussed.
Abstract: Administration of ethanol (2 g/kg, 20% w/v i.p.) to mice produced a significant increase in their locomotor activity. Pretreatment with the monoamine oxidase inhibitor nialamide, whichper se had no marked effect on the locomotor activity, prevented the ethanol-induced locomotor stimulation. The possibility that this effect of nialamide is mediated by a feed-back mechanism is discussed.
TL;DR: Different mechanisms of chemical transmission coexist in advanced nervous systems since, in the distant past, nerve cells originated many times and neurones of a particular ancestry retained a specific type of chemistry from their appearance on.
Abstract: Different mechanisms of chemical transmission coexist in advanced nervous systems since, in the distant past, nerve cells originated many times and neurones of a particular ancestry retained a specific type of chemistry from their appearance on. Diversification of transmission mechanism within the inherited type would be an additional source of transmitter heterogeneity while a kind of selection could reduce the diversity of transmitters during evolution.
TL;DR: It is concluded that physostigmine plus phentolamine, like insulin, appear to stimulate a neurogenic mechanism leading to an activation of adrenomedullary tyrosine hydroxylase, which appears to operate independently of adrenamedullary hormone release and may stimulate catecholamine synthesis even at elevated adrenal catechlamine levels.
Abstract: The adrenomedullary hormone release induced by physostigmine 0.5 to 1 mg/kg i.p. in rats was markedly potentiated by the α-adrenergic blocking agent phentolamine. This drug combination caused a considerable elevation of adrenal dopamine, a decrease in adrenalβ-hydroxylated catecholamines and an increase in plasma catecholamine levels. The monoexponential disappearance of dopamine after treatment with α-methyltyrosine was accelerated by physostigmine plus phentolamine, which thus seem to increase the rate of dopamine synthesis considerably, presumably by activating tyrosine hydroxylase.
TL;DR: The topographical and subcellular distribution of GAD has been studied in Deiters’ nucleus, the cerebellum, hippocampus and substantia nigra, and the effect of lesions of nerve pathways has been examined and showed that GAD is localized in Purkinje cells and probably also in neurones confined to the Cerebellar cortex.
Abstract: The topographical and subcellular distribution of GAD has been studied in Deiters’ nucleus, the cerebellum, hippocampus and substantia nigra, and the effect of lesions of nerve pathways has been examined. The results showed that GAD is localized in Purkinje cells and probably also in neurones confined to the cerebellar cortex. In the hippocampus GAD is localized in intrinsic neurones, some of which are likely to be the basket cells. In the substantia nigra GAD is localized in nerve terminals the density of which may be highest in the pars compacta. The axons to which these terminals belong probably originate in the neostriatum or globus pallidus.
TL;DR: The data indicate that moderate hypoxia may retard the conversion of tyrosine to dopa, which may be related to the O2 requirement of this reaction, however, this effect can be overcome by neurogenic stimuli, presumably via an activation of adrenal tyosine hydroxylase.
Abstract: Hypoxia, with or without hypercapnia, was induced by exposing rats to various gas mixtures for 45 min. In addition, some of the rats were exposed to electrical foot shocks for 15 min. Rats were either untreated by drugs or received inhibitors of catecholamine synthesis or metabolism. The adrenals and blood plasma were analyzed for dopa, and the adrenals for dopamine (DA) and adrenaline + noradrenaline.
TL;DR: A comparison of release of various amines by field stimulation and amantadine indicated that the extragranular binding site prefers amines with a catechol group (NE and dopamine) to those without (octopamine, tyramine) and that the beta hydroxyl group is not a significant factor in binding.
Abstract: Rat heart slices were incubated with tritium-labeled norepinephrine (NE) or other related amines, exposed to amphetamine or electric field stimulation, and the tritium efflux measured. Pretreatment with reserpine plus the monoamine oxidase inhibitor, pheniprazine, greatly decreased NE efflux following field stimulation, but markedly enhanced amphetamine-induced NE efflux. Pretreatment with 6-hydroxydopamine abolished this effect of amphetamine. Treatment of slices with guanethidine,α-methylnorepinephrine or amantadine also abolished or greatly diminished the amphetamine effect, while phenoxybenzamine or tetrabenazine were without effect. Although amphetamine also released metaraminol, an amine shown to be granule bound even in reserpine-treated systems, amantadine did not, suggesting that amantadine releases amines specifically from an extragranular neuronal binding site. A comparison of release of various amines by field stimulation (a measure of granule amine) and amantadine (a measure of extragranular amine) indicated that the extragranular binding site prefers amines with a catechol group (NE and dopamine) to those without (octopamine, tyramine) and that the beta hydroxyl group is not a significant factor in binding. The extragranular binding site may normally serve as a link in the intraneuronal catecholamine transport system.
TL;DR: Aqueous extracts of sheep pineal bodies and sheep cerebral cortex were separated on Sephadex G-25 and G-10 and several distinct peaks could be distinguished showing excitation and fluorescence maxima resembling those of indoles.
Abstract: Aqueous extracts of sheep pineal bodies and sheep cerebral cortex were separated on Sephadex G-25 and G-10. Several distinct peaks could be distinguished showing excitation and fluorescence maxima resembling those of indoles. However, in sheep pineal extract one peak was observed with different excitation and fluorescence maxima which could not be observed in sheep cerebral cortex. Using two-dimensional thinlayer chromatography a substance designated A was isolated and purified, showing excitation maxima at 298 nm and 358 nm, and a fluorescence maximum at 440 nm. Rf values of this substance A in 7 different solvent systems in thinlayer chromatography are presented. The results of paper electrophoresis experiments are also described.
TL;DR: In vagotomized adult cats with the spinal cord transected at T2, short trains of electrical pulses delivered to the central gray substance of the midbrain and the ventral hippocampus initiated a phase reversal in respiration from expiration to inspiration.
Abstract: In vagotomized adult cats with the spinal cord transected at T2, short trains of electrical pulses delivered to the central gray substance of the midbrain and the ventral hippocampus initiated a phase reversal in respiration from expiration to inspiration. A transition from inspiration to expiration, however, was not observed. It is suggested that this phase-switch may be mediated via a reticular formation input into the medulla rather than via the pontine “synchronizing mechanisms”.
TL;DR: It is suggested that granular vesicles contain catecholamines and substance P, and that scorpion toxin by releasing both substances, decreases the number of these vesicle.
Abstract: The effect of purified toxin obtained from the venom of the Brazilian scorpionTityus serrulatus on the small and large granular vesicles and on the large agranular vesicles of the Auerbach's plexus of the rat was investigated. Two segments of the rat ileum were immersed in an isolated organ bath containing Jalon's solution and toxin (15μg/ml) was added to one of these baths (9 exps.). The vesicles were counted in 1300 transversely cut axons and the number of vesicles per 100μ
2 of axonal area was estimated. The toxin did not produce any change in the morphology of the vesicles, but differences in the distribution of the vesicles were found. In the treated group a decrease in the number of the granular (dense) vesicles and an increase in the number of the agranular vesicles was observed. Our findings suggest that granular vesicles contain catecholamines and substance P, and that scorpion toxin by releasing both substances, decreases the number of these vesicles.
TL;DR: In normal rats and in rats subjected to various stimulations known to induce vasopressin release, such as ether-stress, haemorrhage, intracarotic injection of hypertonic saline, and two days of dehydration, the ultrastructural changes of neurosecretory nerve-endings has been analysed.
Abstract: Chez des rats normaux et soumis a diverses stimulations de la liberation de vasopressine (stress a l'ether, hemorragie, injection intracarotidienne hypertonique et deshydratation de deux jours), nous avons analyse les modifications ultrastructurales des terminaisons neurosecretoires. Les granules elementaires conservent leur contenu dense, et leur nombre ne semble pas varier dans de fortes proportions. Chez les rats normaux comme les stimules, des densifications juxtamembranaires sont presentes et des microvesicules de type synaptique sont en contact etroit avec celles-ci. Des images suggerant un processus d'exocytose ont ete observees, mais elles restent toujours tres rares, meme chez les rats stimules, ce qui empeche toute etude quantitative. Des images d'exocytose simultanees a partir d'une meme terminaison ont ete notees. Enfin, des figures suggerent une vesiculisation de la membrane de certains granules apres decharge de leur contenu. Ce phenomene peut etre a l'origine d'une categorie de microvesicules de type synaptique. Une autre categorie de cette population de microvesicules peut etre constituee par micropinocytose. Le nombre global de ces microvesicules est augmente apres stimulation. Si l'existence d'une excretion par exocytose ne peut etre mise en doute, les investigations ultrastructurales visant a determiner son importance dans des circonstances physiologiques restent decevantes. Etant donne que ce mode de liberation est toujours tres difficile a mettre directement en evidence, notre resultat ne peut etre considere comme concluant, du moins quant a un role exclusif de l'exocytose.
TL;DR: In the parkinsonian patients the content of dopamine in the caudate nucleus was raised higher when L-Dopa treatment was combined with a decarboxylase inhibitor than when L -Dopa was given alone.
Abstract: Previous studies have shown that the dopamine content in the caudate nucleus decreases in Parkinson's disease. The present study has corroborated these findings in man andin vivo. In addition for the first timein vivo presence of dopamine in the non parkinsonian human nucleus has been shown morphologically with histofluorescence method. In the parkinsonian patients the content of dopamine in the caudate nucleus was raised higher when L-Dopa treatment was combined with a decarboxylase inhibitor than when L-Dopa was given alone.
TL;DR: Some of the knowledge now available concerning the spinal autonomic processes in the term of sympathetic and parasympathetic reflex paths have been summarized in this chapter.
Abstract: Some of the knowledge now available concerning the spinal autonomic processes in the term of sympathetic and parasympathetic reflex paths have been summarized in this chapter.
TL;DR: Two of the main biochemical features characteristic for oncogenic RNA (oncorna) viruses have been detected in human glioblastoma and a high molecular weight RNA species was found in the subcellular fraction with the highest reverse transcriptase activity.
Abstract: Two of the main biochemical features characteristic for oncogenic RNA (oncorna) viruses have been detected in human glioblastoma. In all tumors tested so far a RNA instructed DNA polymerase (“reverse transcriptase”) activity was present which exhibited the criteria specific for oncorna viruses. It was stimulable by the synthetic polynucleotide poly-rA: oligo-dT, it was almost insensitive to actinomycin D but very sensitive to ethidiumbromide. Using the simultaneous detection test, a high molecular weight RNA species was found in the subcellular fraction with the highest reverse transcriptase activity.
TL;DR: The effect of an experimentally induced stress reaction on the amount of “Gomori-positive” granules, demonstrable in the median eminence of bilaterally adrenalectomized rats was studied and it is assumed that the granules represent the morphological correlate of the corticotropin-releasing factor (CRF).
Abstract: The effect of an experimentally induced stress reaction on the amount of “Gomori-positive” granules, demonstrable in the median eminence of bilaterally adrenalectomized rats was studied. Application of formalin s.c. or histamine i.m. from the 15th to the 17th day p.o., or i.p. injection of Pyrifer® from the 15th to 21st day p.o., with simultaneous administration of 1% NaCl drinking fluid, has no effect on the amount of granules. On the other hand, the amount of granules diminishes if the animals, during a 3-day treatment with formalin, histamine or Pyrifer®, are given solely tap water to drink. Water deprivation from the 15th to the 17th day after bilateral adrenalectomy also causes a marked reduction in the amount of granules. It is assumed that the granules represent the morphological correlate of the corticotropin-releasing factor (CRF). The findings are related to the results of pharmacological studies on the behaviour of the CRF-activity during stress.
TL;DR: The fine structure of synapses was studied in the cat superior cervical ganglion under various experimental conditions and the presence of choline in the performed experiments was found to play an essential role not only in maintaining the intraganglionic nerve transmission, but also in preserving the normalfine structure of presynaptic terminals.
Abstract: The fine structure of synapses was studied in the cat superior cervical ganglion under various experimental conditions. The presence of choline in the performed experiments was found to play an essential role not only in maintaining the intraganglionic nerve transmission, but also in preserving the normal fine structure of presynaptic terminals. Results obtained shed more light on other aspects of the vesicle hypothesis elucidating one of the cellular mechanisms by which the disappearance of synaptic vesicles in stimulated cholinergic nerve terminals could be interpreted.
TL;DR: Unsettled problems concerning the local organization of the intramural nervous system (nerve fibres, ganglion cells and enterochromaffin cells) and the neural control of bowel movement are discussed.
Abstract: The results of neurohistological investigations of the intestine, performed during the last 2 ½ years are presented. The material is based on 98 rectum biopsies (including 43 showing a normal innervation, 28 of morbus Hirschsprung, 6 of atresia ani, 9 of morbus Down, one of Niemann-Pick, 5 of which cases were accompanied by different cerebral symptoms), 8 duodenal biopsies accompanied by different clinical symptoms, and one surgical specimen of the appendix. The clinical relevance and practical diagnostic value of neurohistological investigations on bioptic material of the intestine is discussed. Besides, the progress in research due to more specific techniques now available is demonstrated. Unsettled problems concerning the local organization of the intramural nervous system (nerve fibres, ganglion cells and enterochromaffin cells) and the neural control of bowel movement are discussed.
TL;DR: The release of noradrenaline from the sympathetic nerve endings (varicosities) is discussed in relation to the economy of the amine storage granules, their content of NA, and the rate of contribution of new granules to the nerve terminals via intra-axonal transport.
Abstract: The release of noradrenaline (NA) from the sympathetic nerve endings (varicosities) is discussed in relation to the economy of the amine storage granules, their content of NA, and the rate of contribution of new granules to the nerve terminals via intra-axonal transport.
TL;DR: It is suggested that the cholinergic influence on the normal as well as the caffeine-stimulated locomotor activity requires the cooperation of central catecholamine neurons.
Abstract: The stimulation of locomotor activity induced by caffeine was studied in mice, grouped 3 by 3. Atropine, 8 mg/kg, which by itself did not appreciably stimulate locomotor activity, markedly increased the hyperactivity elicited by 10 mg/kg caffeine. Benztropine also increased the locomotor stimulation observed after caffeine. However, the stimulatory effect of benztropine alone, in contrast to atropine, was apparent even at low doses. Physostigmine, 0.1 mg/kg preceeded by N-methylatropine, 1 mg/kg, slightly if at all decreased the normal locomotor activity. However, it significantly diminished the stimulation elicited by caffeine. Some animals were treated with reserpine, 10 mg/kg, 6 h beforehand. The reserpineinduced suppression of locomotor activity was reversed by combined treatment with ET 495 and clonidine, agents assumed to stimulate central dopamine and noradrenaline receptors, respectively. This reversing effect was increased by caffeine. Atropine or physostigmine did not appreciably affect the ET 495+ clonidine reversal, nor did they change the effect of caffeine. It is suggested that the cholinergic influence on the normal as well as the caffeine-stimulated locomotor activity requires the cooperation of central catecholamine neurons.