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PubMed1998

Excitatory amino acid neurotransmission. Pathways for metabolism, storage and reuptake of glutamate in brain.

In the nervous system, glutamate is an excitatory aminoacid which at higher concentrations has been implicated in a number of disorders. Glutamate is stored in presynaptic vesicles and is released by calcium-dependent exocytosis. After its action on ionotropic receptors (iGluR, related to ionic channels) or metabotropic receptors (mGluR, related to metabolic formation of second messengers), glutamate can be removed from the synaptic cleft through two processes: re-uptake back into pre-synaptic terminals or diffusion out of synaptic cleft for uptake by glial cells. This is achieved by glutamate transporters. In pre-synaptic terminals, glutamate is packed into the specialized secretory vesicles by means of a specific vesicular transporter. The level of glutamate available for neurosecretion is regulated by the vesicular transport activity. In order to achieve a proper concentration of the neurotransmitter in synaptic vesicles, glutamate must be synthesized. Glutamine is obtained in astroglial cells from the glutamate reuptaken, and as it has no neurotransmitter activity, it is the metabolite which regenerates glutamate in neurones (glutamate-glutamine cycle). Moreover, glutamate is also obtained from glucose by an intermediate of TCA cycle. In this paper we want to introduce some aspects of glutamate biosynthesis and release: glutamate receptors, neurotransmitter uptake by the glutamate transporters and neurotransmitter inactivation and new formation by metabolism.

Amino Acid Transport System X-AG↗
PubMed2002

Bi-directional coupling between dihydropyridine receptors and ryanodine receptors.

The control of calcium signaling between plasma membrane dihydropyridine receptors (DHPRs or L-type calcium channels) and ryanodine receptors (RyRs or calcium release channels) located in the endoplasmic/sarcoplasmic reticulum (ER/SR) underlies a broad array of functions including skeletal muscle contraction, cardiac performance, arteriole tone, neurosecretion, synaptic plasticity, and gene regulation. It has long been appreciated that DHPR activation of RyRs and subsequent calcium release from intracellular stores represents a key event in the control of these processes. In excitable cells, DHPRs trigger the release of intracellular calcium by promoting the opening of nearby RyRs (termed orthograde coupling). Interestingly, the signaling interaction between DHPRs and RyRs is often bi-directional such that the calcium-conducting activity of DHPR channels is also regulated by its interaction with the RyR (termed retrograde coupling). Recent data indicate that skeletal, cardiac, and neuronal cells utilize fundamentally distinct DHPR/RyR bi-directional coupling mechanisms (chemical and mechanical) in order to control the efficiency, fidelity, and activity of each of these two essential calcium channels. This review will focus on evaluating the nature and molecular determinants of these coupling mechanisms, as well as the extent to which excitable cell function is influenced by bi-directional DHPR/RyR calcium signaling.

Animals↗
PubMed1990

Potentiation of norepinephrine secretion by angiotensin II in the isolate rabbit iris-ciliary body.

The prejunctional effects of angiotensin II (AII) on stimulation-evoked secretion of 3H-norepinephrine (3H-NE) were investigated by in vitro methods in isolated, superfused rabbit iris-ciliary body preparations. AII (0.1-10 nM) concentration-dependently enhanced the field- stimulated release of 3H-NE (EC50 = 0.1 nM), nearly doubling evoked neurotransmitter release with no apparent effect on spontaneous 3H-NE efflux. The response to 1 nM AII was abolished by the selective AII receptor antagonist saralasin [( Sar1,Val5, Ala8]-angiotensin II; 500 nM), which alone did not modify 3H-NE overflow. AII-mediated effects on neurosecretion were partially additive to those of forskolin and were not potentiated by phosphodiesterase inhibition, suggesting that AII utilizes a mechanism other than increased cAMP synthesis to facilitate neurotransmitter release. AII also strongly enhanced calcium ionophore (A23187)-induced 3H-NE release in iris-ciliary body segments, indicating that AII can modulate calcium-dependent exocytosis at step(s) distal to calcium influx. These results demonstrate that sympathetic nerves in the rabbit eye contain prejunctional, facilitatory AII receptors, and support the possible involvement of the renin-angiotensin system in regulation of ocular sympathetic neurotransmission in vivo.

1-Methyl-3-isobutylxanthine↗
PubMed1982

Human catecholamine storage vesicle proteins.

Catecholamines in the adrenal medulla and sympathetic nerve are stored in vesicles, along with numerous proteins and peptides; both catecholamines and proteins are released by and are markers of exocytosis during sympathoadrenal neurosecretion. The proteins include the enzyme dopamine-beta-hydroxylase and the chromogranins, a group of molecules of largely undetermined function. We have isolated catecholamine storage vesicles (chromaffin granules) from bovine adrenal medulla and human pheochromocytoma. The numerous soluble proteins in the granules: (a) have a spectrum of sizes; (b) have a spectrum of charges; and (c) display considerable interspecies qualitative homology. Dopamine-beta-hydroxylase (DBH) was isolated from human and bovine vesicles by Concanaval in A affinity chromotography. DBH is a tetrameric glycoprotein consisting of 2 non-covalently joined dimeric subunits, each of which is 2 disulfide linked monomers; interspecies molecular weight differences were noted. Ongoing studies concern chromogranin A, the quantitatively major vesicle protein, in bovine and human vesicles.

Adrenal Gland Neoplasms↗
PubMed1988

Angiotensin and the lamina terminalis: illustrations of a complex unity.

The subfornical organ, the median preoptic nucleus, and the OVLT are arranged in a dorsal to ventral column to form the lamina terminalis ("end wall") of the third cerebral ventricle. In the decade of the 1970s, several labs showed that angiotensin II produces many of its effects in the brain by interacting with the structures of the lamina terminalis. This review concentrates on drinking behavior and on two structures: The subfornical organ as an important sensor of blood-borne angiotensin, and the median preoptic nucleus as a sensitive zone for central angiotensin. In the 1980s, histochemistry and tract-tracing have begun to clarify the structural framework for a complex of interactions. All three structures of the lamina terminalis are filled with angiotensin immunoreactive neural processes and angiotensin binding sites. The evidence suggests that angiotensinergic axons have intrinsic and extrinsic origins. Neurosecretion of angiotensin is apparent in some inbred strains of rats. It is concluded that the lamina terminalis is best considered a single functional entity tuned to the detection of fluid imbalance as signaled by angiotensin.

Angiotensin II↗
PubMed1998

Mechanism of peroxide-induced potentiation of sympathetic neurotransmission in bovine irides: role of extracellular calcium.

Hydrogen peroxide (H2O2) and enzymes that regulate its metabolism are present in tissues of the anterior segment of the eye. We have previously shown that in vitro, H2O2 can enhance sympathetic neurotransmission in irides from several mammalian species. In the present study, we investigated the role of extracellular calcium in H2O2-induced potentiation of sympathetic neurotransmission in the bovine isolated iris. Isolated bovine hemiirides were incubated in a bicarbonate-buffered, carbogen-gassed Krebs buffer solution containing [3H]-norepinephrine ([3H]NE) for 60 min. After incubation, tissues were prepared for studies of [3H]NE release using the superfusion method. Release of [3H]NE was elicited by consecutive trains of electrical field stimulation. Removal of calcium from the buffer solution attenuated field-stimulated [3H]NE overflow in isolated, superfused bovine irides without affecting basal tritium efflux. H2O2 (1 mM) enhanced evoked [3H]NE release to the same extent in tissues exposed to buffer solutions containing normal calcium (1.3 mM) as in those containing low calcium (0.13 mM) or zero calcium. However, in the presence of zero-calcium buffer solution containing the chelator, EDTA (1 mM), H2O2 (1 mM) caused a gradual and sustained increase in basal tritium efflux. In buffer solutions containing high calcium (1.95 mM), the magnitude of H2O2-induced increase in field-stimulated [3H]NE release was significantly (P < 0.05) attenuated. Although the neuronal calcium channel antagonist omega-conotoxin (20 nM) inhibited [3H]NE by 25%, it had no effect on H2O2 (1 mM)-induced potentiation of evoked [3H]NE overflow. We conclude that while trace amounts of extracellular calcium are necessary for H2O2-induced enhancement of sympathetic neurotransmission, increasing extracellular (buffer) calcium concentration impaired peroxide-induced enhancement of [3H]NE release. Furthermore, voltage-activated calcium channels may not be directly involved in peroxide-induced alteration of adrenergic neurosecretion in bovine isolated irides.

Animals↗
PubMed2003

Neuronal calcium sensor-1 and phosphatidylinositol 4-kinase beta regulate IgE receptor-triggered exocytosis in cultured mast cells.

We examined the possible occurrence and function of neuronal Ca(2+) sensor 1 (NCS-1/frequenin) in the mast cell line rat basophilic leukemia, RBL-2H3. This protein has been implicated in the control of neurosecretion from dense core granules in neuronal cells as well as in the control of constitutive secretory pathways in both yeast and mammalian cells. We show that RBL-2H3 cells, secretory cells of the immune system, endogenously express the 22-kDa NCS-1 protein as well as an immune-related 50-kDa protein. Both proteins associate in vivo with phosphatidylinositol 4-kinase beta (PI4Kbeta) and colocalize with the enzyme in the Golgi region. We show further that overexpression of NCS-1 in RBL-2H3 cells stimulates the catalytic activity of PI4Kbeta, increases IgE receptor (FcepsilonRI)-triggered hydrolysis of phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)), and stimulates FcepsilonRI-triggered, but not Ca(2+) ionophore-triggered, exocytosis. Conversely, expression of a kinase-dead mutant of PI4Kbeta reduces PI4Kbeta activity, decreases FcepsilonRI-stimulated phosphatidylinositol 4,5-bisphosphate hydrolysis, and blocks FcepsilonRI-triggered, but not Ca(2+) ionophore-triggered, exocytosis. Our results indicate that PI(4)P, produced by the Golgi-localized PI4Kbeta, is the rate-limiting factor in the synthesis of the pool of PI(4,5)P(2) that serves as substrate for the generation of lipid-derived second messengers in FcepsilonRI-triggered cells. We conclude that NCS-1 is involved in the control of regulated exocytosis in nonneural cells, where it contributes to stimulus-secretion coupling by interacting with PI4Kbeta and positive regulation of its activity.

1-Phosphatidylinositol 4-Kinase↗
PubMed1999

Intracellular Ca(2+) oscillations in luteinizing hormone-releasing hormone neurons derived from the embryonic olfactory placode of the rhesus monkey.

To understand the mechanism of pulsatile luteinizing hormone-releasing hormone (LHRH) release, we examined whether cultured LHRH neurons exhibit spontaneous intracellular Ca(2+) ([Ca(2+)](i)) signaling. The olfactory placode and the ventral migratory pathway of LHRH neurons from rhesus monkey embryos at embryonic ages 35-37 were dissected out and cultured on glass coverslips. Two to five weeks later, cultured cells were labeled with fura-2 and examined for [Ca(2+)](i) signaling by recording changes in [Ca(2+)](i) every 10 sec for 30-175 min. Cells were fixed and immunostained for LHRH and neuron-specific enolase. In 20 cultures, 572 LHRH-positive cells exhibited [Ca(2+)](i) oscillations at an interpulse interval (IPI) of 8.2 +/- 0.7 min and a duration of 88.8 +/- 2.9 sec. LHRH-negative neurons in culture exhibited only occasional [Ca(2+)](i) oscillations. In 17 of 20 cultures with LHRH-positive cells, [Ca(2+)](i) oscillations occurred synchronously in 50-100% of the individual cells, whereas [Ca(2+)](i) oscillations in cells in the remaining three cultures did not synchronize. Strikingly, in 12 of 17 cultures the synchronization of [Ca(2+)](i) oscillations repeatedly occurred in complete unison at 52.8 +/- 3.0 min intervals, which is similar to the period observed for LHRH release, whereas in 5 of 17 cultures the less tight synchronization of [Ca(2+)](i) oscillations repeatedly occurred at 23.4 +/- 4.6 min intervals. IPI of [Ca(2+)](i) oscillations in cells with tight synchronization and less tight synchronization did not differ from IPI in cells without synchronization. The results indicate that LHRH neurons derived from the monkey olfactory placode possess an endogenous mechanism for synchronization of [Ca(2+)](i) oscillations. Whether synchronization of [Ca(2+)](i) oscillations relates to neurosecretion remains to be investigated.

Activity Cycles↗
PubMed2000

P2Y purinoceptors inhibit exocytosis in adrenal chromaffin cells via modulation of voltage-operated calcium channels.

We have used combined membrane capacitance measurements (C(m)) and voltage-clamp recordings to examine the mechanisms underlying modulation of stimulus-secretion coupling by a G(i/o)-coupled purinoceptor (P2Y) in adrenal chromaffin cells. P2Y purinoceptors respond to extracellular ATP and are thought to provide an important inhibitory feedback regulation of catecholamine release from central and sympathetic neurons. Inhibition of neurosecretion by other G(i/o)-protein-coupled receptors may occur by either inhibition of voltage-operated Ca(2+) channels or modulation of the exocytotic machinery itself. In this study, we show that the P2Y purinoceptor agonist 2-methylthio ATP (2-MeSATP) significantly inhibits Ca(2+) entry and changes in C(m) evoked by single 200 msec depolarizations or a train of 20 msec depolarizations (2.5 Hz). We found that P2Y modulation of secretion declines during a train such that only approximately 50% of the modulatory effect remains at the end of a train. The inhibition of both Ca(2+) entry and DeltaC(m) are also attenuated by large depolarizing prepulses and treatment with pertussis toxin. Inhibition of N-type, and to lesser extent P/Q-type, Ca(2+) channels contribute to the modulation of exocytosis by 2-MeSATP. The Ca(2+)-dependence of exocytosis triggered by either single pulses or trains of depolarizations was unaffected by 2-MeSATP. When Ca(2+) channels were bypassed and exocytosis was evoked by flash photolysis of caged Ca(2+), the inhibitory effect of 2-MeSATP was not observed. Collectively, these data suggest that inhibition of exocytosis by G(i/o)-coupled P2Y purinoceptors results from inhibition of Ca(2+) channels and the Ca(2+) signal controlling exocytosis rather than a direct effect on the secretory machinery.

Adenosine Triphosphate↗
PubMed2001

Intrahippocampal infusions of k-atp channel modulators influence spontaneous alternation performance: relationships to acetylcholine release in the hippocampus.

One mechanism by which administration of glucose enhances cognitive functions may be by modulating central ATP-sensitive potassium (K-ATP) channels. K-ATP channels appear to couple glucose metabolism and neuronal excitability, with channel blockade increasing the likelihood of neurosecretion. The present experiment examined the effects of glucose and the direct K-ATP channel modulators glibenclamide and lemakalim on spontaneous alternation performance and hippocampal ACh release. Rats received either artificial CSF vehicle or vehicle plus drug for two consecutive 12 min periods via microdialysis probes (3 mm; flow rate of 2.1 microliter/min) implanted in the left hippocampus. During the second 12 min period, rats were tested for spontaneous alternation performance. Dialysate was simultaneously collected for later analysis of ACh content. Both glucose (6.6 mm) and glibenclamide (100 micrometer) significantly increased alternation scores compared with those of controls. Conversely, lemakalim (200 micrometer) significantly reduced alternation scores relative to those of controls. Simultaneous administration of lemakalim with either glucose or glibenclamide resulted in alternation scores not significantly different from control values. All drug treatments enhanced hippocampal ACh output relative to control values. The results demonstrate that K-ATP channel modulators influence behavior when administered directly into the hippocampus, with channel blockers enhancing and openers impairing spontaneous alternation performance, thus supporting the hypothesis that glucose enhances memory via action at central K-ATP channels. That lemakalim, as well as glibenclamide and glucose, increased hippocampal ACh output suggests a dissociation between the effects of K-ATP channel modulators on behavior and hippocampal ACh release.

Acetylcholine↗
PubMed2001

[Peptidergic mechanisms of hypothermia-induced seizures in rats during early ontogenesis].

Arginine-vasopressin reduced the tonic-clonic seizures' latency as well as the duration of the seizures brain-stem generalisation on the 3rd and 5th postpartum days in rats. The reduced latency was also observed after the PACAP38 low doses administration, whereas higher doses diminished and then enhanced the threshold of generalised hyperthermia-induced seizures on the 3rd and 5th days and the 7th and 9th days, resp. The arginine-vasopressin-treated animals had a dramatically enhanced duration of the tonic-clonic seizures up to the epileptic status on the 9th postpartum day. The findings suggest the PACAP involvement in mechanisms of experimental febrile seizures through its effect upon arginine-vasopressin neurosecretion.

Animals↗
PubMed2001

Cdk5 on the brain.

Mammalian brains are highly compartmentalized into groups of functionally specialized neurons. Cell migration and neurite outgrowth must be tightly orchestrated to achieve this level of organization. A small serine/threonine kinase that shows homology to cyclin-dependent kinases (Cdks) has emerged as an important regulator of neuronal migration. Cdk5, unlike other Cdks, is not regulated by cyclins, and its activity is primarily detected in postmitotic neurons in developing and adult nervous systems. This review describes work indicating that Cdk5 links extracellular signaling pathways and cytoskeletal/membrane systems to direct neuronal migration, axon growth, and possibly neurosecretion. Despite its importance, unchecked Cdk5 activity is toxic to neurons, and may underlie some of the pathologies associated with neurodegenerative disorders such as Alzheimer's disease and amyotrophic lateral sclerosis.

Alzheimer Disease↗
PubMed2001

Peptidergic neurohemal system of an insect: mass spectrometric morphology.

Neuropeptides are by far the most diverse group of messenger molecules in insects. To understand cell signaling and function, it is essential to reveal the complete neuropeptide profile of a single neuron/nerve/neurohemal organ first. In this study, matrix-assisted laser desorption ionization time of flight (MALDI-TOF) mass spectrometry was used to analyze the peptidergic system of an insect, focussing on the neurohemal structures. Major neurohemal organs were investigated, including the retrocerebral complex, perisympathetic organs, and all nerves supplying these organs with neurosecretions. Additionally, peripheral neurohemal release sites such as the dilator muscle of the antennal circulatory organ and lateral heart nerves were studied, as well as parts of the stomatogastric nervous system. The following neuropeptide families were analyzed: kinins, allatostatins, leucomyosuppressin, corazonin, adipokinetic hormones, myoinhibitory peptide, sulfakinins, periviscerokinins, YLSamide, VEAacid, SKNacid, proctolin, the head peptide, and pyrokinins. Beyond a contribution to a map of the distribution of neuropeptides in a neurohemal system, the following conclusions can be drawn from these experiments. (1) Nearly all abundant peaks in the different mass spectra represent peptides that have already been identified. (2) Although only adult males were used in this study, variations in the peptide abundances were observed that are possibly correlated with different physiological/developmental conditions. (3) Peptides have a body-region-specific distribution in the neurohemal system. (4) A clear compartmentalisation of the retrocerebral complex could be observed.

Amino Acid Sequence↗
PubMed2000

Hypothalamo-neurohypophysial magnocellular neuroendocrine system of field voles after acute heat or cold stress.

Hypothalamo-neurohypophysial magnocellular neuroendocrine system (H-NH MC NES) of field voles was described in normal conditions and after acute heat or cold stress. 60 mature males of field voles were used for examinations after 2 weeks of adaptation to stable conditions of laboratory keeping. 10 animals were the controls. Another group of 25 field voles were subjected to sudden cold of -15 degrees C for 3 hours. The third group of 25 field voles were subjected to sudden heat of +32 degrees C for 3 hours. Neurosecretory material in paraffin 6 microns sections was stained with paraaldehyde fuchsin (fixed in Bouine fluid in the modyfication of Bock et al. 1968) and tigroid was stained with toluidine blue (fixed in Carnoy fluid). Routine staining with hematoxylin and eosin was used for comparison. It was found that H-NH MC NES in field voles has similar body structure as that described in many reports for laboratory H-NH MC NES of rodents. Supraoptic nucleus (SON) consisted of large multipolar neurocytes and paraventricular nucleus (PVN) consisted of slightly smaller neurocytes. PVN also included areas with small neurocytes. Acute heat or cold stress evoked enhanced concentration of neurosecret in SON and PVN and in the remaining H-NH MC NES structures of field voles simultaneously a decrease of tigroid contents was observed in neurocytes of SON and PVN after heat stress.

Animals↗
PubMed2002

Identification of the differentiation-associated Na+/PI transporter as a novel vesicular glutamate transporter expressed in a distinct set of glutamatergic synapses.

Glutamate transport into synaptic vesicles is a prerequisite for its regulated neurosecretion. Here we functionally identify a second isoform of the vesicular glutamate transporter (VGLUT2) that was previously identified as a plasma membrane Na+-dependent inorganic phosphate transporter (differentiation-associated Na+/P(I) transporter). Studies using intracellular vesicles from transiently transfected PC12 cells indicate that uptake by VGLUT2 is highly selective for glutamate, is H+ dependent, and requires Cl- ion. Both the vesicular membrane potential (Deltapsi) and the proton gradient (DeltapH) are important driving forces for vesicular glutamate accumulation under physiological Cl- concentrations. Using an antibody specific for VGLUT2, we also find that this protein is enriched on synaptic vesicles and selective for a distinct class of glutamatergic nerve terminals. The pathway-specific, complementary expression of two different vesicular glutamate transporters suggests functional diversity in the regulation of vesicular release at excitatory synapses. Together, the two isoforms may account for the uptake of glutamate by synaptic vesicles from all central glutamatergic neurons.

Adenosine Triphosphate↗
PubMed1975

[Large cell neurosecretory nuclei of the anterior hypothalamus of mice following exposure to antibodies to nerve growth factor].

Studies of morphology of the secretory hypothalamo-neurohypophyseal system under conditions of inhibition of the function of the peripheral region of the sympathetic nervous system were carried out. Desympathyzation was achieved by administration to newly born animals of antibodies to the factor of growth of nerves. In addition to the survey histological methods, morphometry, autoradiography and spectrophotometric investigations were also used. The aim of the work was to establish with the help of the methods referred to above the functional state of the hypothalamo-neurohypophyseal secretory system (HNSS) under deep immunological desympathyzation of the organism. The data obtained confirm the existence of a functional connection between the peripheral region of the sympathetic nervous system and HNSS. A hypofunctional state of the sympathetic department caused a rise in the functional activity to HNSS--in supraoptic and paraventricular nuclei of the hypothalamus there were observed enlarged neurones and their nuclei; this was accompanied by an intensification of the biosynthesis processes and secretion of neurosecretory material, neurohypophysis containing lesser amounts of neurosecret than in the norm. The rise of the functional activity of HNSS was accompanied by a higher specific hormonal effect upon the periphery (the effect of the hormone on "target"), which was confirmed by manifestations of working hypertrophy of the medullar of kidneys. The reaction of HNSS was apparently mediated through a complex of pathological changes in the organism and was directed at the maintenance of the optimal tonus of vessels and at preservation of homoestasis as a whole.

Animals↗
PubMed2002

Von Hippel-Lindau tumor suppressor protein transforms human neuroblastoma cells into functional neuron-like cells.

Von Hippel-Lindau (VHL) tumor suppressor protein is expressed in neurons of the central nervous system and plays an important role during the neuronal differentiation of central nervous system progenitor cells. To elucidate the neuronal differentiating potential of VHL protein in neuroblastoma cells, we overexpressed or inhibited VHL protein in human neuroblastoma cells (SY-SH5Y), and examined the morphological change, expressions of neuronal markers, and electrophysiological functions. Here we show that with VHL gene transduction SY-SH5Y cells stably expressing the VHL protein had neurite-like processes with varicosities, showed the distinct expression of the neuronal markers neuropeptide Y and neurofilament 200, acquired regulated neurosecretion competence in response to depolarizing and cholinergic stimuli, and had large voltage-gated fast sodium currents and delayed rectifier potassium (Kv) currents compatible with those of functional neurons. In addition, they displayed inactivated ether-á-go-go potassium channels related to the promotion of the cell cycle and to the termination of differentiation. Also, by treatment with retinoic acid, they rapidly underwent cell death related to apoptosis. These findings suggest that the induction of neuronal function by VHL protein is associated with down-regulation of the cell cycle. In contrast, the inhibition of endogenous expression of VHL protein with antisense-orientated VHL gene transduction reduced such neuronal properties inherent to these cells, including the capacity for activation of ether-á-go-go channels. In conclusion, VHL protein has a neuronal differentiating potential to transform neuroblastoma cells into functional neuron-like cells. Our finding of the neuronal differentiation of neuroblastoma cells under the control of the VHL gene may contribute to the development of clinical techniques for neuronal regeneration in the case of intractable neuronal diseases and for differentiation therapy against neuroblastomas.

Apoptosis↗
PubMed1992

[Stage T1 malignant tumors of the arythenoid. Analysis of a series of 26 cases].

26 malignant tumours of the arytenoid classified as T1 according to the UICC 1987, were treated in the ENT and Cervico-Facial Surgery wards to Hospital Laennec between 1961 and 1990. The natural history of these lesions, locoregional efficiency of the different treatments used, the part played by chemotherapy, survival, causes of death and therapeutic modalities used as a last measure, have been analysed. The frequency of tumours with neuroendocrine has been emphasized. Such a diagnosis should be questioned when the initial biopsy does not diagnose a well differentiated epidermoid carcinoma. The use of argyrophil colouring in order to find neurosecretive granules helps in carrying out the diagnosis. The treatment of tumours, classed T1 N0 M0, of the arytenoid, is based on partial, laryngeal surgery associated with a preventive, jugulo-carotidian-ipsilateral ganglionary intervention.

Actuarial Analysis↗