833 resultados para cholinergic neurotransmission


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In this study we investigated the effect of the anteroventral third ventricle (AV3V) lesion on the pressor, bradycardic, natriuretic, kaliuretic, and dipsogenic responses induced by the injection of the cholinergic agonist carbachol into the lateral preoptic area (LPOA) in rats. Male Holtzman rats with sham or electrolytic AV3V lesion were implanted with stainless steel cannula directly into the LPOA. Injection of carbachol (7.5 nmol) into the LPOA of sham rats induced natriuresis (405 ± 66 μEq/120 min), kaliuresis (234 ± 44 μEq/120 min), water intake (9.5 ± 1.7 ml/60 min), bradycardia (-47 ± 11 bpm), and increase in mean arterial pressure (28 ± 3 mmHg). Acute AV3V lesion (1-5 days) reduced the natriuresis (12 ± 4 μEq/120 min), kaliuresis (128 ± 27 μEq/120 min), water intake (1.7 ± 0.9 ml/60 min), and pressor responses (14 ± 4 mmHg) produced by carbachol into the LPOA. Tachycardia instead of bradycardia was also observed. Chronic (14-18 days) AV3V lesion reduced only the pressor response (10 ± 2 mmHg) induced by carbachol. These results showed that acute, but not chronic, AV3V lesion reduced the natriuretic, kaliuretic, and dipsogenic responses to carbachol injection into the LPOA. The pressor response was reduced in acute or chronic AV3V-lesioned rats. The results suggest that the lateral areas may control the fluid and electrolyte balance independently from the AV3V region in chronic AV3V-lesioned rats. © 1992.

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We studied the nicotine stimulation of the amygdaloid complex (AMG) on sodium and water intake in satiated and water-deprived rats. Nicotine produced no change in sodium or water intake in satiated animals when injected directly into the AMG. In water-deprived animals, nicotine injected into the AMG (basolateral nuclei) only blocked sodium chloride intake. We have previously demontrated that carbachol inhibits water and sodium intake in both satiated and water-deprived animals injected into the AMG. Injection of hexamethonium into the AMG totally blocked water intake in satiated and water-deprived animals. Hexamethonium injected into the AMG prior to nicotine produced no change in sodium intake. Thus, the present data suggest that sodium and water intake are mediated by a specific population of cholinoceptive neurons in the amygdaloid complex.

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We investigated the effects of losartan, an AT 1-receptor blocker, and ramipril, a converting enzyme inhibitor, on the pressor response induced by angiotensin II (ANG II) and carbachol (a cholinergic receptor agonist). Male Holtzman rats (250-300 g) with a stainless steel cannula implanted into the lateral ventricle (LV) were used. The injection of losartan (50 nmol/l μl) into the LV blocked the pressor response induced by ANG II (12 ng/l μl) and carbachol (2 nmol/l μl). After injection of ANG II and carbachol into the LV, mean arterial pressure (MAP) increased to 31 ± 1 and 28 ± 2 mmHg, respectively. Previous injection of losartan abolished the increase in MAP induced by ANG II and carbachol into the LV (2 ± 1 and 5 ± 2 mmHg, respectively). The injection of ramipril (12 ng/l μl) prior to carbachol blocked the pressor effect of carbachol to 7 ± 3 mmHg. These results suggest an interaction between central cholinergic pathways and the angiotensinergic system in the regulation of arterial blood pressure.

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The present study was undertaken to look for the effect of chloroethylclonidine (CEC) on prejunctional alpha-2 autoreceptors of the canine saphenous vein. The effect was tested on tritium overflow evoked by electrical stimulation from tissues preloaded with 0.2 μM 3H- norepinephrine. Yohimbine (3-300 nM) and CEC (1-125 μM) increased and UK- 14,304 reduced the overflow of tritium evoked by 300 pulses (1 Hz). The maximal increase of tritium overflow caused by yohimbine was much higher than that caused by CEC: 3.82 and 1.74 times, respectively. CEC (5 μM) abolished both the inhibition caused by UK-14,304 and the enhancement of tritium overflow caused by yohimbine. However, when CEC was added after yohimbine, it reduced the electrically evoked overflow of tritium, the maximal effect being a reduction of tritium overflow by 35%. Prazosin (1-100 nM) did not change either the inhibitory effect of UK-14,304 or the facilitatory effect of CEC. These results suggest that CEC acts on two different subtypes of prejunctional alpha-2 autoreceptors; on one of them it acts as an antagonist and increases the electrically evoked overflow of tritium (and inhibits both the effect of UK-14,304 and yohimbine); on the other it acts as an agonist and reduces the electrically evoked overflow of tritium. Alternatively, one can admit that CEC is able to inhibit alpha-2 autoreceptors, which causes an increase of the transmitter release, and to activate a nonadrenergic inhibitory receptor thus causing a reduction of the transmitter release.

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Background and Objectives. The analgesic actions of nonsteroidal anti-inflammatory drugs (NSAID) result from the inhibition of the peripheral synthesis of prostaglandins. In spite of the emphasis on the peripheral action, several studies have shown the potential central action of such drugs. In rats, NSAID doses insufficient to block pain when systemically administered were effective when intrathecally injected. This effect could be mediated by interaction with descending serotoninergic ways together with neurotransmission modulation of glycine or N-methyl-D-aspartate receptors. Our goal was to study the effect of different tenoxican doses in the histology of dogs spinal cord and meninges. Methods. Thirty two dogs (7 to 17 kg) were randomly distributed in four groups: G1 - Control with distilled water (DW); G2 - 2 mg tenoxican diluted in DW; G3 - 4 mg tenoxican diluted in DW; G4 - 10 mg tenoxican diluted in DW in a constant volume of 1 ml. Anesthesia was induced with etomidate and fentanyl and dural puncture was performed with a 25G spinal needle in interspace L6-7. Animals were observed for 72 hours and subsequently euthanized by electrocution. Lumbar and sacral spinal cord segments were removed for further histologic examination. Results. All animals were clinically normal during the observation period and there has been no histologic alteration of the nervous system and meninges. Conclusions. In our experimental model intrathecal tenoxican doses up to 10 mg have not triggered nervous tissue or meningeal injuries in dogs.

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Studies of the effect of ethanol on human visual evoked potentials are rare and usually involve chronic alcoholic patients. The effect of acute ethanol ingestion has seldom been investigated. We have studied the effect of acute alcoholic poisoning on pattern-reversal visual evoked potentials (PR-VEP) and flash light visual evoked potentials (F-VEP) in 20 normal volunteers. We observed different effects with ethanol: statistically significant prolonged latencies of F-VEP after ingestion, and no significant differences in the latencies of the PR-VEP components. We hypothesize a selective ethanol effect on the afferent transmission of rods, mainly dependent on GABA and glutamatergic neurotransmission, influencing F-VEP latencies, and no effect on cone afferent transmission, as alcohol doesn't influence PR-VEP latencies.

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In this review the definition of COPD is presented and the epidemiology and risk factors for disease development are briefly discussed. Characteristics clinical features, pulmonary functions indices, radiologics signs and arterial blood gases alterations are presented and discussed. Classification of disease severity and components of COPD management are also described.

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To quantify psychoactive drug use and investigate use-related variables among students of Assis, Brazil, a questionnaire was administered to collect sociodemographic data and identify the pattern of non-medical use of psychoactive drugs in 20% of public and private school students. The largest consumption indexes for lifetime use were seen for alcohol (68.9%) and tobacco (22.7%). Drugs most often used were: solvents (10.0%); marijuana (6.6%); benzodiazepines (3.8%); amphetamines (2.6%); cocaine (1.6%); and anticholinergics (1.0%).

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Alzheimer's disease (AD) is a progressive neurodegenerative pathology with severe economic and social impact. There is currently no cure, although cholinesterase inhibitors provide effective temporary relief of symptoms in some patients. Nowadays drug research and development are based on the cholinergic hypothesis that supports the cognition improvement by regulation of the synthesis and release of acetylcholine in the brain. There are only four commercial medicines approved for treatment of AD and natural products have played an important role in the research for new acetylcholinesterase inhibitors.

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The chronic obstructive lung disease is reviewed with emphasys on its epidemiology and risk factors. The diagnosis, clinical aspects pulmonary, functional alterations and laboratorial findings are discussed. The treatment is also reviewed, based on the actual consensus, considering the following classes of approaches: bronchodilators, inhaled β-agonists, corticoids, methilxanthines, prolonged domiciliar-orygen therapy.

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The maintenance of the arterial pressure in normal levels is important for the homeostasis of body fluids. The central nervous system regulating sympathetic and parasympathetic autonomic efferent can adjust arterial pressure which allows animals or human to face different daily activities with the best performance. Different central areas are responsible for the control of autonomic discharges to cardiovascular system and many of them are also involved in the control of fluid electrolyte balance. One of these areas is the tissue surrounding the anteroventral third ventricle (AV3V region) localized in the forebrain and a main central site for angiotensin II receptors and osmoreceptors. The AV3V lesions impair the development of many models of experimental hypertension in rats and the pressor responses to different stimuli. Lesions of the AV3V region also reduce dipsogenic responses to angiotensin II, central cholinergic activation, water deprivation and increase in plasma osmolarity, atrial natriuretic peptide secretion produced by body fluid expansion and the increase in renal excretion to central cholinergic activation. Recent evidence also suggests the participation of AV3V region in pressor responses produced by the activation of medullary mechanisms.

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The neuromodulatory effect of nitric oxide (NO) on glutamatergic transmission within the NTS related to cardiovascular regulation has been widely investigated. Activation of glutamatergic receptors in the NTS stimulates the production and release of NO and other nitrosyl substances with neurotransmitter/neuromodulator properties. The presence of NOS, including the protein nNOS and its mRNA in vagal afferent terminals in the NTS and nodose ganglion cells suggest that NO can act on glutamatergic transmission. We previously reported that iontophoresis of L-NAME on NTS neurons receiving vagal afferent inputs significantly decreased the number of action potentials evoked by iontophoretic application of AMPA. In addition, iontophoresis of the NO donor papaNONOate enhanced spontaneous discharge and the number of action potentials elicited by AMPA, suggesting that NO could be facilitating AMPA-mediated neuronal transmission within the NTS. Furthermore, the changes in renal sympathetic discharge during activation of baroreceptors and cardiopulmonary receptors involve activation of AMPA and NMDA receptors in the NTS and these responses are attenuated by microinjection of L-NAME in the NTS of conscious and anesthetized rats. Cardiovascular responses elicited by application of NO in the NTS are closely similar to those obtained after activation of vagal afferent inputs, and L-glutamate is the main neurotransmitter of vagal afferent fibers. In this review we discuss the possible neuromodulatory mechanisms of central produced/released NO on glutamatergic transmission within the NTS.

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The control of the blood pressure depends on the activity of select groups of neurons present in the central nervous system. Evidence has demonstrated that the redox state (a balance between oxidizing and reducing species) is involved in the control of neuronal activity, which suggests that the redox state can influence the neuronal transmission within the central nervous system acting on the neuronal modulation of biological functions. For instance, the glutamatergic transmission may be widely affected by reactive oxygen species, oxidizing agents that have been extensively investigated due to their involvement in physiological and pathological processes. In the present article, we discuss the main experimental finds that support the hypothesis that reactive oxygen species have important role in physiological (and pathological) modulation of the cardiovascular function through alterations in the sympathetic and parasympathetic system. Therefore, reactive oxygen species can actively participate in the development of cardiovascular diseases like hypertension when the balance in the redox state is disrupted.

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Zinc (Zn ++) has been shown as an important physiological inhibitor of pituitary PRL release, and Zn ++ and PRL could be involved in a negative feedback regulatory loop. However, this inhibitory effect has not been detected in humans with regard to thyrotropin releasing hormone (TRH), dopamine (DA) and histamine (HA) neurotransmitters. In order to investigate this topic, Zn ++ was acutely and chronically administered to five healthy men to observe the probable inhibitory effect on PRL release during insulin-induced hypoglycemia. The positive PRL response to hypoglycemia has generally been considered to be mediated via the hypothalamus by adrenergic, serotoninergic, histaminergic, opioid-peptidergic and TRH neurotransmitters. The results showed that Zn ++ was not able to inhibit the PRL release during insulin-induced hypoglycemia. Under these conditions, Zn ++ does not block hypothalamic neurotransmitters stimulated by hypoglycemia, thus excluding its clinical application in human beings. On the other hand, the effect of acute stress, such as hypoglycemia, on the serum Zn ++ profile was not observed. ©2006 Dustri-Verlag Dr. K. Feistle.

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Molecular neurobiology has provided an explanation of mechanisms supporting mental functions as learning, memory, emotion and consciousness. However, an explanatory gap remains between two levels of description: molecular mechanisms determining cellular and tissue functions, and cognitive functions. In this paper we review molecular and cellular mechanisms that determine brain activity, and then hypothetize about their relation with cognition and consciousness. The brain is conceived of as a dynamic system that exchanges information with the whole body and the environment. Three explanatory hypotheses are presented, stating that: a) brain tissue function is coordinated by macromolecules controlling ion movements, b) structured (amplitude, frequency and phase-modulated) local field potentials generated by organized ionic movement embody cognitive information patterns, and c) conscious episodes are constructed by a large-scale mechanism that uses oscillatory synchrony to integrate local field patterns. © by São Paulo State University.