Otitis media aguda en Atención Primaria / Acute otitis media in primary care

Objetivos: Debido a la muy alta incidencia de otitis media aguda (OMA) referida en algunos trabajos y a la disponibilidad de una vacuna conjugada para su prevención, hemos estudiado la incidencia de OMA en nuestro medio en los últimos 9 años. Material y métodos: Se realiza el trabajo en el Centro de Salud de Manises, población de 26.000 habitantes (4.560 niños hasta 14 años), a 6 km de Valencia capital. Se obtienen los diagnósticos de otitis de 230.020 consultas entre 1993 y 2001. El criterio diagnóstico de OMA ha sido la presencia de otalgia más algún signo timpánico. Resultados: La OMA ha sido la causa del 4% de todas las consultas. Al cumplir 1 año de vida, el 35,4% de los niños ha tenido algún episodio de OMA, y al cumplir 4 años lo ha sufrido el 84,6%. Ha tenido tres o más cuadros de OMA el 5,7% de los niños al año de vida y el 31,8% al llegar a los 4. Se comprueba que cuanto antes tiene un niño la primera OMA, mayor número de episodios va a tener. La incidencia de mastoiditis es del 0,011%. Se comparan los resultados con los obtenidos por otros autores. Conclusiones: Encontramos una incidencia de OMA más baja que la referida por otros autores, probablemente porque es un trabajo retrospectivo donde sólo se han diagnosticado las OMA sintomáticas (AU)

Objective: In view of the very high incidence of acute otitis media (AOM) in children reported in some studies and the availability of a polysaccharide conjugate vaccine for its prevention, we studied the incidence of AOM in our population over the last nine years. Materials and methods: The research was carried out in the Health Center of Manises, a city 6 kilometers from Valencia, Spain, which has a population of 26,000 inhabitants (4,560 children of up to 14 years of age). The diagnosis was obtained from 230,020 consultations between 1993 and 2001. The diagnostic criteria were earache and any type of tympanic involvement. Results: AOM accounted for 4% of all consultations. Within the first year of life, 35.4% of children had had at least one AOM episode and 84.6% before the fourth year of life. 5.7% of children had had 3 or more AOM episodes within the first year and 31.8% before the fourth. There is a direct relationship between early age at the first episode and the number of episodes of AOM. The incidence of mastoiditis was 0.011%. These results were compared with those obtained by other authors. Conclusions: We found a lower incidence of AOM than that reported by other authors, probably because ours is a retrospective study involving only symptomatic AOM (AU)

[Anti-HBs titers after a vaccination program in children and adolescents. Should a booster dose be given?]. / Títulos de anti-HBs tras un programa de vacunación en niños y adolescentes: revacunar?

OBJECTIVES: To determine the efficacy and immunogenicity achieved 6 years after the start of a massive vaccination campaign against hepatitis B in newborn infants and adolescents (12 years). The persistence of anti-hepatitis B virus surface antigen (HBS) levels and the need for a booster dose were also assessed. MATERIALS AND METHODS: From 1993 to 1997 the Engerix vaccine (10 micrograms) and since then the Recombivax vaccine (5 micrograms). The vaccination schedule was the standard of three doses (0, 1, 6). Blood analyses were used for determination of anti-HBs between October of 1998 and May of 2000. RESULTS: We studied 382 cases. Five years after the first dose, 96.1% (73/76) has anti-HBs and in 75% (57/76) levels were above 10UI/L. Six to seven years after vaccination anti-HBs were detected in 94,1 (32/34) of the children and in 70.6% (24/34) of these, levels were above 10UI/L. CONCLUSIONS: A high percentage of children were found to have good levels of anti-HBs 67 years after vaccination. Recent studies show that booster doses are not required because of the immunologic memory that produces the vaccine. The anti-HB protective level (> or = 10UI/l) should not be taken into consideration because this level is only valid when passive immunity with immunoglobulins is applied.

Rapid eye movement sleep deprivation induces an increase in acetylcholinesterase activity in discrete rat brain regions.

Some upper brainstem cholinergic neurons (pedunculopontine and laterodorsal tegmental nuclei) are involved in the generation of rapid eye movement (REM) sleep and project rostrally to the thalamus and caudally to the medulla oblongata. A previous report showed that 96 h of REM sleep deprivation in rats induced an increase in the activity of brainstem acetylcholinesterase (Achase), the enzyme which inactivates acetylcholine (Ach) in the synaptic cleft. There was no change in the enzyme's activity in the whole brain and cerebrum. The components of the cholinergic synaptic endings (for example, Achase) are not uniformly distributed throughout the discrete regions of the brain. In order to detect possible regional changes we measured Achase activity in several discrete rat brain regions (medulla oblongata, pons, thalamus, striatum, hippocampus and cerebral cortex) after 96 h of REM sleep deprivation. Naive adult male Wistar rats were deprived of REM sleep using the flower-pot technique, while control rats were left in their home cages. Total, membrane-bound and soluble Achase activities (nmol of thiocholine formed min(-1) mg protein(-1)) were assayed photometrically. The results (mean +/- SD) obtained showed a statistically significant (Student t-test) increase in total Achase activity in the pons (control: 147.8 +/- 12.8, REM sleep-deprived: 169.3 +/- 17.4, N = 6 for both groups, P<0.025) and thalamus (control: 167.4 +/- 29.0, REM sleep-deprived: 191.9 +/- 15.4, N = 6 for both groups, P<0.05). Increases in membrane-bound Achase activity in the pons (control: 171.0 +/- 14.7, REM sleep-deprived: 189.5 +/- 19.5, N = 6 for both groups, P<0.05) and soluble enzyme activity in the medulla oblongata (control: 147.6 +/- 16.3, REM sleep-deprived: 163.8 +/- 8.3, N = 6 for both groups, P<0.05) were also observed. There were no statistically significant differences in the enzyme's activity in the other brain regions assayed. The present findings show that the increase in Achase activity induced by REM sleep deprivation was specific to the pons, a brain region where cholinergic neurons involved in REM generation are located, and also to brain regions which receive cholinergic input from the pons (the thalamus and medulla oblongata). During REM sleep extracellular levels of Ach are higher in the pons, medulla oblongata and thalamus. The increase in Achase activity in these brain areas after REM sleep deprivation suggests a higher rate of Ach turnover.

Rapid eye movement sleep deprivation induces an increase in acetylcholinesterase activity in discrete rat brain regions

Some upper brainstem cholinergic neurons (pedunculopontine and laterodorsal tegmental nuclei) are involved in the generation of rapid eye movement (REM) sleep and project rostrally to the thalamus and caudally to the medulla oblongata. A previous report showed that 96 h of REM sleep deprivation in rats induced an increase in the activity of brainstem acetylcholinesterase (Achase), the enzyme which inactivates acetylcholine (Ach) in the synaptic cleft. There was no change in the enzyme's activity in the whole brain and cerebrum. The components of the cholinergic synaptic endings (for example, Achase) are not uniformly distributed throughout the discrete regions of the brain. In order to detect possible regional changes we measured Achase activity in several discrete rat brain regions (medulla oblongata, pons, thalamus, striatum, hippocampus and cerebral cortex) after 96 h of REM sleep deprivation. Naive adult male Wistar rats were deprived of REM sleep using the flower-pot technique, while control rats were left in their home cages. Total, membrane-bound and soluble Achase activities (nmol of thiocholine formed min-1 mg protein-1) were assayed photometrically. The results (mean + or - SD) obtained showed a statistically significant (Student t-test) increase in total Achase activity in the pons (control: 147.8 + or - 12.8, REM sleep-deprived: 169.3 + or - 17.4, N = 6 for both groups, P<0.025) and thalamus (control: 167.4 + or - 29.0, REM sleep-deprived: 191.9 + or - 15.4, N = 6 for both groups, P<0.05). Increases in membrane-bound Achase activity in the pons (control: 171.0 + or - 14.7, REM sleep-deprived: 189.5 + or - 19.5, N = 6 for both groups, P<0.05) and soluble enzyme activity in the medulla oblongata (control: 147.6 + or - 16.3, REM sleep-deprived: 163.8 + or - 8.3, N = 6 for both groups, P<0.05) were also observed. There were no statistically significant differences in the enzyme's activity in the other brain regions assayed. The present findings show that the increase in Achase activity induced by REM sleep deprivation was specific to the pons, a brain region where cholinergic neurons involved in REM generation are located, and also to brain regions which receive cholinergic input from the pons (the thalamus and medulla oblongata). During REM sleep extracellular levels of Ach are higher in the pons, medulla oblongata and thalamus. The increase...

Títulos de antiHBs tras un programa devacunación en niños y adolescentes: ¿revacunar? / Antihepatitis B virus surface antigen titers after a vaccination program in children and adolescents. Should a booster dose be given?

OBJETIVO: Tras haber pasado 6 años desde el inicio de la campaña de vacunación masiva de la hepatitis B en recién nacidos y adolescentes (12 años), se pretende conocer la eficacia e inmunogeneicidad de la misma, la persistencia de la misma, la persistencia de los valores de antihbs y la necesidad de realizar dosis de recuerdo. MATERIAL Y MÉTODOS: Se utilizó la vacuna engerix desde 1993 hasta 1987 (10 mg) y desde entonces la vacuna recombivax (5 mg). El calendario vacunal fue el estándar de 3 dosis (0, 1 y 6 años). Para realizar el estudio se aprovechó cualquier análisis de sangre para cuantificar el título de antihbs, entre octubre de 1998 y mayo de 2000. RESULTADOS: se obtuvieron 382 casos. A los 5 años de la primera dosis, el 96,1% (73/76) tenian antihbs y el 75% (57/76) por encima de 10U/L. A los 6-7 años de la vacunación, en el 94,1% (32/34) de los niños se detectaba antihbs y en el 70,6% (24/34) de éstos por encima de 10/Ul sólo en 5 niños fue negativo el anticuerpo. CONCLUSIÓN: en este estudio se ha encontrado un alto porcentaje de niños con buenos valores de antihbs, tras 6-7 años de la vacunación. La bibliografía reciente demuestra que, dada la memoria inmunológica que produce la vacuna, no es necesaria la revacunación. También debe olvidarse el denominado nivel protectivo de antihbs 10U/l, sólo válido cuando se aplica inmunidad pasiva con inmunoglobulinas (AU)

Sex-dependent differences in the activities of acetylsalicylic acid-esterases in mouse kidneys.

Acetylsalicylic acid (ASA), the most used drug worldwide, is hydrolyzed to salicylic acid and acetate by esterases present in tissues of several species including humans. Sex differences in drug metabolism by rodent liver are documented in the literature. In this paper we report a difference in the activities of the esterases (ASA-esterase I and II) in the kidneys of male and female mice. In this species there is no difference between males and females in liver ASA-esterases (ASA-esterase I: males 38.5 +/- 7.9 (N = 5) and females 31.6 +/- 7.6 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P > 0.05; ASA-esterase II: males 77.3 +/- 17.4 (N = 5) and females 61.4 +/- 15.1 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P > 0.05). However, in the kidneys males presented a much higher enzyme activity than females (ASA-esterase I: males 25.2 +/- 6.3 (N = 5) and females 6.8 +/- 0.6 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P < 0.0002; ASA-esterase II: males 79.8 +/- 10.1 (N = 5) and females 13.0 +/- 1.1 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P < 0.0001). The difference between sexes observed in mouse kidneys could serve as a model to study the molecular basis of this sex difference and also to determine the possible involvement of pituitary and gonadal hormones in this difference in ASA-esterase activities since these hormones control the sex differences in rodent liver enzyme activity.

Sex-dependent differences in the activities of acetylsalicylic acid-esterases in mouse kidneys

Acetylsalicylic acid (ASA), the most used drug worldwide, is hydrolyzed to salicylic acid and acetate by esterases present in tissues of several species including humans. Sex differences in drug metabolism by rodent liver are documented in the literature. In this paper we report a difference in the activities of the esterases (ASA-esterase I and II) in the kidneys of male and female mice. In this species there is no difference between males and females in liver ASA-esterases (ASA-esterase I: males 38.5 ñ 7.9 (N = 5) and females 31.6 ñ 7.6 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P>0.05; ASA-esterase II: males 77.3 ñ 17.4 (N = 5) and females 61.4 ñ 15.1 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P>0.05). However, in the kidneys males presented a much higher enzyme activity than females (ASA-esterase I: males 25.2 ñ 6.3 (N = 5) and females 6.8 ñ 0.6 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P<0.0002; ASA-esterase II: males 79.8 ñ 10.1 (N = 5) and females 13.0 ñ 1.1 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P<0.0001). The difference between sexes observed in mouse kidneys could serve as a model to study the molecular basis of this sex difference and also to determine the possible involvement of pituitary and gonadal hormones in this difference in ASA-esterase activities since these hormones control the sex differences in rodent liver enzyme activity

Gender differences in the activities of aspirin-esterases in rat tissues

The activities of aspirin (acetylsalicylic acid)-esterases were measured in several tissues (liver, kidney, adrenal glands, brain and serum) from adult male and female Wistar rats. In males, both aspirin-esterase I (assayed at pH 5.5) and II (assayed at pH 7.4) activities were higher in liver homogenates when compared to females (aspirin-esterase I: males 48.9 ñ 4.8 (N = 8) and females 29.3 ñ 4.2 (N = 8) nmol of salicylic acid formed min-1 mg protein-1; aspirin-esterase II: males 41.4 ñ 4.1 (N = 8) and females 26.1 ñ 4.5 (N = 8) nmol of salicylic acid formed min-1 mg protein-1, P<0.001). In serum, enzyme activity was higher in females than in males (aspirin-esterase I: males 0.85 ñ 0.06 (N = 6) and females 1.18 ñ 0.11 (N = 6) nmol of salicylic acid formed min-1 mg protein-1; aspirin-esterase II: males 1.03 ñ 0.13 (N = 6) and females 1.34 ñ 0.11 (N = 6) nmol of salicylic acid formed min-1 mg protein-1, P<0.001). In the other tissues assayed, no statistically significant difference between males and females was found. There were no statistically significant differences when the enzymes were assayed in different phases of the estrous cycle in liver and serum. These results show that the differences in aspirin-esterase activity observed between males and females are not due to the estrous cycle. The gender difference obtained in our study may indicate an involvement of gonadal hormones in the control of the hydrolysis of aspirin. This possibility is currently under investigation.

Decreased activity of striatal monoamine oxidase B after rapid eye movement (REM) sleep deprivation in rats.

The striatum seems to be the main brain region involved in stereotyped behavior induced by dopaminergic agonists. Rapid eye movement (REM) sleep deprivation increases dopaminergic agonist-induced stereotypy and produces biochemical changes in striatal dopaminergic neurotransmission. However, the mechanism underlying the increased dopaminergic sensitivity induced by REM sleep deprivation has not been elucidated. In an attempt to determine some of the biochemical changes in striatal dopaminergic neurotransmission that could contribute to REM sleep deprivation effects, we measured the activity of monoamine oxidase (MAO) A and B, the enzymes responsible for dopamine and beta-phenylethylamine (beta-PEA) deamination in striatum. Male adult rats were deprived of REM sleep for 96 h by the flower-pot technique. MAO A and B were assayed radioisotopically in the mitochondrial fraction by standard laboratory procedures, using [14C]-5-hydroxytryptamine (5-HT) and [14C]-beta-phenylethylamine (beta-PEA), as substrates for MAO A and MAO B, respectively. The results showed no significant statistical differences in striatal MAO A activity, whereas a significant decrease in MAO B activity was observed. The results are discussed in terms of the possible involvement of beta-PEA, a striatal endogenous trace amine, which potentiates dopaminergic neurotransmission and may participate in the increased dopaminergic sensitivity observed after REM sleep deprivation.

Gender differences in the activities of aspirin-esterases in rat tissues.

The activities of aspirin (acetylsalicylic acid)-esterases were measured in several tissues (liver, kidney, adrenal glands, brain and serum) from adult male and female Wistar rats. In males, both aspirin-esterase I (assayed at pH 5.5) and II (assayed at pH 7.4) activities were higher in liver homogenates when compared to females (aspirin-esterase I: males 48.9 +/- 4.8 (N = 8) and females 29.3 +/- 4.2 (N = 8) nmol of salicylic acid formed min-1 mg protein-1; aspirin-esterase II: males 41.4 +/- 4.1 (N = 8) and females 26.1 +/- 4.5 (N = 8) nmol of salicylic acid formed min-1 mg protein-1, P < 0.001). In serum, enzyme activity was higher in females than in males (aspirin-esterase I: males 0.85 +/- 0.06 (N = 6) and females 1.18 +/- 0.11 (N = 6) nmol of salicylic acid formed min-1 mg protein-1, aspirin-esterase II: males 1.03 +/- 0.13 (N = 6) and females 1.34 +/- 0.11 (N = 6) nmol of salicylic acid formed min-1 mg protein-1, P < 0.001). In the other tissues assayed, no statistically significant difference between males and females was found. There were no statistically significant differences when the enzymes were assayed in different phases of the estrous cycle in liver and serum. These results show that the differences in aspirin-esterase activity observed between males and females are not due to the estrous cycle. The gender difference obtained in our study may indicate an involvement of gonadal hormones in the control of the hydrolysis of aspirin. This possibility is currently under investigation.

Acetylcholinesterase activity in the pons and medulla oblongata of rats after chronic electroconvulsive shock

An imbalance between cholinergic and noradrenergic neurotransmission has been proposed for the etiology of affective disorders. According to this hypothesis, depression would be the result of enhanced cholinergic and reduced noradrenergic neurotransmission. Repeated electroconvulsive shock (ECS) is an effective treatment for depression; moreover, in laboratory animals it induces changes in brain noradrenergic neurotransmission similar to those obtained by chronic treatment with antidepressant drugs (down-regulation of beta-adrenergic receptors). The aim of the present study was to determine whether repeated ECS in rats changes acetylcholinesterase (Achase) activity. Achase controls the level of acetylcholine (Ach) in the synaptic cleft and its levels seem to be regulated by the interaction between Ach and its receptor. Thus, a decrease in Achase activity would suggest decreased cholinergic activity. Adult male Wistar rats received one ECS (80 mA, 0.2s, 60Hz) daily for 7 days. Control rats were handled in the same way without receiving the shock. Rats were sacrificed 24 h after the last ECS and membrane-bound and soluble Achase activity was assayed in homogenates obtained from the pons and medulla oblongata. A statistically significant decrease in membrane-bound Achase activity (nmol thiocholine formed min-1 mg protein-1) (control 182.6 + 14.8 ECS 162.2 + 14.2, P<0.05) and an increase in soluble Achase activity in the medula oblongata (control 133.6 + 4.2, ECS 145.8 + 12.3, P<0.05) were observed. No statistical differences were observed in Achase activity in the pons. Although repeated ECS induced a decrease in membrane-bound Achase activity, the lack of changes in the pons (control Achase activity: total 231.0 + 34.5, membrane-bound 298.9 + 18.5, soluble 203.9 + 30.9), the region where the locus coeruleus, the main noradrenergic nucleus, is located, does not seem to favor the existence of an interaction between cholinergic and noradrenergic neurotransmission after ECS treatment.

Activities of monoamine oxidase (MAO) A and B in discrete regions of rat brain after rapid eye movement (REM) sleep deprivation.

Rapid eye movement (REM) sleep deprivation increases monoaminergic (noradrenergic and serotonergic) turnover and their metabolites in whole brain of rats. This increase in metabolites may indicate increased activity of the enzymes responsible for the inactivation of monoamines. To test this hypothesis, we assayed the activity of monoamineoxidases (MAOs) A and B in hippocampus, hypothalamus, brainstem and its divisions pons and medulla oblongata in rats deprived of REM sleep for 96 h. REM sleep deprivation was carried out by the flower-pot technique. A control group remained in their home cages. MAO A was assayed by using [14C]-5-hydroxytryptamine as the substrate (50 microM final concentration) and MAO B by using [14C]-beta-phenylethylamine (2 microM final concentration). The enzymes were assayed in the mitochondrial fraction.The results obtained showed that a significant decrease in the activity of MAO A was obtained in the brainstem and an increase in medulla oblongata and no statistical differences in the activity of MAO B in brainstem, pons and medulla oblongata and MAO A in pons; there were also no differences in the activities of both MAO A and B in hippocampus and hypothalamus. Although our results confirmed previous data regarding changes in MAO A activity in brainstem and medulla oblongata, they did not confirm our hypothesis that the increase in monamine turnover and metabolites in the brain would be the result of increased MAO activity.

Chronic imipramine treatment-induced changes in acetylcholinesterase (EC 3.1.1.7) activity in discrete rat brain regions.

Cholinergic as well as monoaminergic neurotransmission seems to be involved in the etiology of affective disorders. Chronic treatment with imipramine, a classical antidepressant drug, induces adaptive changes in monoaminergic neurotransmission. In order to identify possible changes in cholinergic neurotransmission we measured total, membrane-bound and soluble acetylcholinesterase (Achase) activity in several rat brain regions after chronic imipramine treatment. Changes in Achase activity would indicate alterations in acetylcholine (Ach) availability to bind to its receptors in the synaptic cleft. Male rats were treated with imipramine (20 mg/kg, i.p.) for 21 days, once a day. Twenty-four hours after the last dose the rats were sacrificed and homogenates from several brain regions were prepared. Membrane-bound Achase activity (nmol thiocholine formed min-1 mg protein-1) after chronic imipramine treatment was significantly decreased in the hippocampus (control = 188.8 +/- 19.4, imipramine = 154.4 +/- 7.5, P < 0.005) and striatum (control = 850.9 +/- 59.6, imipramine = 742.5 +/- 34.7, P < 0.005). A small increase in total Achase activity was observed in the medulla oblongata and pons. No changes in enzyme activity were detected in the thalamus or total cerebral cortex. Since the levels of Achase seem to be enhanced through the interaction between Ach and its receptors, a decrease in Achase activity may indicate decreased Ach release by the nerve endings. Therefore, our data indicate that cholinergic neurotransmission is decreased after chronic imipramine treatment which is consistent with the idea of an interaction between monoaminergic and cholinergic neurotransmission in the antidepressant effect of imipramine.

Chronic imipramine treatment-induced changes in acetylcholinesterase (EC 3.1.1.7) activity in discrete rat brain regions

Cholinergic as well as monoaminergic neurotransmission seems to be involved in the etiology of affective disorders. Chronic treatment with imipramine, a classical antidepressant drug, induces adaptive changes in monoaminergic neurotransmission. In order to identify possible changes in cholinergic neurotransmission we measured total, membrane-bound and soluble acetylcholinesterase (Achase) activity in several rat brain regions after chronic imipramine treatment. Changes in Achase activity would indicate alterations in acetylcholine (Ach) availability to bind to its receptors in the synaptic cleft. Male rats were treated with imipramine (20 mg/kg, ip) for 21 days, once a day. Twenty-four hours after the last dose the rats were sacrificed and homogenates from several brain regions were prepared. Membrane-bound Achase activity (nmol thiocholine formed min(-1) mg protein(-1) after chronic imipramine treatment was significantly decreased in the hippocampus (control = 188.8 + 19.4, imipramine = 154.4 + 7.5, P<0.005) and striatum (control = 850.9 + 59.6, imipramine = 742.5 + 34.7, P<0.005). A small increase in total Achase activity was observed in the medula oblongata and pons. No changes in enzyme activity were detected in the thalamus or total cerebral cortex. Since the levels of Achase seem to be enhanced through the interaction between Ach and its receptors, a decrease in Achase activity may indicate decreased Ach release by the nerve endings. Therefore, our data indicate that cholinergic neurotransmission is decreased after chronic imipramine treatment which is consistent with the idea of an interaction between monoaminergic and cholinergic neurotransmission in the antidepressant effect of imipramine.

Rapid eye movement (REM) sleep deprivation reduces rat frontal cortex acetylcholinesterase (EC 3.1.1.7) activity.

Rapid eye movement (REM) sleep deprivation induces several behavioral changes. Among these, a decrease in yawning behavior produced by low doses of cholinergic agonists is observed which indicates a change in brain cholinergic neurotransmission after REM sleep deprivation. Acetylcholinesterase (Achase) controls acetylcholine (Ach) availability in the synaptic cleft. Therefore, altered Achase activity may lead to a change in Ach availability at the receptor level which, in turn, may result in modification of cholinergic neurotransmission. To determine if REM sleep deprivation would change the activity of Achase, male Wistar rats, 3 months old, weighing 250-300 g, were deprived of REM sleep for 96 h by the flower-pot technique (N = 12). Two additional groups, a home-cage control (N = 6) and a large platform control (N = 6), were also used. Achase was measured in the frontal cortex using two different methods to obtain the enzyme activity. One method consisted of the obtention of total (900 g supernatant), membrane-bound (100,000 g pellet) and soluble (100,000 g supernatant) Achase, and the other method consisted of the obtention of a fraction (40,000 g pellet) enriched in synaptic membrane-bound enzyme. In both preparations, REM sleep deprivation induced a significant decrease in rat frontal cortex Achase activity when compared to both home-cage and large platform controls. REM sleep deprivation induced a significant decrease of 16% in the membrane-bound Achase activity (nmol thiocholine formed min-1 mg protein-1) in the 100,000 g pellet enzyme preparation (home-cage group 152.1 +/- 5.7, large platform group 152.7 +/- 24.9 and REM sleep-deprived group 127.9 +/- 13.8). There was no difference in the soluble enzyme activity. REM sleep deprivation also induced a significant decrease of 20% in the enriched synaptic membrane-bound Achase activity (home-cage group 126.4 +/- 21.5, large platform group 127.8 +/- 20.4, REM sleep-deprived group 102.8 +/- 14.2). Our results suggest that REM sleep deprivation changes Ach availability at the level of its receptors through a decrease in Achase activity.

Rapid eye movement (REM) sleep deprivation reduces rat frontal cortex acetylcholinesterase (EC 3.1.1.7) activity

Rapid eye movement (REM) sleep deprivation induces severeal behavioral changes. Among these, a decrease in yawning behavior produced by low doses of cholinergic agonists is observed which indicates a change in brain cholinergic neurotransmission after REM sleep deprivation. Acetylcholinesterase (Achase) controls acetylcholine (Ach) availability in the synaptic cleft. Therefore, altered Achase activity may lead to a change in Ach availability at the receptor level which, in turn, may result in modification of cholinergic neurotransmission. To determine if REM sleep deprivation would change the activity of Achase, male Wistar rats, 3 months old, weighing 250-300 g, were deprived of REM sleep for 96 h by the flower-pot technique (N = 12). Two additional groups, a home-cage control (n = 6) and a large platform control (N = 6), were also used. Achase was measured in the frontal cortex using two different methods to obtain the enzyme activity. One method consisted of the obtention of total (900 g supernatant), membrane-bound (100,000 g pellet) and soluble (100,000 g supernatant) Achase, and the other method consisted of the obtention of a fraction (40,000 g pellet) enriched in synaptic membrane-bound enzyme. In both preparations, REM sleep deprivation induced a significant decrease in rat frontal cortex Achase activity when compared to both home-cage and large platform controls. REM sleep deprivation induced a significant decrease of 16 percent in the membrane-bound Achase activity (nmol thiocholine formed min(-1) mg protein(-1) in the 100,000 g pellet enzyme preparation (home-cage group 152.1 + 5.7, large plataform group 152.7 + 24.9 and REM sleep-deprived group 127.9 + 13.8). There was no difference in the soluble enzyme activity. REM sleep deprivation also induced a significant decrease of 20 percent in the enriched synaptic membrane-bound Achase activity (home-cage group 126.4 + 21.5, large platform group 127.8 + 20.4, REM sleep-deprived group 102.8 + 14.2). Our results suggest that REM sleep deprivation changes Ach availability at the level of its receptors through a decrease in Achase activity.

Fluorimetric determination of tissue distribution and differences between the activity of aspirin esterases I and II in mice and rats.

A modification of available fluorimetric methods, based on the native fluorescence of salicylic acid, has been used to assay the activity of aspirin esterases I and II in small amounts of several tissues from rats and mice. The results obtained showed that aspirin esterase I from mouse liver and kidney had the lowest activity and that the activity of aspirin esterase II from these organs was greater than that from the same organs from rats. Liver enzyme kinetics and tissue distribution in rats was shown to be similar to previous data obtained using a spectrophotometric method. This fluorimetric method, which is more sensitive and rapid than the spectrophotometric method, may be useful in studies on aspirin metabolism.

Acetylcholinesterase activity in the pons and medulla oblongata of rats after chronic electroconvulsive shock.

An imbalance between cholinergic and noradrenergic neurotransmission has been proposed for the etiology of affective disorders. According to this hypothesis, depression would be the result of enhanced cholinergic and reduced noradrenergic neurotransmission. Repeated electroconvulsive shock (ECS) is an effective treatment for depression; moreover, in laboratory animals it induces changes in brain noradrenergic neurotransmission similar to those obtained by chronic treatment with antidepressant drugs (down-regulation of beta-adrenergic receptors). The aim of the present study was to determine whether repeated ECS in rats changes acetylcholinesterase (Achase) activity. Achase controls the level of acetylcholine (Ach) in the synaptic cleft and its levels seem to be regulated by the interaction between Ach and its receptor. Thus, a decrease in Achase activity would suggest decreased cholinergic activity. Adult male Wistar rats received one ECS (80 mA, 0.2 s, 60 Hz) daily for 7 days. Control rats were handled in the same way without receiving the shock. Rats were sacrificed 24 h after the last ECS and membrane-bound and soluble Achase activity was assayed in homogenates obtained from the pons and medulla oblongata. A statistically significant decrease in membrane-bound Achase activity (nmol thiocholine formed min-1 mg protein-1) (control 182.6 +/- 14.8, ECS 162.2 +/- 14.2, P < 0.05) and an increase in soluble Achase activity in the medulla oblongata (control 133.6 +/- 4.2, ECS 145.8 +/- 12.3, P < 0.05) were observed. No statistical differences were observed in Achase activity in the pons. Although repeated ECS induced a decrease in membrane-bound Achase activity, the lack of changes in the pons (control Achase activity: total 231.0 +/- 34.5, membrane-bound 298.9 +/- 18.5, soluble 203.9 +/- 30.9), the region where the locus coeruleus, the main noradrenergic nucleus, is located, does not seem to favor the existence of an interaction between cholinergic and noradrenergic neurotransmission after ECS treatment.

Mazindol: efeitos anorético e neurotóxico em ratos jovens e idosos / Mazindol: anoretic and neurotoxic effects in young old rats

Os efeitos da administraçäo crônica do mazindol (5 e 10 mg/kg i.p. e 60 mg/kg s.c) sobre a evoluçäo ponderal e a atividade da tirosina hidroxilase cerebral foram determinados em ratos machos jovens e idosos. O potencial anorético da droga foi observado através da avaliaçäo comparativa do peso corporal dos animais. A atividade da tirosina hidroxilase no estriato foi utilizada como parâmetro indireto da possível neurotoxicidade do mazindol. Nos ratos jovens notou-se uma perda significativa de peso aos 15 dias de tratamento, com recuperaçäo ascendente deste ao longo do tempo. Nos ratos idosos houve também perda de peso significativa; no entanto, tal recuperaçäo näo foi observada. Näo foram detectadas alteraçöes significativas da atividade enzimática em relaçäo aos grupos controles para ambas as idades. Estes resultados säo analisados a partir de dados encontrados na literatura

Daily changes in pentylenetetrazol-induced convulsions and open-field behavior in rats.

Susceptibility to pentylenetetrazol (PTZ)-induced clonic convulsions was measured in rats over the 24-hr light-dark cycle at four-hour intervals. The results showed a higher sensitivity to PTZ around 2200 hr. Other groups of rats were exposed to a four-min open-field session. In the first two min of the session the animals were submitted to open-field environmental stimuli. The next two-min observation occurred with sound and light presented to the animals. Differences through the 24-hr period of the day for both sessions were seen. A reduction in rearing at 2200 hr and increase in defecation at 2200 hr and 0200 hr was observed.