RESUMEN
Although some studies have investigated the effects of dietary L-tryptophan on agonistic behavior, research on adult fish specimens is still lacking. Moreover, submissive behaviors have been generally overlooked. We focused on agonistic behavior between males of the cichlid fish Cichlasoma dimerus, in dyadic encounters held in a novel context after being fed or not with an L-tryptophan enriched diet (TRP) for 2 weeks. We arranged three different dyads: control/control (control conditions: not TRP enriched), control/TRP, and TRP/TRP. We also registered the response of the brain serotonergic system in four brain regions. TRP/TRP dyads showed higher latencies to first attack, lower overall aggression, and lower proportions of bites and passive copings (submissive display) compared to control/control. TRP dominant males performed fewer bites with respect to controls, and subordinate males opposed to TRP males showed fewer passive copings. Higher serotonergic activities were found in subordinates' optic tectum and in the telencephalon and preoptic area/hypothalamus of TRP males. Altogether, results point out that dietary L-tryptophan reduced males' motivation to attack and dominant aggression, which consequently influenced subordinate agonistic repertory. In addition, males within TRP/TRP dyads showed a switch in their behavioral agonistic repertory. These behavioral outcomes were probably due to modifications at brain serotonergic functioning.
Asunto(s)
Conducta Agonística/efectos de los fármacos , Conducta Agonística/fisiología , Conducta Animal/efectos de los fármacos , Conducta Animal/fisiología , Cíclidos/fisiología , Triptófano/farmacología , Animales , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Dieta , Masculino , Serotonina/metabolismoRESUMEN
The hypothalamic neuropeptides of the vasopressin-oxytocin family (and their homologs for non-mammalian species) are key modulators of the Social Brain Network, acting via specific receptors reported in all the nuclei of this network. Different conclusive examples have proven the context-dependency actions of hypothalamic nonapeptides on social behavior in several vertebrate taxa. Teleost fishes provide endless possibilities of experimental model systems to explore the underlying mechanisms of nonapeptide actions on social behavior given that they are the most diverse group of vertebrates. Although it has been difficult to identify commonalities of nonapeptide actions across species, indisputable evidence in many teleost species have demonstrated a clear role of vasotocin in the modulation of aggressive and sexual behaviors. Though Neotropical South American fish contribute an important percentage of teleost diversity, most native species remain unexplored as model systems for the study of the neuroendocrine bases of social behavior. In this review, we will revise recent data on the two model systems of Neotropical fish, South American cichlids and weakly electric fish that have contributed to this issue.
Asunto(s)
Conducta Agonística/efectos de los fármacos , Peces/fisiología , Vasotocina/farmacología , Animales , Modelos Biológicos , Sistemas Neurosecretores/metabolismo , Conducta SocialRESUMEN
Glutathione is the major non-protein thiol to which many different roles in the central nervous system (CNS) are attributed. To further investigate the glutathione response in the CNS, we tested the effect of three stress models on glutathione levels in the brain. We tested the effect of two models of repeated intraspecific agonistic interaction in mice. No influence was observed over the glutathione levels in the mice cerebral cortex, cerebellum, liver, and blood. Acute restraint stress in rats was found to induce an increase in glutathione levels in the cerebellum after 2 and 4 h of immobilization, an effect not observed in the cerebral cortex, striatum, and hippocampus. To investigate the interference of an inhibitor of nitric oxide synthase (NOS), N(omega)Nitro-L-arginine-methyl-ester (L-NAME, 50 mg/kg) was applied i.p. at the beginning of restraint stress. L-NAME alone did not lead to a change in glutathione levels although, in combination with restraint stress, it induced an increase in such levels. This effect was observed in all four structures studied, i.e. cortex, hippocampus, striatum, and cerebellum. The values returned to basal levels after 6h of immobilization. In conclusion, the pattern of dominance, after repeated intraspecific agonistic interaction, was ineffective in producing alterations in brain glutathione, whereas acute restraint stress led to an increase in glutathione levels within a window of 2-4 h, and the inhibition of NOS increased glutathione levels in all studied rat brain structures, suggesting a specificity interference of acute restraint stress with the glutathione system.
Asunto(s)
Encéfalo/metabolismo , Glutatión/metabolismo , Inhibición Neural/fisiología , Óxido Nítrico Sintasa/fisiología , Estrés Fisiológico/metabolismo , Conducta Agonística/efectos de los fármacos , Conducta Agonística/fisiología , Análisis de Varianza , Animales , Conducta Animal , Encéfalo/anatomía & histología , Encéfalo/efectos de los fármacos , Masculino , Ratones , NG-Nitroarginina Metil Éster/farmacología , Inhibición Neural/efectos de los fármacos , Óxido Nítrico Sintasa/antagonistas & inhibidores , Ratas , Ratas Wistar , Restricción Física/métodosRESUMEN
Microinjection of L-glutamic acid into the basal midbrain of the toad Bufo paracnemis induced a series of responses linked to antipredator behavior such as flight, backward locomotion and defensive postures. Furthermore, alerting/orientation occurred in 20% of the animals, a behavior which is probably important for the animal to achieve the above responses. Locomotion occurred in 18% of the toads. The existence of a mesencephalic premotor control for locomotion in these animals is discussed comparatively. All responses were accompanied by changes in arterial pressure, heart rate and intrabuccal pressure. In some animals which exhibited backward locomotion responses, defensive postures and alerting/orientation, bradycardia or cardiac arrest occurred, with no appreciable changes in arterial pressure. This fact is discussed on the basis of studies which have shown the occurrence of similar alterations in situations of fear in other vertebrates. Autonomic changes without other responses occurred in 16% of the animals. Flight behavior was usually observed as a consequence of stimulation of sites located in the anterodorsal tegmental nucleus and lateral portions of the midbrain tegmentum. In contrast, locomotion was obtained by stimulating basal sites of the tegmentum located in the anteroventral nucleus and in the reticular formation lateral to it. Sites related to the remaining behaviors were located more diffusely in the basal midbrain.
Asunto(s)
Conducta Agonística/efectos de los fármacos , Glutamatos/farmacología , Mesencéfalo/efectos de los fármacos , Conducta Predatoria/efectos de los fármacos , Conducta Agonística/fisiología , Animales , Nivel de Alerta/efectos de los fármacos , Nivel de Alerta/fisiología , Sistema Nervioso Autónomo/efectos de los fármacos , Sistema Nervioso Autónomo/fisiología , Presión Sanguínea/efectos de los fármacos , Presión Sanguínea/fisiología , Mapeo Encefálico , Bufonidae , Femenino , Ácido Glutámico , Frecuencia Cardíaca/efectos de los fármacos , Frecuencia Cardíaca/fisiología , Masculino , Mesencéfalo/fisiología , Orientación/efectos de los fármacos , Orientación/fisiología , Conducta Predatoria/fisiologíaRESUMEN
Electrical stimulation of either the midbrain central gray or the medial hypothalamus induces a defense reaction in the rat, characterized mainly by increased locomotion, rearing, and leaping. However, microinjection of the excitatory amino acid glutamate was effective only in the former region. Because excitatory amino acids do not depolarize axons of passage, it was suggested that the hypothalamus is devoid of soma/dendrites of neurons commanding the defense reaction. In the present study, we show that a subtoxic dose (60 pmol) of another excitatory amino acid, kainic acid, injected into the medial hypothalamus significantly enhanced locomotion and rearing of Wistar rats systematically observed in an open field. Similar behavioral changes have been reported following microinjection of drugs impairing GABAergic neurotransmission. Local pretreatment with the GABAA receptor agonist THIP (2 nmol) blocked the effect of kainic acid. Therefore, the medial hypothalamus of the rat seems to contain a population of neuronal cell bodies commanding the defense reaction, which is activated by excitatory amino acids and tonically inhibited by GABAergic fibers.
Asunto(s)
Conducta Agonística/efectos de los fármacos , Anticonvulsivantes/farmacología , Nivel de Alerta/efectos de los fármacos , Conducta Exploratoria/efectos de los fármacos , Hipotálamo Medio/efectos de los fármacos , Isoxazoles/farmacología , Ácido Kaínico/antagonistas & inhibidores , Receptores de GABA-A/efectos de los fármacos , Animales , Mapeo Encefálico , Relación Dosis-Respuesta a Droga , Ácido Kaínico/farmacología , Masculino , Actividad Motora/efectos de los fármacos , Ratas , Ratas Endogámicas , Tiempo de Reacción/efectos de los fármacos , Aislamiento SocialRESUMEN
Grouped, nonkiller and killer animals were centrally injected either with vehicle or with 5,7-dihydroxytryptamine. After a period of 7-10 days, forepaw treading and hindlimb abduction were induced by 5-MeODMT administration in all sham and lesioned rats. As expected, behavioral supersensitivity was observed in grouped and nonkiller lesioned rats. A reduced increase in 5-MeODMT-induced behaviors was obtained in killer lesioned animals. 5-HT uptake studies showed a comparable reduction of 5-HT uptake within all the lesioned rats. This evidence suggests an altered capacity to promote adaptive changes on 5-HT sites in killer rats following the destruction of central serotonergic fibers.
Asunto(s)
Agresión/efectos de los fármacos , Conducta Agonística/efectos de los fármacos , Metoxidimetiltriptaminas/farmacología , Actividad Motora/efectos de los fármacos , Receptores de Serotonina/fisiología , Serotonina/metabolismo , Triptaminas/farmacología , 5,7-Dihidroxitriptamina/toxicidad , Conducta Agonística/fisiología , Animales , Corteza Cerebral/metabolismo , Ventrículos Cerebrales/efectos de los fármacos , Hipocampo/metabolismo , Masculino , Ratones , Ratas , Ratas Endogámicas , Receptores de Serotonina/efectos de los fármacosRESUMEN
1. Benzyleugenol (BE), a phenylpropene derivative, protects rats and mice against maximal electroshock seizures and has a protective index superior to that of phenobarbital. The present paper describes experiments carried out to further characterize the pharmacological and toxicological profile of this compound. 2. BE, at a dose range of 100-400 mg/kg ip, was inactive when tested for the following effects: analgesia, as measured by the hot plate and acetic acid writhing methods; neuroleptic-like effects, when tested by the catalepsy and palpebral ptosis, conditioned avoidance response and apomorphine-induced stereotypies methods; and anxiolytic effects, measured by the shock-elicited aggressiveness of mice. In contrast, tolerance to the anticonvulsant effect of BE, at dose range of 240-800 mg/kg orally, developed in mice and rats after 10 to 40 days of continued treatment. 3. BE, at dose range of 104-800 mg/kg orally, proved to be remarkably safe when chronically administered to laboratory animals. Thus, 3 to 6 month administration of large BE doses to rats and mice did not affect body weight, behavioral measures, serum and blood tests, or hematological parameters. Anatomopathological examinations of viscera of BE-treated animals did not reveal alterations which could be attributed to drug treatment. 4. Daily treatment up to 3 months of male rats and mice with BE, at a dose range of 80-800 mg/kg orally, did not affect the reproductive capacity of the animals. Pregnant females treated with BE during different periods of gestation gave birth to litters similar to those of control females; when adult, BE and control litters performed equally well in a passive avoidance task. 5. These results were compared with those of known anti-epileptic drugs, such as phenytoin, phenobarbital and valproic acid, and it is suggested that BE deserves further research as a potential candidate for the treatment of epilepsy.
Asunto(s)
Anticonvulsivantes , Electrochoque , Eugenol/análogos & derivados , Conducta Agonística/efectos de los fármacos , Animales , Catalepsia/inducido químicamente , Depresión Química , Relación Dosis-Respuesta a Droga , Tolerancia a Medicamentos , Eugenol/farmacología , Eugenol/toxicidad , Femenino , Masculino , Ratones , Ratones Endogámicos , Dimensión del Dolor , Embarazo , Ratas , Ratas Endogámicas , Reproducción/efectos de los fármacos , Conducta Estereotipada/efectos de los fármacosRESUMEN
We measured the aggressive behavior of isolated mice treated or not with d,1-amphetamine (6.0 mg/kg, ip) and injected with different doses of d,1-propranolol (10.0, 20.0 or 30.0 mg/kg, ip) or haloperidol (0.5 or 1.0 mg/kg). d,1-Amphetamine (6.0 mg/kg, ip) decreased the aggressiveness of the isolated mice and induced stereotyped behavior. Haloperidol antagonized amphetamine-induced stereotypy, increased the latency to the 1st attack and decreased duration of fighting and frequency of attacks in mice treated or not with amphetamine. d,1-Propranolol did not change stereotypy but decreased aggressiveness in a dose-dependent way, being more effective against aggression induced by isolation per se. These results are discussed in terms of the interference of the drugs with the activity of either catecholaminergic neurons or midbrain reticular formation. The latter effect seems to be the most likely explanation for the observed anti-aggressive effects of haloperidol and d-1, propranolol.