ABSTRACT
Restraint water-immersion stress (RWIS), a compound stress model, has been widely used to induce acute gastric ulceration in rats. A wealth of evidence suggests that the central nucleus of the amygdala (CEA) is a focal region for mediating the biological response to stress. Different stressors induce distinct alterations of neuronal activity in the CEA; however, few studies have reported the characteristics of CEA neuronal activity induced by RWIS. Therefore, we explored this issue using immunohistochemistry and in vivo extracellular single-unit recording. Our results showed that RWIS and restraint stress (RS) differentially changed the c-Fos expression and firing properties of neurons in the medial CEA. In addition, RWIS, but not RS, induced the activation of corticotropin-releasing hormone neurons in the CEA. These findings suggested that specific neuronal activation in the CEA is involved in the formation of RWIS-induced gastric ulcers. This study also provides a possible theoretical explanation for the different gastric dysfunctions induced by different stressors.
Subject(s)
Animals , Rats , Action Potentials , Physiology , Analysis of Variance , Central Amygdaloid Nucleus , Pathology , Corticotropin-Releasing Hormone , Metabolism , Disease Models, Animal , Gastric Mucosa , Pathology , Gene Expression Regulation , Physiology , Neurons , Physiology , Patch-Clamp Techniques , Proto-Oncogene Proteins c-fos , Metabolism , Rats, Wistar , Stress, Physiological , Physiology , Stress, PsychologicalABSTRACT
<p><b>OBJECTIVE</b>To reveal the nongenomic effect of aldosterone on the regulation of sodium intake in the nucleus tractus solitarius (NTS) and the role of central nucleus of the amygdala (CeA) in regulating this effect.</p><p><b>METHODS</b>Adult male SD rats were divided into four groups and underwent operations to induce bilateral CeA electrolytic lesions (400 μA, 25 s; =28), bilateral sham CeA lesions (=28), unilateral CeA lesions (=28), or unilateral sham CeA lesions (=26). After 3 days of recovery, the rats received implantation of a stainless steel 23-gauge cannula wih two tubes into the NTS followed by a recovery period of 7 days. The rats in each group were then divided into two subgroups for microinjection of aldosterone (50 ng/μL) or control solution in the NTS, and the cumulative intake within 30 min of 0.3 mol/L NaCl solution was recorded for each rat.</p><p><b>RESULTS</b>Bilateral CeA lesions (3 days) eliminated the increased 0.3 mol/L NaCl intake induced by aldosterone microinjected into the NTS (0.3±0.04 mL in CeA lesion group 1.3±0.3 mL in sham lesion group). Unilateral CeA lesion (3 days) reduced aldosterone-induced increase of NaCl intake in the first 15 min ( < 0.05) but not in 15-30 min ( > 0.05). In rats with sham lesions, aldosterone (50 ng/μL) still induced a significant increase in NaCl intake[1.3±0.3 mL 0.25±0.02 mL in the control group; F (3, 224)=24.0, < 0.05].</p><p><b>CONCLUSIONS</b>The regulation of sodium intake by aldosterone is subjected to descending facilitatory modulation by the bilateral CeA, and CeA integrity is essential for aldosterone to execute the nongenomic effect in regulating rapid sodium intake.</p>
ABSTRACT
Binge alcohol drinking during adolescence has been associated with neurotoxicity and increased risk for the development of alcohol use disorders. There is evidence that acute and chronic ethanol administration alters c-fos expression, an indirect index of cellular activity, in different brain regions in adult rats. We evaluate here if a binge-like pattern of ethanol exposure during adolescence has a relevant impact on basal and/or ethanol-stimulated regional c-fos activity during adulthood. For that aim, Sprague-Dawley rats PND 25 were saline pre-treated, (SP group) or binge-ethanol pre-treated (BEP group) for twoconsecutive days, at 48-h intervals, over a 14-day period (PND 25 to PND 38). At adult stage (PND 63) and following 25 ethanol-free days, we evaluated c-fos immunoreactivity in response to saline or acute ethanol (1.5 or 3.0 g/kg) in the hypothalamus and amygdala. We found that acute ethanol administration dose-dependently increased c-fos activity in the the Paraventricular nucleus of the hypothalamus (PVN). Interestingly, binge-ethanol exposure during adolescence significantly reduced basal c-fos activity during adulthood in the Central nucleus of the amygdala (CeA) and the Arcuate nucleus of hypothalamus (Arc). We conclude that binge-like ethanol administration during adolescence causes long-term disturbances in basal neural activity in brain areas critically involved with ethanol consumption.
El consumo en atracón durante la adolescencia está asociado con neurotoxicidad y con el riesgo de desarrollar un trastorno en el uso de alcohol. Diversos estudios muestran que la administración aguda y crónica de alcohol en ratas adultas altera la expresión de c-fos, un marcador indirecto de actividad celular, en diferentes áreas cerebrales. Nosotros evaluamos si el patrón de consumo de alcohol en atracón durante la adolescencia tiene un impacto en la actividad basal de c-fos en esas regiones activadas por el alcohol. Utilizamos ratas Sprague-Dawley en su día post-natal 25 (PND25) tratadas con suero salino (grupo SP) o con etanol tipo atracón (grupo BEP) durante dos días consecutivos, en intervalos de 48 h, durante 14 días (PND25- PND38). En la edad adulta (PND63) y después de 25 días sin etanol, evaluamos la inmunorreactividad para c-fos en respuesta a una administración aguda de suero salino o etanol (1,5 ó 3,0 g/kg) en diferentes regiones cerebrales. La administración de alcohol incrementó de manera dosis-dependiente la actividad de c-fos en el núcleo paraventricular del hipotálamo. Además la exposición a etanol tipo atracón durante la adolescencia disminuyó la actividad basal de c-fos en la adultez en el núcleo central de la amígdala y en el núcleo arqueado del hipotálamo. Concluimos que el consumo de alcohol en atracón durante la adolescencia causa problemas a largo plazo en la actividad basal de regiones cerebrales implicadas en el consumo de alcohol.
Subject(s)
Animals , Rats , Paraventricular Hypothalamic Nucleus/drug effects , Arcuate Nucleus of Hypothalamus/drug effects , Proto-Oncogene Proteins c-fos/drug effects , Ethanol/administration & dosage , Central Amygdaloid Nucleus/drug effects , Immunohistochemistry , Age Factors , Ethanol/pharmacologyABSTRACT
The reinforcement omission effect (ROE) has been attributed to both motivational and attentional consequences of surprising reinforcement omission. Recent evidence suggests that the basolateral complex of the amygdala is involved in motivational components related to reinforcement value, whereas the central nucleus of the amygdala is involved in the processing of the attentional consequences of surprise. This study was designed to verify whether the mechanisms involved in the ROE depend on the integrity of either the basolateral amygdala complex or central nucleus of the amygdala. The ROE was evaluated in rats with lesions of either the central nucleus or basolateral complex of the amygdala and trained on a fixed-interval schedule procedure (Experiment 1) and fixed-interval with limited hold signaled schedule procedure (Experiment 2). The results of Experiment 1 showed that sham-operated rats and rats with lesions of either the central nucleus or basolateral area displayed the ROE. In contrast, in Experiment 2, subjects with lesions of the central nucleus or basolateral complex of the amygdala exhibited a smaller ROE compared with sham-operated subjects. Thus, the effects of selective lesions of amygdala subregions on the ROE in rats depended on the training procedure. Furthermore, the absence of differences between the lesioned groups in either experiment did not allow the dissociation of attentional or motivational components of the ROE with functions of specific areas of the amygdala. Thus, results did not show a functional double-dissociation between the central nucleus and basolateral area in the ROE.
Subject(s)
Animals , Rats , Amygdala , Conditioning, Operant , Reinforcement, PsychologyABSTRACT
Reinforcement omission has been used as a procedure for the evaluation of attentional and motivational processes. Studies show that the activation of some amygdala nuclei may be involved in the modulation of these processes. This study examined the reinforcement omission effects on behavioral repertoire of rats with lesions in the central nucleus and basolateral complex of the amygdala, using classical conditioning and non-contingent reinforcement schemes. Each trial constituted of a 20 second tone, always followed by the delivery of water, in the 19th second. In the sessions involving omission, the water was delivered in half of the trials. The results showed that all groups responded to the omission and only the Basolateral group showed effect in the "Rearing" category, in the period after the omission. These results highlight the need to consider the involvement of a more complex neural network for evaluation of these effects.
A omissão de reforço tem sido usada como procedimento de avaliação dos processos atencionais e motivacionais. Estudos mostram que a ativação de alguns núcleos da amígdala pode estar envolvida na modulação destes processos. O presente trabalho examinou os efeitos da omissão do reforço no repertório comportamental de ratos com lesões no núcleo central e complexo basolateral da amígdala, utilizando-se de esquemas de condicionamento clássico e reforçamento não-contingente. Cada prática constituía de um sinal sonoro de 20 segundos, sempre seguido da liberação de água, no 19º segundo. Nas sessões que envolviam omissão, a água era liberada em metade das práticas. Os resultados mostraram que todos os grupos responderam à omissão e somente o grupo Basolateral apresentou efeito na categoria "Levantar-se", no período após a omissão. Estes resultados apontam a necessidade de se considerar o envolvimento de uma rede neural mais complexa para avaliação destes efeitos.