Galanin (GAL) and neuropeptide Y (NPY) are neuropeptides involved in behaviors associated with anxiety. Both neuropeptides interact in several central functions. However, the potential behavioral and cellular interactions between them in anxiety are unknown. GAL was found to act through GAL receptor 2 (GALR2) to enhance NPYY1 receptor (NPYY1R)-mediated anxiolytic behaviors in rats. Using receptor autoradiography, c-Fos expression and in situ proximity ligation assay, the medial paracapsular intercalated nuclei of the amygdala were determined to be a key area in the interaction probably involving the formation of GALR2/NPYY1R heteroreceptor complexes. In cell cultures costimulation of GALR2 and NPYY1R induced changes in the functions of these receptors. The changes involved a potentiation of the decrease in the phosphorylation of CREB induced by NPYY1R and a delay in the internalization of NPYY1R. These results indicate that GALR2/NPYY1R interactions can provide a novel integrative amygdaloid mechanism in anxiety.

Galanin (GAL) is a peptide involved in multiple functions, including central cardiovascular control. In this review, the role of GAL and its fragments in the modulation of cardiovascular neuronal networks in the nucleus of the solitary tract is presented, including its interaction with the classical neurotransmitters and other neuropeptides involved in cardiovascular responses in this nucleus. First, we describe the cardiovascular responses of GAL and the pathway involved in these responses. Then we summarize findings obtained in our laboratory on how GAL, through its receptors, interacts with two other neuropeptides -Neuropeptide Y and Angiotensin II and their receptors -as they have particularly conspicuous cardiovascular effects. All these results strengthen the role of GAL in central cardiovascular control and indicate the existence of interactions among GAL receptor subtypes and a 2 -adrenergic receptors, AT1, and Y1 receptor subtypes. These interactions are crucial for understanding the integrative mechanisms responsible for the organization of the cardiovascular responses from the NTS.

The GABA, antagonist CGP 35348 was intraperitoneally given in doses of 100, 300, and 900 mglkg to old rats. These rats were earlier chronically provided with EEG and EMG electrodes. Sleep recordings based on visual inspection of EEG and EMG recordings were made for 3 h post injection, and spontaneous behaviour in the recording cage was additionally observed. With 100 and 300 mglkg, the drug produced an increase in the duration of REM sleep compared to the saline-injected control group. The REM sleep latency was correspondingly reduced. Non-REM sleep and total sleep duration increased and an s-shaped dose-response relationship was found. Explorative behaviour was diminished after injections with 100 and 300 mgl kg CGP 35348. The number and duration of spike-wave discharges were reduced after all doses of CGP 35348 and during all 3 recording hours. The latter outcomes confirm the strong suppressive action of this drug on spike-wave discharges; these effects have also been reported in models of absence epilepsy. The hypnotic properties and especially the increase in REM sleep after the administration of CGP 35348 deserve attention considering the paucity of drugs which facilitate REM sleep. The discovery of drugs promoting REM sleep might have theoretical as well as clinical consequences.

Los trastornos de ansiedad son, en la actualidad, enfermedades psiquiátricas muy frecuentes e incapacitantes. Las mujeres en edad reproductiva son más vulnerables a desarrollar trastornos de ansiedad, aproximadamente entre 2 a 3 veces más que los hombres. Ser hombre o mujer no sólo puede influir en la prevalencia de los trastornos mentales, sino también en la manifestación y expresión de los síntomas, la voluntad para solicitar asistencia médica o psicológica, el curso de la enfermedad, incluso en la respuesta al tratamiento. Cada vez hay pruebas más sólidas de que existen diferencias entre ambos sexos respecto a la anatomía cerebral, la neuroquímica y los patrones de activación y respuesta a los estímulos ambientales; diferencias que pueden influir en la etiología y el curso de los trastornos psiquiátricos. Sin embargo, poco se conoce sobre los factores de riesgo que inducen a las mujeres a desarrollar ciertas psicopatologías. Por ello, en este trabajo pretendemos presentar una breve revisión sobre los aspectos psicobiológicos que pueden contribuir a las diferencias de sexo en los trastornos de ansiedad.

No abstract