A potential role of hippocampus on impulsivity and alcohol consumption through CB1R.

There are a few studies suggesting that the hippocampus is involved in the regulation of impulsivity, and which attempt to explain drug seeking behavior in addiction. In addition, cannabinoid receptor 1 (CB1R) is highly expressed in the hippocampus (HPP). To further understand the potential role of the hippocampal CB1R in impulsive and drug seeking behaviors, we characterized impulsivity in adolescent and adult male rats, by means of a delay discounting task (DDT) by evaluating preference and seeking motivation for alcohol (10 % v/v) consumption, and analyzing CB1R expression in CA1, CA3 and the dentate gyrus (DG) of the HPP as well as in the medial prefrontal cortex (mPFC). Our results show that adolescent rats display more impulsive choices than adult rats in the DDT. The k value is statistically higher in adolescents, further supporting that they are more impulsive. Besides, adolescent rats have higher forced and voluntary alcohol consumption and display a higher alcohol conditioned place preference (CPP) vs. adult rats. In addition, CB1R expression in CA3 and the DG is higher in adolescent vs. adult rats. Our data further support the role of the hippocampus in impulsivity with the potential involvement of the endocannabinoid system, considering that CB1R in CA3 and DG is higher in adolescents, who display impulsivity and alcohol seeking and consumption.

[Sleep genes]. / Genes del sueño.

INTRODUCTION: Sleep is a non-learned adaptive strategy that depends on the expression of several neurotransmitters and other molecules. The expression of some of these molecules depends on a number of different genes. Sleep disorders are associated with an inadequate expression of some molecules, which therefore indicates that these genes that code for these molecules participate in the regulation of normal sleep. AIM: To discuss the evidence on gene regulation over the occurrence of sleep and its architecture, as well as of sleep disorders, which supports the participation of specific genes. DEVELOPMENT: We describe the evidence on sleep in mammals, particularly in humans, in addition to studies with twins that demonstrate the influence of genes on sleep regulation. We also discuss several sleep disorders, which in this study only serves to emphasise how certain specific genes, under normal conditions, participate in the expression of sleep. Furthermore, evidence is also provided for other molecules, such as endocannibinoids, involved in sleep regulation. Lastly, we report on studies conducted with different strains of mice that show differences in the amount of sleep they express, possibly as an epiphenomenon of their different genetic loads. CONCLUSIONS: A number of different genes have been described as those responsible for making us sleep, although sleeping also depends on our interaction with the environment. This interaction is what makes us express sleep at times that are best suited to favouring our survival.

Genes del sueño / Sleep Genes

Resumen. Introducción. El sueño es una estrategia adaptativa no aprendida que depende de la expresión de diversos neurotransmisores y otras moléculas. La expresión de varias de estas moléculas depende de diversos genes. Alteraciones del dormir se asocian con una inadecuada expresión de algunas moléculas, que indican entonces que estos genes que codifican estas moléculas participan en la regulación del sueño normal. Objetivo. Discutir la evidencia de la regulación de los genes sobre la ocurrencia del sueño y su arquitectura, así como de alteraciones del sueño, que sustenta la participación de genes específicos. Desarrollo. Se describe la evidencia sobre el sueño en mamíferos, particularmente en humanos, así como estudios con gemelos que evidencian la influencia genética en la regulación del sueño. Posteriormente, se discuten algunas alteraciones del sueño, que en esta revisión sólo sirven para enfatizar cómo ciertos genes específicos, en condiciones normales, participan en la expresión del sueño. Además, se da evidencia sobre otras moléculas, como los endocannabinoides, que participan en la regulación del sueño. Por último, se describen los estudios con diferentes cepas de ratones que manifiestan diferencias en la cantidad de sueño que expresan, posiblemente como epifenómeno de sus diferentes cargas genéticas. Conclusiones. Se han descrito diversos genes que nos hacen dormir, aunque dormir también depende de la interacción con el medio ambiente. Esta interacción es la que nos hace expresar el sueño en los momentos más convenientes para sobrevivir (AU)

Summary. Introduction. Sleep is a non-learned adaptive strategy that depends on the expression of several neurotransmitters and other molecules. The expression of some of these molecules depends on a number of different genes. Sleep disorders are associated with an inadequate expression of some molecules, which therefore indicates that these genes that code for these molecules participate in the regulation of normal sleep. Aim. To discuss the evidence on gene regulation over the occurrence of sleep and its architecture, as well as of sleep disorders, which supports the participation of specific genes. Development. We describe the evidence on sleep in mammals, particularly in humans, in addition to studies with twins that demonstrate the influence of genes on sleep regulation. We also discuss several sleep disorders, which in this study only serves to emphasise how certain specific genes, under normal conditions, participate in the expression of sleep. Furthermore, evidence is also provided for other molecules, such as endocannibinoids, involved in sleep regulation. Lastly, we report on studies conducted with different strains of mice that show differences in the amount of sleep they express, possibly as an epiphenomenon of their different genetic loads. Conclusions. A number of different genes have been described as those responsible for making us sleep, although sleeping also depends on our interaction with the environment. This interaction is what makes us express sleep at times that are best suited to favouring our survival (AU)