Mice genetically deficient in vasopressin V1a and V1b receptors are resistant to jet lag.
Science
; 342(6154): 85-90, 2013 Oct 04.
Article
em En
| MEDLINE
| ID: mdl-24092737
ABSTRACT
Jet-lag symptoms arise from temporal misalignment between the internal circadian clock and external solar time. We found that circadian rhythms of behavior (locomotor activity), clock gene expression, and body temperature immediately reentrained to phase-shifted light-dark cycles in mice lacking vasopressin receptors V1a and V1b (V1a(-/-)V1b(-/-)). Nevertheless, the behavior of V1a(-/-)V1b(-/-) mice was still coupled to the internal clock, which oscillated normally under standard conditions. Experiments with suprachiasmatic nucleus (SCN) slices in culture suggested that interneuronal communication mediated by V1a and V1b confers on the SCN an intrinsic resistance to external perturbation. Pharmacological blockade of V1a and V1b in the SCN of wild-type mice resulted in accelerated recovery from jet lag, which highlights the potential of vasopressin signaling as a therapeutic target for management of circadian rhythm misalignment, such as jet lag and shift work.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Receptores de Vasopressinas
/
Síndrome do Jet Lag
Limite:
Animals
Idioma:
En
Ano de publicação:
2013
Tipo de documento:
Article