Diurnal variation of NMDA receptor expression in the rat cerebral cortex is associated with traumatic brain injury damage.

OBJECTIVE: Data from our laboratory suggest that recovery from a traumatic brain injury depends on the time of day at which it occurred. In this study, we examined whether traumatic brain injury -induced damage is related to circadian variation in N-methyl-D-aspartate receptor expression in rat cortex. RESULTS: We confirmed that traumatic brain injury recovery depended on the time of day at which the damage occurred. We also found that motor cortex N-methyl-D-aspartate receptor subunit NR1 expression exhibited diurnal variation in both control and traumatic brain injury-subjected rats. However, this rhythm is more pronounced in traumatic brain injury-subjected rats, with minimum expression in those injured during nighttime hours. These findings suggest that traumatic brain injury occurrence times should be considered in future clinical studies and when designing neuroprotective strategies for patients.

Does the neuroprotective role of anandamide display diurnal variations?

The endocannabinoid system is a component of the neuroprotective mechanisms that an organism displays after traumatic brain injury (TBI). A diurnal variation in several components of this system has been reported. This variation may influence the recovery and survival rate after TBI. We have previously reported that the recovery and survival rate of rats is higher if TBI occurs at 1:00 than at 13:00. This could be explained by a diurnal variation of the endocannabinoid system. Here, we describe the effects of anandamide administration in rats prior to the induction of TBI at two different times of the day: 1:00 and 13:00. We found that anandamide reduced the neurological damage at both times. Nevertheless, its effects on bleeding, survival, food intake, and body weight were dependent on the time of TBI. In addition, we analyzed the diurnal variation of the expression of the cannabinoid receptors CB1R and CB2R in the cerebral cortex of both control rats and rats subjected to TBI. We found that CB1R protein was expressed more during the day, whereas its mRNA level was higher during the night. We did not find a diurnal variation for the CB2R. In addition, we also found that TBI increased CB1R and CB2R in the contralateral hemisphere and disrupted the CB1R diurnal cycle.

Sleep deprivation has a neuroprotective role in a traumatic brain injury of the rat.

During the process of a brain injury, responses to produce damage and cell death are activated, but self-protective responses that attempt to maintain the integrity and functionality of the brain are also activated. We have previously reported that the recovery from a traumatic brain injury (TBI) is better in rats if it occurs during the dark phase of the diurnal cycle when rats are in the waking period. This suggests that wakefulness causes a neuroprotective role in this type of injury. Here we report that 24h of total sleep deprivation after a TBI reduces the morphological damage and enhances the recovery of the rats, as seen on a neurobiological scale.

Neuroprotección y traumatismo craneoencefálico / Neuroprotection and traumatic brain injury

Durante un proceso de lesión cerebral, por ejemplo en un traumatismo craneoencefálico, se activan respuestas que inducen daño cerebral o muerte celular; sin embargo, también se inducen respuestas de protección que intentan mantener la integridad y funcionalidad del cerebro; esto se conoce como neuroprotección. Efectivamente, posterior a un TCE, se desencadenan mecanismos que traen como consecuencia liberación de neurotransmisores excitadores tales como el glutamato, lo que provoca una entrada masiva de Ca²+ en las neuronas, activación de proteasas, lipasas, sintasa de óxido nítrico, endonucleasas, producción de radicales libres y potencialmente necrosis o apoptosis. Aunque hay reportes de sustancias neuro o cerebroprotectoras desde hace más de 50 años, es al final de la década de los ochenta del siglo pasado cuando comienza a aparecer un gran número de publicaciones tratando de entender los mecanismos neuroprotectores desencadenados por un insulto al cerebro. En este trabajo revisamos brevemente el concepto, la epidemiologia y los diversos agentes que se han utilizado para disminuir el daño causado por un traumatismo craneoencefálico.

During a process of brain injury, e.g. head injury, responses to induce brain damage and / or cell death are activated, but also protective responses that attempt to maintain the integrity and functionality of the brain are induced. This is known as neuroprotection. Indeed a head injury triggers mechanisms that result in release of excitatory neurotransmitters such as glutamate, which causes an influx of Ca²+ into neurons, activation of proteases, lipases, nitric oxide synthase, endonucleases, free radicals production and potentially necrosis and / or apoptosis. Although the brain or neuroprotective substances research has more than 50 years, is at the end of the decade of 80's of last century when it began to appear a large number of publications trying to understand the neuroprotective mechanisms triggered by an insult to the brain. In this paper we briefly review the concept, epidemiology and strategies that have been used to minimize the damage caused by brain injury.

Recovery after a traumatic brain injury depends on diurnal variations effect of cystatin C.

Many studies indicate that the hour of the day at which the onset of stroke occurs is very important in patient recovery. Furthermore, multiple studies have been conducted which show that ischemia in rats produces different magnitudes of injury depending on the hour of the day at which it was induced. Using a traumatic brain injury (TBI) model, we analyzed the effect of the time of day on the recovery of rats and obtained a higher survival rate if TBI was induced at 01:00 h as compared with TBI induced at 13:00 h. We also analyzed the effect of the protease inhibitor cystatin C (CC) on the recovery of rats from TBI and found that it increased mortality and bleeding, and that these effects were more pronounced at 13:00 h.