Growth hormone improves hippocampal adult cell survival and counteracts the inhibitory effect of prolonged sleep deprivation on cell proliferation

García-García, Fabio; Herrán-Arita, Alberto K. De la; Juárez-Aguilar, Enrique; Regalado-Santiago, Citlalli; Millán-Aldaco, Diana; Blanco-Centurión, Carlos; Drucker-Colı́n, René

doi:10.1016/j.brainresbull.2011.01.003

Cited by 34 publications

(15 citation statements)

References 61 publications

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“…Although not classically considered to be a neurotrophic factor, accumulating evidence indicates that GH plays an important role in the regeneration of neural cells. [13][14][15] Our results indicate that GH treatment is also useful in promoting sciatic nerve regeneration, thus supporting the possibility of using the hormone, alone or in combination with other therapeutic approaches, for treatment of peripheral nerve injuries.…”

supporting

confidence: 61%

“…49 In addition, GH is known to play a major role in neural development 50 and several lines of evidence suggest that the GH/GHR pathway also plays a role in neuroregeneration. [13][14][15] In this regard, it should be highlighted that GH therapy has been proven to exert beneficial effects on the treatment of several central nervous system pathologies, including cerebral palsy 51,52 and the neurological sequelae of traumatic brain injury or oncological brain surgery. 53 GH treatment may have several advantages over other neurotrophic factors.…”

Section: Discussionmentioning

confidence: 99%

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Growth hormone treatment enhances the functional recovery of sciatic nerves after transection and repair

et al. 2012

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supporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Growth hormone treatment enhances the functional recovery of sciatic nerves after transection and repair

et al. 2012

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“…AcPb is also implicated in hippocampal synaptogenesis (Huang et al 2011, Yoshida et al 2012). Extended sleep deprivation compromises hippocampal neogenesis and proliferation (Guzmin-Marin 2003; Garcia-Garcia et al 2011). Recent evidence indicates that the type I IL1 receptor and glucocorticoids mitigate the detrimental effects of sleep loss on cell survival (Mueller et al 2014).…”

Section: Discussionmentioning

confidence: 99%

The neuron-specific interleukin-1 receptor accessory protein is required for homeostatic sleep and sleep responses to influenza viral challenge in mice

Davis

Dunbrasky

Oonk

et al. 2015

Brain, Behavior, and Immunity

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Interleukin-1β, (IL1) is involved in sleep regulation and sleep responses induced by influenza virus. The IL1 receptor accessory protein (AcP) and an alternatively spliced isoform of AcP found primarily in neurons, AcPb, form part of the IL1 signaling complex. IL1-induced sleep responses depend on injection time. In rat cortex, both IL1 mRNA and AcPb mRNA peak at Zeitgeber Time (ZT) 0 then decline over the daylight hours. Sleep deprivation enhances cortical IL1 mRNA and AcPb mRNA levels, but not AcP mRNA. We used wild type (WT) and AcPb knockout (KO) mice and performed sleep deprivation between ZT10-20 or between ZT22-8 based on the time of day expression profiles of AcPb and IL1. We hypothesized that the magnitude of the responses to sleep loss would be strain- and time of day-dependent. In WT mice, NREMS and REMS rebounds occurred regardless of when they were deprived of sleep. In contrast, when AcPbKO mice were sleep deprived from ZT10-20 NREMS and REMS rebounds were absent. The AcPbKO mice expressed sleep rebound if sleep loss occurred from ZT22-8 although the NREMS responses were not as robust as those that occurred in WT mice. We also challenged mice with intranasal H1N1 influenza virus. WT mice exhibited the expected enhanced sleep responses. In contrast, the AcPbKO mice had less sleep after influenza challenge compared to their own baseline values and compared to WT mice. Body temperature and locomotor activity responses after viral challenge were lower and mortality was higher in AcPbKO than in WT mice. We conclude that neuron-specific AcPb plays a critical role in host defenses and sleep homeostasis.

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“…Damaged neurons from TBI are often found in regions controlling behavior (Garcia-Garcia et al, 2011), which may result in increased neuropsychiatric symptoms characteristic of many neurodegenerative diseases. In a rodent model of sleep disruption and fragmentation, for example, animals displayed more impulsive-like behavior and had increased levels of corticosterone (Tartar et al, 2009).…”

Section: Mechanistic Consequences Of Sleep Disruptionmentioning

confidence: 99%

Sleep disruption and the sequelae associated with traumatic brain injury

Lucke‐Wold

Smith

Nguyen

et al. 2015

Neuroscience & Biobehavioral Reviews

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Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy.

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Growth hormone improves hippocampal adult cell survival and counteracts the inhibitory effect of prolonged sleep deprivation on cell proliferation

Cited by 34 publications

References 61 publications

Growth hormone treatment enhances the functional recovery of sciatic nerves after transection and repair

Growth hormone treatment enhances the functional recovery of sciatic nerves after transection and repair

The neuron-specific interleukin-1 receptor accessory protein is required for homeostatic sleep and sleep responses to influenza viral challenge in mice

Sleep disruption and the sequelae associated with traumatic brain injury

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