Growth Hormone: Why not ? Rescues Hippocampal Synaptic Function after Sleep Deprivation and Medication


Growth Hormone Rescues Hippocampal Synaptic Function after Sleep Deprivation

Our results identify growth hormone as a critical mediator linking sleep to normal synaptic function of the hippocampus.

Hippocampal CA1 neurons from sleep-deprived animals had reduced NMDAR-mediated synaptic currents, reduced NMDA receptor-dependent LTP, and reduced synaptic NR2B subunit expression.

Restoring growth hormone to sleep-deprived animals caused recovery of NMDAR function, NMDA receptor-dependent synaptic plasticity, and synaptic NMDAR subunit expression.

The NMDAR, of course is a specific type of ionotropic glutamate receptor. It is named this because the agonist molecule N-methyl-D-aspartate (NMDA) binds selectively to it, and not to other glutamate receptors. , a cellular mechanism for learning and memory.

In this study, LTP was deficient in hippocampal slices from sleep-deprived animals, which had a lower NR2B subunit level. Growth hormone restoration to sleep-deprived animals rescued LTP Subunit NR2B of the NMDAR is critical for targeting activated calcium-calmodulin-dependent protein kinase II, a downstream target for Ca2+ during LTP induction Ca2+ flux through NMDARs is thought to be critical in synaptic plasticity

Sleep is required for, and sleep loss impairs, normal hippocampal synaptic N-methyl-d-aspartate (NMDA) glutamate receptor function and expression, hippocampal NMDA receptor-dependent synaptic plasticity, and hippocampal-dependent memory function.

Changes seen during normal aging further emphasize the critical role of growth hormone/IGF-I in maintaining memory function. Circulating growth hormone and IGF-I are decreased during aging , and growth hormone or IGF-I treatment improves memory-dependent performance . Aged rats show impaired hippocampal LTP and hippocampal-dependent learning and memory that have been linked to decreased NR2B expression

Although sleep is essential, the signals linking sleep to hippocampal function are not known. One potential signal is growth hormone. Secretion of pituitary growth hormone is strongly related to sleep. A major surge of growth hormone secretion occurs during sleep, and sleep deprivation suppresses growth hormone secretion

Growth hormone is released during sleep, and its release is suppressed during sleep deprivation. If growth hormone links sleep to hippocampal function, then restoration of growth hormone during sleep deprivation should prevent adverse consequences of sleep loss. In men, even more so than women, about 75% of your total HGH is produced as a consequence of SlowWaveSleep Periods

(whereas it’s only about 50% for women)

It is no coincidence that the secretion of Growth Hormone Pulses is associated with slow wave sleep. Slow Wave Sleep is related to neurogenesis and in particular to the sequence of stages required to yield new mature differentiated cells in the various areas of the brain. Of course we know what a preponderance of neurogenesis occurs within the hippocampal area, and, in particular, the dentate gyrus, closely apposed toe CA1

This, NR2B subunit is mainly present in immature neurons and in extrasynaptic locations, The NR2B is predominant in the early postnatal brain, but the number of NR2A subunits grows with age, and eventually NR2A subunits outnumber NR2B. There is a universal similarity (if not absolute identity) between the sequences of events and the relevant factors in adult neurogenesis and in embryological and early post natal development.

So we can see that what is likely happening here is that the growth hormone is exerting its effects via its role in the sequence of neurogenesis stages as the pluripotent progenitors first proliferate and then are ready for differentiation stages, which apparently required HGH>

Growth Hormone production and availability is a key signal during the course of the process of neurogenesis…in the differentiation stage of the process, but not the proliferation stage. Accordingly therefore HGH as a growth factor of importance in the process of neurogenesis would be naturally expected.

The fact that neurogenesis and the aspects of SWS including memory consolidiation with which it is associated are key players in the processing of new experience and the availability of that experience to future moments and to adaptive learning during those moments simply fits perfectly with the findings here.

And,yes, this finding is probably relevant to the fact that we seem to get less and less cognitively sharp with age. Presumably the modicum of new neurons that is produced as we age along with the diminished HGH secretion is associated with that aging deterioration

This study just speaks of sleep deprivation in a general sense . Sleep deprivation itself has long been associated with impairment of learning and memory . Also, like growth hormone, sleep deprivation affects hippocampal synaptic plasticity by altering NMDAR expression and function

But if you are one of the millions who is staking sleep medicine of one kind or another (Zolpidem or Zopiclone or whatever) you can be sure that you are not getting proper sleep with the proper sleep architecture…even though you may be knocked for 7 or 8 hours.

Thus to us it makes eminent good sense for every physician who prescribes some so called “sleep medication” all of which diminish slow wave sleep and diminsh Growth Hormone production, even while you are thinking that you are getting true sleep…to also consider and probably prescribe HGH as part of the treatment. But we cannot expect that kind of caring care, can we?

To test this hypothesis, we examined rat hippocampus for spontaneous excitatory synaptic currents in CA1 pyramidal neurons, long-term potentiation in area CA1, and NMDA receptor subunit proteins in synaptic membranes.

Three days of sleep deprivation caused a significant reduction in NMDA receptor-mediated synaptic currents compared with control treatments.

When rats were injected with growth hormone once per day during sleep deprivation, the loss of NMDA receptor-mediated synaptic currents was prevented.

Growth hormone injections also prevented the impairment of long-term potentiation that normally follows sleep deprivation. In addition, sleep deprivation led to a selective loss of NMDA receptor 2B (NR2B) from hippocampal synaptic membranes, but normal NR2B expression was restored by growth hormone injection.

There seems to be all the reason in the world to take HGH to retain good performance and cognitive funciont the next day and to keep your hippocampus functioning up to par.

Of course, they won’t tell you this. And your doctors will pretend they know nothing about t. They’ d much prefer to sit on the side lines watch you erode day after day, or should we say “night after night” while filling yourself with the sleep meds “du jour’ instead of providing you with HGH to keep your brain at optimal level of function.

OF course, the researchers and pharma are an equally cowardly lot because until the do the proper research, the HGH is not likely to be insurable. And since it costs about $700 per month, it’s beyond most people’s budgets.

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