Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, July 14, 2016

Is silence golden? Effects of auditory stimuli and their absence on adult hippocampal neurogenesis

I bet your doctor hasn't even come up with this simple stroke protocol in the 2.5 years since it came out. A fireable offense in my book, including the stroke department head and the hospital president. The contradictions between this and enriched environment will need to be answered by your doctor. Do not try silence on your own, that would be too dangerous unless your doctor has prescribed it.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4087081/
From http://www.lifehack.org/377243/science-says-silence-much-more-important-our-brains-than-thought

Abstract

We have previously hypothesized that the reason why physical activity increases precursor cell proliferation in adult neurogenesis is that movement serves as non-specific signal to evoke the alertness required to meet cognitive demands. Thereby a pool of immature neurons is generated that are potentially recruitable by subsequent cognitive stimuli. Along these lines, we here tested whether auditory stimuli might exert a similar non-specific effect on adult neurogenesis in mice. We used the standard noise level in the animal facility as baseline and compared this condition to white noise, pup calls, and silence. In addition, as patterned auditory stimulus without ethological relevance to mice we used piano music by Mozart (KV 448). All stimuli were transposed to the frequency range of C57BL/6 and hearing was objectified with acoustic evoked potentials. We found that except for white noise all stimuli, including silence, increased precursor cell proliferation (assessed 24 h after labeling with bromodeoxyuridine, BrdU). This could be explained by significant increases in BrdU-labeled Sox2-positive cells (type-1/2a). But after 7 days, only silence remained associated with increased numbers of BrdU-labeled cells. Compared to controls at this stage, exposure to silence had generated significantly increased numbers of BrdU/NeuN-labeled neurons. Our results indicate that the unnatural absence of auditory input as well as spectrotemporally rich albeit ethological irrelevant stimuli activate precursor cells—in the case of silence also leading to greater numbers of newborn immature neurons—whereas ambient and unstructured background auditory stimuli do not.
Keywords: Plasticity, Stem cells, Hippocampus, Mouse, Learning

Introduction

Adult neurogenesis adds plasticity to the dentate gyrus of the hippocampus and is involved in key functions such as pattern separation (Aimone et al. 2010; Clelland et al. 2009) and avoidance of catastrophic interference (Appleby and Wiskott 2009; Wiskott et al. 2006) by adding flexibility to the network in situations where novel information has to be integrated into established representations (Garthe et al. 2009; Dupret et al. 2008). Adult neurogenesis is regulated by behavioral activity. Both physical activity and exposure to a challenging environment increase adult neurogenesis but do so by different means (Kronenberg et al. 2003). Non-specific stimuli like physical activity enhance the proliferation of precursor cells and lead to an increased potential in form of a larger pool of “neuroblasts” and immature neurons that can be recruited in case of a cognitive challenge. In contrast, exposure to an enriched environment promotes the survival of newborn neurons. Accordingly, the two interventions turned out to be additive in their effect (Fabel et al. 2009).
The new immature neurons own particular functionality in that they are more likely to generate action potentials in response to incoming stimuli due to their particular balance between excitatory and inhibitory input (Marin-Burgin et al. 2012). The threshold for LTP induction is reduced in these neurons (Schmidt-Hieber et al. 2004; Snyder et al. 2001). In fact, the LTP that is measurable in the dentate gyrus under physiological conditions is contributed by the newborn neurons during this critical period of their development (Garthe et al. 2009; Saxe et al. 2006). Thus, the immature new neurons are assumed to be more easily excitable than older cells, biasing the input towards the more plastic subpopulation of cells (Marin-Burgin et al. 2012). The hypothesis is that this mechanism allows flexible adaptation and learning of new information in previously established contexts. Non-specific stimuli would increase precursor cell proliferation to increase a pool of cells that can be recruited if cognitive demand arises (for detailed discussion see: Fabel et al. 2009).
The finding that exercise would have this effect on proliferation raised the question, whether other non-specific stimuli would also lead to an increased availability of potentially recruitable cells. Presumably, the intrinsic stimulus during physical activity essentially consists of proprioception and vision. Likewise, there are numerous reports on links between the vestibular system and hippocampal function [(Brandt et al. 2005); see Ref. Smith et al. (2010) for review] even though effects on adult neurogenesis have not yet been specifically addressed. In order to identify relevant sensory stimuli independent of locomotion, we here focused on auditory input as a potential signal to affect adult hippocampal neurogenesis.
Noise trauma with inner ear hair cell loss has led to a reduction of precursor cell proliferation in the hippocampus of rats (Kraus et al. 2010). A potential positive regulatory effect of sound on the early steps of adult hippocampal neurogenesis, however, has not yet been explored. We asked how different types of auditory stimuli would affect the baseline regulation of adult hippocampal neurogenesis (Fig. 1a).
Fig. 1
Regulation of adult hippocampal neurogenesis in dependency of auditory stimuli. a We used two different approaches to address both proliferation and survival/differentiation by injection of BrdU either 24 h before daily sounds exposure or after ...
We used ambient noise in the animal facility (animal house noise) as baseline and exposed our mice to four different conditions: (1) white noise as unstructured auditory stimulus; (2) mouse pup calls as structured stimulus that is for mice common and relevant; (3) Mozart piano music as a structured stimulus, unknown and presumably irrelevant to mice; and (4) silence.

More at link.


No comments:

Post a Comment