Author Archives: johnwschmidt

About johnwschmidt

Exploring medical physiology.

Protein Kinase M and LTP

My previous blog post was also about LTP: long-term potentiation of synapses. Here, the topic is what has been called late-LTP (L-LTP), a strengthening of synapses that can last for months in the hippocampus of laboratory animals. Molecular and cellular … Continue reading

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Presynaptic Endocannabinoid-initiated LTP

“LTP” is long-term potentiation, a type of synaptic plasticity found in the hippocampus that is involved in episodic memory storage. A recent research article reports on the mechanism by which endocannabinoid signaling affects the induction of hippocampal long-term potentiation (LTP). … Continue reading

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Circadian Pacemaker

In my previous blog post, I mentioned that the GHSR1 ghrelin receptor has a high level of activity independent of ghrelin binding.  Recently, an “orphan” G Protein-coupled Receptor (GPCR) (Gpr176) has been implicated in the function of the circadian pacemaker of … Continue reading

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Ghrelin is a vertebrate peptide hormone that has been most heavily studied for its role as a signalling molecule that is made in the gastrointestinal tract and which can modulate the behavior of ghrelin receptors on neurons, both in the … Continue reading

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From the World Health Organization’s Measles Fact sheet (Updated November 2014): Measles information from the U.S. Centers for Disease Control: Manual for the Surveillance of Vaccine-Preventable Diseases, Chapter 7: Measles The CDC measles outbreak webpage. California Department of Public Health … Continue reading

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Narrated PowerPoint Presentations

I previously blogged about using ProfCast to add audio narration to PowerPoint presentations. I had better results recording audio using the internal microphone of a Macintosh than the internal microphone of an HP laptop, but I was left wanting to … Continue reading

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Amyloid β-protein and Synaptophysin

Amyloid β-peptide is normally produced in the brain from the amyloid precursor protein (APP). The amyloid cascade hypothesis of Alzheimer disease says that abnormal accumulation in the brain of amyloid β-peptide (Aβ) causes disruption of synaptic neurotransmission and, eventually, the death of neurons … Continue reading

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