Chronic Exposure to High Altitude: Synaptic, Astroglial and Memory Changes.
Rupali Sharma1,2, Nathan P Cramer2,3, Bayley Perry1,2
1Department of Pathology, F. Edward Hébert School of Medicine Uniformed Services University of the Health Sciences (USU), Bethesda, MD, USA.
Scientific Reports
|November 13, 2019
Summary
Chronic high altitude exposure impairs learning and memory in mice. This cognitive decline is linked to region-specific molecular changes in synaptic proteins and glial markers in the brain.
Area of Science:
- Neuroscience
- Altitude Physiology
- Molecular Biology
Background:
- Long-term high altitude (HA) operations can cause health issues.
- Chronic exposure to high altitude (CEHA) is linked to cognitive deficits.
- Understanding the molecular basis of CEHA-induced cognitive impairment is crucial.
Purpose of the Study:
- To investigate the effects of CEHA on cognitive function in mice.
- To examine changes in synaptic protein expression in response to CEHA.
- To explore region-specific molecular alterations in the brain following CEHA.
Main Methods:
- Mice were exposed to chronic high altitude (5000m for 12 weeks).
- Cognitive functions, including learning and memory, were assessed.
- Synaptic protein levels (e.g., synaptophysin, PSD-95) and glial markers were measured using molecular techniques.
- Ultrastructural analyses were performed on hippocampal synapses.
Main Results:
- CEHA mice showed deficits in learning and memory associated with hippocampal function.
- Decreased levels of synaptophysin and spinophilin were observed in the olfactory cortex.
- Reduced levels of PSD-95, GAP43, and GFAP were found in the cerebellum.
- Synaptophysin and PSD-95 levels were also decreased in the brainstem.
- No significant differences in hippocampal synaptic density or morphology were noted.
Conclusions:
- CEHA exposure leads to cognitive impairment in mice.
- Cognitive deficits are associated with region-specific molecular changes in synaptic proteins and glial markers.
- These findings suggest complex neuroplasticity mechanisms underlying brain adaptation to chronic high altitude.
Related Concept Videos
Role of Neurotransmitters in Memory
2.3K
Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is...
Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is...
2.3K
Long-term Depression
3.0K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...
Calcium Ion Concentration Mechanism
If over...
3.0K
Long-term Depression
32.9K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
32.9K
Alzheimer's Disease: Overview
1.5K
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
1.5K
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists
479
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
479
Long-term Potentiation
58.0K
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
58.0K


