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Alcohol use disorder can vary in severity. Alcohol dependence can impact stress and other disorders in many ways. [70] For example, stress-related disorders such as anxiety and PTSD are known to increase risk of alcohol use disorder (AUD), and they are often co-morbid. Mental disorders that pair with AUD can impacts the brain in many ways.
Intrinsic stress can be acutely and chronically experienced by a person. [8] The varying effects of stress on performance or stress hormones are often compared to or known as "inverted-u" [10] which induce areas in learning, memory and plasticity. [8] Chronic stress can affect the brain structure and cognition.
Two molecular mechanisms for synaptic plasticity involve the NMDA and AMPA glutamate receptors. Opening of NMDA channels (which relates to the level of cellular depolarization) leads to a rise in post-synaptic Ca 2+ concentration and this has been linked to long-term potentiation, LTP (as well as to protein kinase activation); strong depolarization of the post-synaptic cell completely ...
Anxiety is the Big Bad Wolf of the modern wellness conversation: How to get rid of it, how to get to sleep with it, how to meditate it away. But what if there’s another way of interpreting anxiety?
It is also used at most synapses that are "modifiable", i.e. capable of increasing or decreasing in strength. Modifiable synapses are thought to be the main memory-storage elements in the brain. Excessive glutamate release can overstimulate the brain and lead to excitotoxicity causing cell death resulting in seizures or strokes. [22]
Synapses that have undergone LTP tend to have stronger electrical responses to stimuli than other synapses. The term long-term potentiation comes from the fact that this increase in synaptic strength, or potentiation, lasts a very long time compared to other processes that affect synaptic strength. [1]