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Effects Biological impact Intense psychological stress caused by unwanted, troublesome memories can cause brain structures such as the amygdala, hippocampus and frontal cortex to become activated, as they process the memory.
Related to this, there is some neuroimaging fMRI evidence that those who are susceptible to PTSD have a hippocampus with a reduced size. These children suffer academically and socially due to symptoms like fragmentation of memoryintrusive thoughts, dissociation and flashbacks, all of which may be related to hippocampal dysfunction.
Physical aggression, conflicts and moodiness cause dysfunction in relationships with families, spouse, children and significant others. Depressionsevere anxiety and fear commonly stem from traumatic memories.
These memories become consolidatedstable, and enduring long-term memories LTMs through the synthesis of proteins only a few hours after the initial experience.
The release of the neurotransmitter Norepinephrine Noradrenaline plays a large role in consolidation of traumatic memory. Stimulation of beta-adrenergic receptors during arousal and stress strengthens memory consolidation. Increased release of Stress effects and management proposal inhibits the prefrontal cortexwhich plays a role in emotion control as well as extinction or suppression of memory.
Additionally, the release also serves to stimulate the amygdala which plays a key role in generating fear behaviors.
Reconsolidation after retrieval can be used to strengthen existing memories and update or integrate new information.
This allows a memory to be dynamic and plastic in nature. Just like in consolidation of memory, reconsolidation, involves the synthesis of proteins. Inhibition of this protein synthesis directly before or after retrieval of a traumatic memory can disrupt expression of that memory.
This is done by reactivating a memory so that it causes the process of reconsolidation to begin. One source described the process this way: The administration of several different types of protein synthesis antagonists can be used to block protein synthesis that occurs after a traumatic memory is reactivated.
The inhibition of creation of new proteins will stop the reconsolidation process and make the memory imperfect. Molecular Consolidation theory says that memory is created and solidified or consolidated by specific chemical reactions in the brain.
Initially, memories exist in a plastic, labile state before they are more solidly encoded. It has been argued that memory consolidation occurs more than once- each time a memory is recalled, it returns to a labile state.
It states that things which cause memory loss after initial learning can also lead to memory loss after reactivation or retrieval  and it is by applying a pharmacological intervention at this plastic point whereby a traumatic memory can be erased.
The importance of the amygdala Human brain in the coronal orientation. Amygdalae are shown in dark red. The amygdala is an important brain structure when it comes to learning fearful responses, in other words, it influences how people remember traumatic things.
An increase in blood flow to this area has been shown when people look at scary faces, or remember traumatic events.
It is likely that the amygdala is necessary for the memory enhancing effects of glucocorticoids and epinephrine.
Anisomycin The consolidation of memory requires the synthesis creation of certain proteins in the amygdala. Disruption of protein synthesis in the amygdala has been shown to prevent long-term memory for fear conditioning.
In tests where it is delivered to the lateral and basal nuclei in the amygdala of rats, the rats demonstrated that they had forgotten fear responses that they had been conditioned to display. U0 U is a MAPK inhibitor, it disrupts the synthesis of the proteins required to reconsolidate memory.
Research has shown that administration of this drug in rats is correlated with a reduction in synaptic potentiation in the lateral amygdala. This means that the neurons in this area which are selective for a certain fear memory fire less easily in response to the memory when affected by the drug as compared to the ease with which they fire without the drug present.
This was observed by recording brain activity in the amygdala of these rats when presented with tones they had been conditioned to fear.
Research exploring the idea that blocking these receptors would disrupt the creation of proteins necessary for consolidating fearful memories in the amygdala.
Propranolol is one such blocker, and in studies was shown to prevent the expression and return of fear in human subjects  Another study showed that emotionally arousing stories generally predicted better memory recall than stories which were less so.
Subjects who read or listened to these arousing stories were less able to remember the details in response to multiple choice questions or in free recall when they had been given a dose of propranolol prior to the story exposure.
Knowing this, researchers hypothesized that hyper-activating these receptors instead of blocking them would enhance their activity, and increase forgetting. D-cycloserine is a chemical which enhances agonist the activity of the NMDA receptors.HiddenLevers is a risk technology platform, providing next-level applications, analytics and economic research for the wealth management space.
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