Some recent studies are investigating pseudo memory and its mechanisms. Real memories depend on drawing in the past, retrieving information, recalling past events and re-encoding these items by recombining (rearranging) them with new information, creating a new memory. However, sometimes failures in this system lead to memory errors that cooperate with improper memory generation. In this article, there is information about some neuropharmacological aspects as possible mechanisms of agonist and antagonist modulation of wrong memory.
Dopaminergic Modulation of True Memories
The prefrontal cortex plays an important role in mediating working memory observed in neuroimaging and neurophysiology studies in monkeys and humans. Studies have shown dopaminergic modulation of executive functions, working memory, and emotion. Studies with monkeys have shown that activation of dopamine D 1 receptors in the prefrontal cortex is required for the expression of working memory. Also, in humans, there is evidence of the dominant role of the dopamine D 1 receptor in working memory. However, other studies with dopaminergic D 2 receptor antagonists and agonists have also shown that humans and monkeys play a role in memory study. Takahashi et al., Hippocampal D 2 receptors also played a role in executive functions and verbal fluency traits.
Some neurological and psychiatric pathologies such as Parkinson’s disease, schizophrenia, autism, attention deficit, Huntington’s disease, and frontal lobe lesions have emotional process disorders. All these pathologies involve the dopaminergic system, which suggests the participation of dopamine in emotion. Moreover, emotional processes depend on different structures; Most of these include the limbic system with dopaminergic innervation. Many biochemical, pharmacological, and neuroimaging studies reinforce the idea of a dopaminergic additive to emotion. A study on Parkinson’s disease shows that the abnormal state of the dopaminergic system compromises the normal functioning of the amygdala. Some studies show dopaminergic D involvementc. (2 receptors in emotional memory)
It is important to evaluate the effect of certain drugs acting on various neurotransmitter systems on the functioning of memory for emotional stimuli, because healthy people process emotional parts differently than those without emotional content. This often results in emotional events being more likely to be reversed than neutral events. The finding that emotions affect the performance of episodic memory has led some researchers to investigate the effect of emotions on the production of false memories. While these studies provide different results, perhaps stemming from the various methods used, they all suggest that emotion interferes with signs of false memories.
Dopaminergic and Other Neurotransmitter System Modulation of False Memories
The antipsychotics are haloperidol and sulpyrite, two studies using dopamine D 2 drugs increased false memory rates but had an effect on real memory, these are receptor antagonists adjusted to evaluate pseudo-memory dopaminergic modulation. Other neurotransmitter system effects on the production of false memories, dextroamphetamines, & # 916; It has been studied in trials with (9) -tetrahydrocannabinol (THC) and benzodiazepines (diazepam and lorazepam). The effects of caffeine and alcohol on real and false memories have also been studied.
Ballard observed that dextroamphetamine (AMP) increased errors during memory access. In another study, the same author found that AMP increased memory correct but not false compared to placebo, but AMP increased false memory compared to THC. In 1999, Blair and Curran observed that diazepam selectively impaired the subjects’ ability to recognize angry expressions, but did not affect the recognition of other emotional expressions on the face. One study has shown that diazepam and lorazepam impair conscious recall associated with correct memories that are not false. Caffeine appears to increase the strength of the connections between list words and critical attractions, thus reinforcing both real and false memories.
Another study in 2012 observed more false positive responses from polydrug users such as ecstasy than non-users. The increased frequency of long-term ecstasy use was positively associated with memories when digested prior to encoding. But differently, it confirmed that misrecognition increased when amphetamine was swallowed before being withdrawn. In contrast, alcohol decreases semantic activation, leading to a decrease in false memories and rejection of false memories often seen with placebo. The second effect of alcohol may be due to its ability to disrupt the tracking processes established in coding. Milani and Curran compared the effect of low dose with high dose of alcohol on the recall experience of misleading memory.
They found high levels of inaccurate recall and recognition in both treatments and confirmed that a small dose of alcohol did not alter too much inaccurate memory measurement, but did alter the pattern of the recall experience in terms of recall and cognition responses. Specifically, it increased the level of recall responses to misidentifications (critical attractions). An autobiographical study reported that compared to placebo, lorazepam increased levels of conscious recall as assessed by ‘recall’ responses for both real and false memories, and caused an overestimation of personal significance and emotional intensity of past events.
Emotion facilitates real memory performance compared to neutral content events. However, in situations with negative emotional content, released stress and high cortisol levels, the opposite should happen; that is, there is a deterioration in the performance of processes such as perception and memory. This mechanism can be represented on a graph with one of the inverse “U” curves. These high stress situations will be represented on the decreasing part of the curve; this means that emotion has a facilitating effect on coding, but if the level of emotion is exaggerated, the effect is just the opposite. Presumably, in extreme stressful situations, with a high level of attention and arousal, an exaggerated processing of the relevant stimuli (central directions) of the event occurs, which is detrimental to the processing of environmental (irrelevant) stimuli. This imbalance during encoding can facilitate the formation of false memories through errors when re-encoding some memory traces.
Some possible mechanisms of pseudo-memory dopaminergic modulation proposed by the authors of this research will be the dopamine effect (1) to study memory / executive functions with the corticostriatal hippocampus-prefrontal D. Dopaminergic modulation with 2 Ge, (2) 2 dopaminergic modulation, the amygdala’s response to emotionally charged stimuli, and (3) dopaminergic modulation of the decision-making process (via the striatum). Other possible failures in coding by other neurotransmitters may also contribute to false memory formation. However, the precise mechanisms of other neurotransmitter systems, as well as their role in the production of false memories, await clarification in the future.
Activation (agonism) or blockade (antagonism) of the receptors can have different effects on the emotional judgment of the stimulus and can stimulate or distort real or false memories depending on the drug and system studied. Studying false memories is a challenging field of neuroscience that is extraordinarily fascinating, with many questions yet to be elucidated in a way that new methods and tools of neuropsychological rehabilitation may be proposed in the future.
Writer: Ozlem Guvenc Agaoglu