![]() Recently, we observed in a genetically engineered mouse model, that the induced loss of neuroplastin resulted in retrograde amnesia of associative memories ( Bhattacharya et al., 2017). However, the specificity and mechanisms of memory loss induced by psychoactive drugs are not precisely understood. Experimentally, retrograde amnesia can be induced by some psychoactive drugs from which alcohol is the most prominent (for review: Lee et al., 2009). Besides studies of patients suffering from retrograde amnesia which often lead to rather anecdotal knowledge, experimental access to retrograde amnesia is very limited. In contrast to learning or memory acquisition studies, the literature on experimentally induced retrograde amnesia is very scarce. In particular, associative memories underlie post-traumatic stress disorder because the traumatic experience is linked to the memory of other stimuli/items/signals that later on may become triggers for the painful/traumatic recall. Furthermore, an increasing number of patients suffers from post-traumatic stress disorder (according to the United States National Center for PTSD 7 or 8 out of 100 people will experience PTSD at some point in their live 1). Indeed, forgetting “negative” experiences and emphasizing “good” memories may help coping with life and generating optimism ( Nørby, 2018). However, in cases of traumatic experiences or negatively connotated “bad” memories, forgetting may be highly welcome. Usually, “normal” forgetting ( Nørby, 2018), such as forgetting information without significance, is not referred to as retrograde amnesia although the mechanisms underlying forgetting and retrograde amnesia may not be distinct.įorgetting relevant information and memory loss commonly have negative connotations. Memories can be affected by retrograde amnesia generally but also distinct types of memories such as associative memories may be selectively compromised. Traumatic events can be a direct impact by injury, viral or bacterial infections, malnutrition (Korsakoff’s syndrome), or psychoactive drugs and also psychogenic experiences (for review, see Squire and Alvarez, 1995). Retrograde amnesia may be caused by a single specific traumatic event or it may accompany brain disorders or malfunctions. Retrograde amnesia is the backward loss of memories and is distinguished from forward anterograde amnesia, which is the inability to acquire new memories. The possibility to elicit retrograde amnesia in a controlled manner allows to investigate the underlying mechanisms and may provide a deeper understanding of the molecular and circuit processes of memory. Therefore, neuronal loss of neuroplastin may block the retrieval and storage of associative memories by interference with Ca 2+ signaling cascades. Neuroplastin is tightly linked to the expression of the main Ca 2+ extruding pumps, the plasma membrane calcium ATPases (PMCAs). Recently, we observed that neuronal loss of neuroplastin resulted in retrograde amnesia specifically for associative memories. In this review, I will discuss a new genetic approach to induce retrograde amnesia in a mouse model and raise the hypothesis that retrograde amnesia is caused by altered intracellular calcium homeostasis. ![]() External or internal impacts like traumatic brain injury, stroke, or electroconvulsive treatments may similarly result in variable degrees of retrograde amnesia. Apart from models and diseases in which neurodegeneration or dementia like Alzheimer’s disease result in loss of memory, retrograde amnesia can be elicited by various drugs of which alcohol is the most prominent one and exemplifies the non-specific effects and the variable duration. In contrast to the many experimental models addressing learning deficits caused by anterograde amnesia, the incapability to acquire new information, retrograde amnesia could so far only be investigated sporadically in human patients and in a limited number of model systems. In general, memories and learning are associated with a positive connotation although the extinction of unpleasant experiences and memories of traumatic events may be highly welcome. Loss of memories may be caused in two ways: either by loss/erasure of the memory itself or by the inability to access the memory, which is still present. ![]() ![]() ![]() Often, the trigger for retrograde amnesia is a traumatic event. The successful acquisition and memory of information is required before retrograde amnesia may occur. Retrograde amnesia is the inability to remember events or information. ![]()
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