101 However, the difference in craving was not long-lasting, as t

101 However, the difference in craving was not long-lasting, as the experimental and placebo levels of craving were not statistically different 1 week after the intervention. One possibility for this absence of a difference is that propranolol impairment was transient. Another possibility, suggested by a visual inspection of the graphical presentation of the effect (Figure 1), is that the propranolol-induced impairment in craving is relatively constant. Future research should examine whether reduction in craving translates to a reduction in relapse rates and substance abuse. Implications of forgetting for clinical

practice: some #selleck chemical keyword# speculative ideas Constitutive forgetting may provide important functional contributions to the hippocampus. For example, the loss of hippocampus-dependent spatial and contextual memory may be instrumental for http://www.selleckchem.com/products/pacritinib-sb1518.html generalization effects and the development of schemas.102 On the other hand, because systematic forgetting processes may control the life-time of memories,

their deregulation could lead to accelerated and Inhibitors,research,lifescience,medical even pathological forms of memory loss, as seen in senescence and some dementias, such as Alzheimer’s disease (AD). In the latter, β-amyloid causes increases in postsynaptic calcium, which promotes internalization and altered trafficking of synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) Inhibitors,research,lifescience,medical and NMDA receptors, notably increased AMPA removal by engaging Inhibitors,research,lifescience,medical pathways involved in LTD.103 This suggests that forgetting processes as described above may be involved in the pathology of AD, and the accelerated forgetting of episodic content typical for the disease might drive the autobiographical impairment and eventual loss of a self-narrative. It is thus possible that the eventual synapse loss and cell death, which characterize the final stages of AD, are driven in part by forgetting processes that spiral out of control. Traditional views of AD assume that dementia is the

Inhibitors,research,lifescience,medical result of neuron death or dysfunction in the affected areas. While provocative but possible, one explanation for this condition is that uncontrolled forgetting maybe be one of the mechanisms leading to cell dysfunction and death. Therapeutic approaches could therefore target certain steps in molecular pathways associated with forgetting, and possibly at time points well before the devastating stages AV-951 of the disease manifest. Drugs that affect the synaptic removal of AMPA receptors might prove effective in preventing steps that eventually lead to synapse deterioration, as synapse stability critically depends on the glutamate (GluA2) and AMPA receptors.104 In animal models, it has been shown that the peptide GluA23Y, which competitively prevents internalization of GluA2-dependent AMPA receptors, can prevent long-term depression, a possible physiological model of plasticity mechanisms involved in forgetting.

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