Mechanisms learning impairment

Anxiety is a normal part of mental life and plays a crucial role in human psychological development and other forms of learning. Although systematic studies are lacking, suppression of normal levels of anxiety could impair the development of adaptive coping mechanisms. On the other hand, disabling anxiety impairs adaptation as well and is associated with significant morbidity and mortality. 

At low doses, ketamine may result in impairment of attention, learning ability, and memory, and at high doses it has been associated with delirium, amnesia, impaired motor function, hypertension, depression, and respiratory depression (Krystal et al. 1994). Another mechanism of action appears to be a blocking of the reuptake of catecholamines. This effect leads to an increase in heart rate and blood pressure (Reich and Silvay 1989). 

While the conditional gene knockout experiments are supportive of a role for the NMDA receptors in memory, they are less than fully conclusive in linking the synaptic coincidence-detection feature of the NMDA receptor to memory formation. Like all loss-of-function studies, CA1-specific gene-knockout experiments could, in theory, produce memory impairment via a mechanism independent of the coincidence-detection function of the NMDA receptor. For example, one may argue that the physical absence of the NMDA receptor channels may cause subtle structural reconfiguration at the synapse, thereby altering normal synaptic transmission. Therefore, the memory impairment in CA1-specific NR1 knockout mice does not allow a firm conclusion that the coincidence-detection function of NMDA receptors controls learning and memory processes at the cellular level. 

Sullivan, J.M Cellular and molecular mechanisms underlying learning and memory impairments produced by cannabinoids, Learn. Mem. 2000, 7, 132-139. 

Considerable evidence that endocannabinoid actions in the brain impair learning and memory has also been collected. Most of the evidence comes from studies in which CB 1 antagonists improve learning or memory (Lichtman 2000 Shiflett et al. 2004 Terranova et al. 2005 Wolf and Leander 2003). These antagonists can also reverse the amnestic effects of agents such as (3-amyloid and scopolamine (Mazzola et al. 2003 Takahashi et al. 2005). Thus, it appears that activation of CB1 receptors, presumably following release of brain endocannabinoids, has actions that counteract mechanisms involved in learning and memory. 

Straiker A, Mackie K (2005) Depolarization-induced suppression of excitation in murine autaptic hippocampal neurones. J Physiol 569(Pt 2) 501—17 Sullivan JM (2000) Cellular and molecular mechanisms underlying learning and memory impairments produced by cannabinoids. Learn Mem 7(3) 132-9 Sugiura T, Kondo S, Sukagawa A, Nakane S, Shinoda A, Itoh K, Yamashita A, Waku K (1995) 2-Arachidonoylglycerol a possible endogenous cannabinoid receptor ligand in brain. Biochem Biophys Res Commun 215(1) 89—97... 

The influences of vanadium compounds on cardiovascular function, a major complication of diabetes, has been reviewed [144], One of the first papers on the antidiabetic effects of oral administration of vanadium compounds (vanadyl sulfate) to rats with STZ-induced diabetes showed improvement of diabetes-impaired cardiac function [122], Recent work has focused on the correction of metabolic defects of diabetes by vanadium and learning more about the immediate mechanism of the antidiabetic effect. The assumption is made that amelioration of the basic metabolic problems of diabetes by vanadium or any other drug will alleviate the long-term complication arising from disease. Diet supplementation with minerals, such as chromium, appears to complement traditional treatments of diabetes to slow the development of complications. Mineral supplementation is believed to be most effective when dietary supplementation is used to correct a deficiency of a mineral [145],... 

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