Neuroplasticity

In view of the important role of ROCK-II in mediating various neuroplastic events in the CNS, we undertook a study to determine if chronic lithium or VPA regulates the protein levels of ROCK-II. These studies showed that 3-4 weeks of lithium or VPA administration brings about an 25-45% increase in the levels of particulate ROCK-II in FCx, with the lithium-induced increases reaching statistical significance. 

Manji HK, Rajkowska G, Chen G. Neuroplasticity and cellular resilience in mood disorders. Millennium article. Mol Psych 2000 5 578-593. 

STRESS, GLUCOCORTICOIDS AND NEUROPLASTICITY IN THE PATHOLOGY OF MOOD DISORDERS 895... 

The potential hyperactivation of the HPA axis in mood disorders has been revisited in recent years, in large part due to the growing recognition of the specific brain areas in which atrophy (loss), a neuroplastic event, may be present in many patients. To what extent these findings of atrophy represent the sequelae of the biochemical changes (for example, in glucocorticoid levels) accompanying repeated affective episodes, remains to be fully elucidated. 

Evidence accumulating from various laboratories has clearly demonstrated that lithium, at therapeutically relevant concentrations, exerts significant effects on the PKC signaling cascade. Current data suggest that chronic lithium attenuates PKC activity, and down-regulates the expression of PKC isozymes V in the frontal cortex and hippocampus [79, 80], Chronic lithium has also been demonstrated to dramatically reduce the hippocampal levels of a major PKC substrate, myristoylated-alanine-rich C kinase substrate (MARCKS), which has been implicated in regulating long-term neuroplastic events. 

Calcium ions play a critical role in regulating the synthesis and release of neurotransmitters, in neuronal excitability, and in long-term neuroplastic events, and it is thus not surprising that a number of studies have investigated intracellular Ca2+ in peripheral cells, particularly in bipolar disorder. 

Thus, the evidence that stress, and the stress hormone corticosterone, may cause changes in hippocampal structure, hippocampal connections, and changes in gene and protein expression, suggest that viable targets of anxiolytic agents are cellular signaling pathways involved in neuroplasticity and the maintenance of cellular resilience. 

Primary hyperalgesia occurs within the zone of injury and is caused by changes at the injury site itself. Secondary hyperalgesia occurs around the zone of injury and results from neuroplasticity and remodelling. 

Balfour DJ (2002) Neuroplasticity within the mesoaccumbens dopamine system and its role in tobacco Dependence, Curr Drug Targets CNS Neurol Disord 1 413-21 Balfour DJ (2004) The neurobiology of tobacco dependence a preclinical perspective on the role of the dopamine projections to the nucleus accumbens. Nicotine Tob Res 6 899-912 Barik J, Wonnacott S (2006) Indirect modulation by alpha7 nicotinic acetylcholine receptors of noradrenaline release in rat hippocampal slices interaction with glutamate and GABA systems and effect of nicotine withdrawal. Mol Pharmacol 69 618-628... 

D Sa C, Duman RS (2002) Antidepressants and neuroplasticity. Bipolar Disord 4 183-194 De Vry J (1995) 5-HTlA receptor agonists recent developments and controversial issues. Psychopharmacology (Berl) 121 1-26... 

Konradi C and Heckers S. Antipsychotic drugs and neuroplasticity Insights into the treatment and neurobiology of schizophrenia. Biol Psychiatry 2001 50 729-742. 

Azmitia E.C. (1999). Serotonin neurons, neuroplasticity and homeostasis of neural tissue. Neuropsychopharmacology 11 33 S 5 S. 

Stress, Neuroplasticity, and the Hypothalamic-Pituitary-Adrenal Axis... 

Taupin, P. (2006). Adult neurogenesis and neuroplasticity. Restor Neurol Neurosci, 24. 9-15. 

Mao, J. NMDA and opioid receptors their interactions in antinociception, tolerance and neuroplasticity, Brain Res. Rev. 1999, 30, 289-304. 

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