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Title: Nitric oxide system and basal ganglia physiopathology
Authors: Bel, Elaine del
Bermudez-Echeverry, Marcela
Salum, Christiane
Raisman-Vozari, Rita
Keywords: Nitric oxide
Basal ganglia
Physiology, Pathological
Issue Date: 2007
Publisher: Transworld Research Network
Citation: Del Bel, E., Bermudez-Echeverry, M., Salum, C., & Raisman-Vozari, R. (2007). Nitric oxide system and basal ganglia physiopathology. In G. Di Giovanni & E. Esposito (Eds.), The basal ganglia pathophysiology : recent advances 2007. (pp. 129-158). Kerala: Transworld Research Network.
Abstract: Nitric oxide (NO) is a pleiotropic molecule that is needed for physiological functions, especially in the brain NO induces vasodilatation, inhibits apoptosis and plays an important role in memory processes. A population of interneurons has been distinguished in the striatum by nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) staining, an enzyme that is identical with NO synthase (NOS). These interneurons are aspiny cells with dendritic branches and axonal arborisation extending to form a wide field. Single action potentials in these cells produce large inhibitory postsynaptic currents in medium-sized spiny neurons. Release of NO from these neurons facilitates the concurrent release of dopamine and glutamate (GLU). Although the influence of NOS-positive interneurons on striatal neuronal activity remains to be thoroughly characterized, evidence has accumulated suggesting that NO signaling may mediate and/or regulate multiple aspects of striatal neurotransmission. Striatal NO signaling has a major impact on the responsiveness of dopaminergic (DA) neurons to electrical stimulation of the striatum and to some extent, the prefrontal cortex. Moreover, it is likely that NO signalling plays an important role in regulating the activity of striatal output neurons. Thus, striatal NOS interneurons may be critically involved in integrating corticostriatal sensorimotor information within striatal networks and synchronizing the activity of functionally related striatonigral sub-systems. Our studies showed that systemic injections of the inhibitors of NOS decrease either elevate plus maze exploration or rearing in an open field arena. These results may involve motor effects of these compounds, since inhibitors of NOS induced catalepsy in mice. This effect was also found in rats after systemic, intracebroventricular or intrastriatal administration. Chronic NO synthesis inhibition induces plastic changes in NO producing neurons in areas related to motor control. In the same way, the application of NOS inhibitor twice a day, during four days caused cross-tolerance to the cataleptic effect of haloperidol. This raises the possibility that such treatments could decrease motor side effects associated with antipsychotic medications. However, NO can be harmful mainly under oxidative stress conditions due to the oxidation and nitrotyrosilation of functional proteins. Considerable existing evidences indicate a role for NO–DA interactions in pathophysiological conditions such as Parkinson's disease (PD) and schizophrenia. However, the findings on the impact of nitrergic mechanisms in schizophrenia and PD are contradictory. In addition, the slow progression of these diseases, complicates experimental approaches to modeling their pathophysiological mechanism. Inducing experimental Parkinson in rats we found an interaction between NO system and neurodegenerative processes in the nigrostriatal pathway. Because NOS is an enzyme widely distributed and involved in a plethora of necessary physiological responses inside and outside the brain, the role of NO in human neurodegenerative disease is not as easily understood.
ISBN: 8178952688
Appears in Collections:The basal ganglia pathophysiology : recent advances

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