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Nigrostriatal dopaminergic neurons

Does hyperthermia decrease negative feedbaek in nigrostriatal dopaminergic neurons Pharmacol Toxicol 62 344-445, 1988. [Pg.339]

Cheramy, A., Nieoullon, A., and Glowinski, J. (1978) GABAergic processes involved in the control of dopamine release from nigrostriatal dopaminergic neurons in the cat. Eur. J. Pharmacol., 48 281-295. [Pg.89]

Jones IW, Bolam JP, Wonnacott S (2001) Presynaptic localisation of the nicotinic acetylcholine receptor beta2 subunit immunoreactivity in rat nigrostriatal dopaminergic neurones. J Comp Neurol 439 235-247... [Pg.200]

Datla KP, Zbarsky V, Rai D, Parkar S, Osakabe N, AruomaOI, DexterDT(2007) Short-term supplementation with plant extracts rich in flavonoids protect nigrostriatal dopaminergic neurons in a rat model of Parkinson s disease. J Am CoU Nutr 26 341-349... [Pg.95]

Figure 4. Representation of the classification of the dopamine receptor based on its coupling with adenylate cyclase activity. DA+ receptors (left) are coupled to adenylate cyclase through the Ns GTP-binding protein (91) with secondary activation of adenylate cyclase. DA. receptors (middle) are coupled through the Ni GTP-binding protein, thus resulting in inhibition of cyclic AMP formation. DA0 receptors (right) are those uncoupled to cyclic AMP formation, the example being possibly some autoreceptors on nigrostriatal dopaminergic neurons. Figure 4. Representation of the classification of the dopamine receptor based on its coupling with adenylate cyclase activity. DA+ receptors (left) are coupled to adenylate cyclase through the Ns GTP-binding protein (91) with secondary activation of adenylate cyclase. DA. receptors (middle) are coupled through the Ni GTP-binding protein, thus resulting in inhibition of cyclic AMP formation. DA0 receptors (right) are those uncoupled to cyclic AMP formation, the example being possibly some autoreceptors on nigrostriatal dopaminergic neurons.
Nirenberg MJ, Vaughan RA, Uhl GR, Kuhar MJ, Pickel VM (1996b) The dopamine transporter is localized to dendritic and axonal plasma membranes of nigrostriatal dopaminergic neurons. J Neurosci 76 436 147. [Pg.102]

Txvo balanced systems are important in the extrapyramidal control of motor activity at the level of the corpus striatum and substantia nigra in one the neurotransmitter is acetylcholine in the other it is a dopamine. In Parkinson s disease there is degenerative loss of nigrostriatal dopaminergic neurons and the sjunptoms and signs of the disease are due to dopamine depletion. [Pg.422]

Saporito MS, Brown EM, Miller MS, Carswell S (1999) CEP 1347/ KT 7515, an inhibitor of c-jun N terminal kinase activation, attenuates the 1 methyl 4 phenyl tetrahyopyridine mediated loss of nigrostriatal dopaminergic neurons in vivo. J Pharmocol Exp Ther 288 421 27. [Pg.587]

Akathisia occurred in five fairly young patients after subcutaneous or oral sumatriptan (19). The symptoms were short-lived. Increased serotonergic activity, leading to inhibition of nigrostriatal dopaminergic neurons and extrapyramidal symptoms, was the postulated mechanism. A similar mechanism has been thought to provoke the same symptoms with serotonin re-uptake inhibitors. [Pg.3526]

Nicotine decelerates aging of nigrostriatal dopaminergic neurons (8) and it has been suggested that nicotine may relieve the symptoms of Parkinson s disease (7). [Pg.52]

Due to its enhancer effect (-)-deprenyl protects the nigrostriatal dopaminergic neurons against selectively acting neurotoxins (Knoll 1978 Harsing et al. 1979 Cohen et al. 1984 Finnegan et al. 1990 Vizuete et al. 1993 Wu et al. 1993), and facilitates scavenger function in the striatum (Knoll 1988, 1990 Carrillo et al. 1991,1992). [Pg.86]

Since the diagnosis of Parkinson s disease is the unequivocal proof that the age-related irreversible deterioration of the nigrostriatal dopaminergic neuronal system has already surpassed a critical level in the patient, and the disease is incurable, prevention remains the only chance for the future to fight off Parkinson s disease. The daily administration of a small dose of a synthetic mesencephalic enhancer substance from sexual maturity until death presents itself as a proper method for reaching this aim. [Pg.91]

Knoll J (1986c) Role of B-type monoamine oxidase inhibition in the treatment of Parkinson s disease. An update. In Shah NS, Donald AG (eds) Movement disorders. Plenum Press, New York, pp 53-81 Knoll J (1987) / -(-) Deprenyl (Selegiline, Movergan ) facilitates the activity of the nigrostriatal dopaminergic neuron. J Neural Transm 25 45-66 Knoll J (1988) The striatal dopamine dependency of lifespan in male rats. [Pg.152]


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See also in sourсe #XX -- [ Pg.91 ]




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