Research reportElectrophysiological effects of MK-801 on rat nigrostriatal and mesoaccumbal dopaminergic neurons☆
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CSF dopamine is elevated in first-episode psychosis and associates to symptom severity and cognitive performance
2023, Schizophrenia ResearchCharacterisation of methylphenidate-induced excitation in midbrain dopamine neurons, an electrophysiological study in the rat brain
2022, Progress in Neuro-Psychopharmacology and Biological PsychiatryAmeliorating effects of berberine on MK-801-induced cognitive and motor impairments in a neonatal rat model of schizophrenia
2019, Neuroscience LettersCitation Excerpt :This discrepancy can be attributed to the involvement of other neurotransmitters such as GABA and dopamine. Although MK-801 increases dopamine, previous studies show that imbalance at the rotarod test is known as a “non-dopamine dependent” motor function [36,37]. Considering that various receptors and neurotransmitters may be involved in the effects of BBR on motor coordination in the rotarod test, elucidating the exact mechanism underlying this effect will require further studies.
Effects of Low Doses of Ketamine on Pyramidal Neurons in Rat Prefrontal Cortex
2018, NeuroscienceCitation Excerpt :Ro25 also decreased SO size (F3,27 = 11.16, p < 0.001), but it increased SO frequencies (F3,12 = 8.03, p < 0.01, n = 9, Fig. 4B). Like PCP and MK801, ketamine has been shown to excite midbrain DA neurons (French, 1992; Zhang et al., 1992) and increases PFC DA release (Lindefors et al., 1997; Lorrain et al., 2003; Moghaddam et al., 1997), raising the possibility that part of ketamine’s effect on the PFC is indirectly mediated through DA. Consistent with this possibility, some of PCP’s effects on PFC neurons are blocked by DA receptor antagonists including fluphenazine (Gratton et al., 1987; Kargieman et al., 2007).
Inhibition of kynurenine aminotransferase II reduces activity of midbrain dopamine neurons
2016, NeuropharmacologyCitation Excerpt :Although only one dose of MLA was administered (4 mg/kg) our results support the notion that blockade of the glycine site of the NMDA receptor, rather than antagonism of the α7* nicotinic receptor, is the mechanism by which KYNA modulates firing rate on midbrain DA neurons. Furthermore, these results are in line with previous studies where systemic administration of NMDA receptor antagonists, such as PCP, MK-801, and L-701,324, are associated with increased firing rate and percent burst firing in midbrain DA neurons (French et al., 1991, 1993; Zhang et al., 1992; Schwieler et al., 2006). In the present study, administration of PF-04859989 was associated with a marked lowering (75%) in whole brain KYNA (5 mg/kg, i.p. n = 5) 5 h after administration.
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A preliminary report of portions of this work was presented at the Dopamine 90 satellite meeting of the 11th congress of IUPHAR, Como, Italy, 8–11 July, 1990.