Author
E. Pileblad
Bio: E. Pileblad is an academic researcher. The author has contributed to research in topics: Dopaminergic & Homovanillic acid. The author has an hindex of 1, co-authored 1 publications receiving 86 citations.
Topics: Dopaminergic, Homovanillic acid, Antagonist, Dizocilpine, Dopamine
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TL;DR: The stimulation of locomotor activity following D-CPPene treatment does not seem to be mediated through activation of central dopaminergic systems, however, haloperidol pretreatment antagonized this locomotor response, indicating that the dopaminaergic system plays a permissive role in this context.
Abstract: Following intraperitoneal administration of the non-competitive N-methyl-D-aspartate (NMDA) antagonist dizocilpine (MK-801), levels of the dopamine (DA) metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) increased in mouse striatum and limbic forebrain When dizocilpine was given to animals treated with NSD 1015, an inhibitor of 3,4-dihydroxyphenylalanine (DOPA) decarboxylase and monoamine oxidase, there was an increase in levels of DOPA and 3-methoxytyramine (3-MT) These findings suggest that dizocilpine stimulates DA synthesis and release in mouse brain Following dizocilpine treatment a clear-cut increase in spontaneous locomotor activity was observed, probably partly due to enhanced dopaminergic tone The competitive NMDA antagonist D-CPPene produced locomotor stimulation as well, but in contrast to following dizocilpine treatment levels of 3-MT decreased Thus the stimulation of locomotor activity following D-CPPene treatment does not seem to be mediated through activation of central dopaminergic systems However, haloperidol pretreatment antagonized this locomotor response, indicating that the dopaminergic system plays a permissive role in this context
87 citations
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TL;DR: The prefrontal cortex (PFC) has long been known to be involved in the mediation of complex behavioral responses and the findings concerning the function or role of the mPFC are relatively inconsistent, the question is addressed whether these inconsistencies might be related to the anatomical and functional heterogeneity of this brain area.
472 citations
TL;DR: Taking together, neurochemical systems of the basal ganglia significantly contribute to intact response initiation by mechanisms which are only partly consistent with predictions of the current functional scheme of theBasal ganglia, suggesting functional differences of the output structures.
214 citations
TL;DR: The present results indicate that nicotinic acetylcholine receptors in the ventral tegmental area are involved in the positive reinforcing effects of ethanol and could represent a new pharmacological treatment principle against alcohol abuse.
200 citations
TL;DR: Evidence is provided that ethanol-induced activation of the mesolimbic dopamine system (increased dopamine synthesis and release) may be mediated via stimulation of central nicotinic acetylcholine receptors, suggested to be useful in the treatment of alcoholism.
191 citations
TL;DR: The inhibition of NMDA and AMPA receptors by agents acting at different recognition sites produces qualitatively different behavioral consequences.
Abstract: Locomotor activity, ataxia, and stereotypy were assessed in the open field after administration of NMDA and AMPA antagonists acting by different mechanisms. The interaction with glutamatergic receptors was confirmed in the binding assay. (+)MK-801 and phencyclidine (PCP) produced similar changes in horizontal activity, i.e., a strong increase from the begining of the test. Ketamine, and to a lesser extent, memantine, enhanced horizontal activity at the later observation periods only. Amantadine and NBQX produced a slight inhibition, while GYKI-52466, d -cycloserine, (+R)-HA-966, CGP-37849, and dextromethorphan were ineffective. Vertical activity (rearings) were inhibited by most agents except GYKI-52466 and gly-B partial agonists. At higher doses ataxia was seen after: MK-801, PCP, ketamine, memantine, amantadine, CGP-37849, dextromethorphan, and GYKI-52466. Hence, the inhibition of NMDA and AMPA receptors by agents acting at different recognition sites produces qualitatively different behavioral consequences.
184 citations