ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Monoamine oxidase inhibition causes a long-term prolongation of the dopamine-induced responses in rat midbrain dopaminergic cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 39 citations in OpenAlex.
- Review
- Metabolic hormone action in the VTA: Reward-directed behavior and mechanistic insights.Physiology & behavior · 2023Review
- Reversal of dopamine-mediated firing inhibition through activation of the dopamine transporter in substantia nigra pars compacta neurons.British journal of pharmacology · 2018Article
- Dopamine neuronal loss contributes to memory and reward dysfunction in a model of Alzheimer's disease.Nature communications · 2017Article
- Obesity attenuates D2 autoreceptor-mediated inhibition of putative ventral tegmental area dopaminergic neurons.Physiological reports · 2014Article
- PINK1 heterozygous mutations induce subtle alterations in dopamine-dependent synaptic plasticity.Movement disorders : official journal of the Movement Disorder Society · 2014Article
- Obesity decreases excitability of putative ventral tegmental area GABAergic neurons.Physiological reports · 2013Article
- Medical management of levodopa-associated motor complications in patients with Parkinson's disease.CNS drugs · 2007Review
- Effects of monoamine oxidase inhibitors on cocaine discrimination in rats.Behavioural pharmacology · 2006Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The way monoamine oxidase (MAO) modulates the depression of the firing rate and the hyperpolarization of the membrane caused by dopamine (DA) on rat midbrain dopaminergic cells was investigated by means of intracellular recordings in vitro. The cellular responses to DA, attributable to the activation of somatodendritic D2/3 autoreceptors, were prolonged and did not completely wash out after pharmacological blockade of both types (A and B) of MAO. On the contrary, depression of the firing rate and membrane hyperpolarization induced by quinpirole (a direct D2 receptor agonist) were not affected by MAO inhibition. Furthermore, although the inhibition of DA reuptake by cocaine and nomifensine caused a short-term prolongation of DA responses, the combined inhibition of MAO A and B enzymes caused a long-term prolongation of DA effects. Moreover, the effects of DA were not largely prolonged during the simultaneous inhibition of MAO and the DA reuptake system. Interestingly, the actions of amphetamine were not clearly augmented by MAO inhibition. From the present data it is concluded that the termination of DA action in the brain is controlled mainly by MAO enzymes. This long-term prolongation of the dopaminergic responses suggests a substitutive therapeutic approach that uses MAO inhibitors and DA precursors in DA-deficient disorders in which continuous stimulation of the dopaminergic receptors is preferable.
Indexed as
Identifiers
9065488PMC6573484W1565746371What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.