Actions of methylphenidate on dopaminergic neurons of the ventral midbrain

Federici, Mauro; Geracitano, Raffaella; Bernardi, Giorgio; Mercuri, Nicola Biagio

doi:10.1016/j.biopsych.2004.11.030

Cited by 50 publications

(34 citation statements)

References 34 publications

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“…A similar leftward shift of the DA concentration effect curve has been observed with other uptake blockers, suggesting that this value is a typical feature encountered when DAT is pharmacologically inhibited (Federici et al 2005;Lacey et al 1990;Mercuri et al 1991).…”

Section: Discussionsupporting

confidence: 76%

“…Consequently, during the action of MDMA, DA, normally released from the soma and dendrites of the dopaminergic cells in the extracellular space (Cheramy et al 1981), is not properly cleared by the blocked DAT. Actions similar to those caused by MDMA on the dopaminergic neurons, which are also reserpine-resistant and carbidopa-sensitive, have been described at the neuronal level and said to be caused by the DA uptake blockers cocaine, amineptine, and methylphenidate (Federici et al 2005;Lacey et al 1990;Mercuri et al 1991). Thus, cocaine-like actions of MDMA could be consistent with the firing inhibition of the mesencephalic DAergic neurons (Einhorn et al 1988;Lacey et al 1990).…”

Section: Discussionmentioning

confidence: 92%

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Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

Federici

Sebastianelli

Natoli

et al. 2007

Biological Psychiatry

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 92%

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

Federici

Sebastianelli

Natoli

et al. 2007

Biological Psychiatry

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“…As expected for a DAT blocker (15), this drug, at concentrations of 3 M, enhanced the amplitude of the dopaminergic signal, whereas at 10 M it depressed DA transmission. Methylphenidate slowed the decay of the signal, increasing the half-decay phase (Fig.…”

Section: Control Of Da Release By Cocaine and Cocaine-like Drugs-supporting

confidence: 75%

Paradoxical Abatement of Striatal Dopaminergic Transmission by Cocaine and Methylphenidate

Federici

Latagliata

Ledonne

et al. 2014

Journal of Biological Chemistry

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Background:The dopamine transporter (DAT) regulates the outflow of dopamine from synapses. Results: We present evidence that the DAT blockers cocaine and methylphenidate increase or reduce the release of DA in the striatum. Conclusion:The reducing effects on DA release are not dependent on a typical blockade of DAT. Significance: The paradoxical blunting of dopamine (DA) release could account for differential effects of psychostimulants.

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“…In this context, Chase and colleagues [18] showed that MPH administration alters c-fos expression in the brain of juvenile rats. Decreased activity of dopaminergic neurons [19,20], increase in the levels of cyclic adenosine monophosphate (cAMP) response element-binding (CREB) protein and Homer 1A transcript [13,14], as well as increase in corticosterone levels following restraint stress [15] have also been reported after MPH treatment. Recently, it has been shown that chronic treatment with MPH at early age causes excitotoxicity associated to inhibition of glutamate uptake and disturbances in the Na + ,K + -ATPase in the prefrontal cortex [21].…”

mentioning

confidence: 96%

Methylphenidate Causes Behavioral Impairments and Neuron and Astrocyte Loss in the Hippocampus of Juvenile Rats

et al. 2016

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Although the use, and misuse, of methylphenidate is increasing in childhood and adolescence, there is little information about the consequences of this psychostimulant chronic use on brain and behavior during development. The aim of the present study was to investigate hippocampus biochemical, histochemical, and behavioral effects of chronic methylphenidate treatment to juvenile rats. Wistar rats received intraperitoneal injections of methylphenidate (2.0 mg/kg) or an equivalent volume of 0.9 % saline solution (controls), once a day, from the 15th to the 45th day of age. Results showed that chronic methylphenidate administration caused loss of astrocytes and neurons in the hippocampus of juvenile rats. BDNF and pTrkB immunocontents and NGF levels were decreased, while TNF-α and IL-6 levels, Iba-1 and caspase 3 cleaved immunocontents (microglia marker and active apoptosis marker, respectively) were increased. ERK and PKCaMII signaling pathways, but not Akt and GSK-3β, were decreased. SNAP-25 was decreased after methylphenidate treatment, while GAP-43 and synaptophysin were not altered. Both exploratory activity and object recognition memory were impaired by methylphenidate. These findings provide additional evidence that early-life exposure to methylphenidate can have complex effects, as well as provide new basis for understanding of the biochemical and behavioral consequences associated with chronic use of methylphenidate during central nervous system development.

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Actions of methylphenidate on dopaminergic neurons of the ventral midbrain

Cited by 50 publications

References 34 publications

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

Electrophysiologic Changes in Ventral Midbrain Dopaminergic Neurons Resulting from (+/−) -3,4-Methylenedioxymethamphetamine (MDMA—“Ecstasy”)

Paradoxical Abatement of Striatal Dopaminergic Transmission by Cocaine and Methylphenidate

Methylphenidate Causes Behavioral Impairments and Neuron and Astrocyte Loss in the Hippocampus of Juvenile Rats

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