D1-dopamine and α1-adrenergic receptors co-localize in dendrites of the rat prefrontal cortex

Mitrano, Darlene A.; Paré, Jean‐François; Smith, Yoland

doi:10.1016/j.neuroscience.2013.11.002

Cited by 25 publications

(35 citation statements)

References 49 publications

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“…Indeed, there is direct anatomical evidence showing that α 1 ‐ARs exist in pre‐synaptic terminals of glutamate synapses in the PFC (Mitrano et al . , ), which is consistent with our current electrophysiological results. In our experiments, the selection of 100 μM Phe was mainly based on our previous experiments examining the effect of Phe on synaptic transmission in the mPFC (Luo et al .…”

Section: Discussionsupporting

confidence: 93%

Phenylephrine enhances glutamate release in the medial prefrontal cortex through interaction with N‐type Ca²⁺ channels and release machinery

Luo

Tang

et al. 2014

Journal of Neurochemistry

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a 1 -adrenoceptors (a 1 -ARs) stimulation has been found to enhance excitatory processes in many brain regions. A recent study in our laboratory showed that a 1 -ARs stimulation enhances glutamatergic transmission via both pre-and postsynaptic mechanisms in layer V/VI pyramidal cells of the rat medial prefrontal cortex (mPFC). However, a number of presynaptic mechanisms may contribute to a 1 -ARs-induced enhancement of glutamate release. In this study, we blocked the possible post-synaptic action mediated by a 1 -ARs to investigate how a 1 -ARs activation regulates pre-synaptic glutamate release in layer V/VI pyramidal neurons of mPFC. We found that the a 1 -ARs agonist phenylephrine (Phe) induced a significant enhancement of glutamatergic transmission. The Phe-induced potentiation was mediated by enhancing pre-synaptic glutamate release probability and increasing the number of release vesicles via a protein kinase C-dependent pathway. The mechanisms of Phe-induced potentiation included interaction with both glutamate release machinery and N-type Ca 2+ channels, probably via a presynaptic G q /phospholipase C/protein kinase C pathway. Our results may provide a cellular and molecular mechanism that helps explain a 1 -ARs-mediated influence on PFC cognitive functions.

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Section: Discussionsupporting

confidence: 93%

Phenylephrine enhances glutamate release in the medial prefrontal cortex through interaction with N‐type Ca²⁺ channels and release machinery

Luo

Tang

et al. 2014

Journal of Neurochemistry

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“…These two models are not necessarily mutually exclusive. We have shown that α1ARs and D1Rs colocalize on glutamatergic neuronal elements in the mPFC (Mitrano et al, 2014), and previous studies suggest that α1AR signaling restrains D1 signaling in mPFC pyramidal neurons (Trovero et al, 1994). Thus, supranormal D1 activation in the mPFC following DBH inhibition may result from a combination of increased DA release from noradrenergic terminals and decreased NE-α1AR transmission, thereby allowing D1 signaling to proceed unchecked.…”

Section: Discussionmentioning

confidence: 67%

Norepinephrine regulates cocaine-primed reinstatement via α1-adrenergic receptors in the medial prefrontal cortex

et al. 2017

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Drug-primed reinstatement of cocaine seeking in rats is thought to reflect relapse-like behavior and is mediated by the integration of signals from mesocorticolimbic dopaminergic projections and corticostriatal glutamatergic innervation. Cocaine-primed reinstatement can also be attenuated by systemic administration of dopamine β-hydroxylase (DBH) inhibitors, which prevent norepinephrine (NE) synthesis, or by α1-adrenergic receptor (α1AR) antagonists, indicating functional modulation by the noradrenergic system. In the present study, we sought to further discern the role of NE in cocaine-seeking behavior by determining whether α1AR activation can induce reinstatement on its own or is sufficient to permit cocaine-primed reinstatement in the absence of all other AR signaling, and identifying the neuroanatomical substrate within the mesocorticolimbic reward system harboring the critical α1ARs. We found that while intracerebroventricular infusion of the α1AR agonist phenylephrine did not induce reinstatement on its own, it did overcome the blockade of cocaine-primed reinstatement by the DBH inhibitor nepicastat. Furthermore, administration of the α1AR antagonist terazosin in the medial prefrontal cortex (mPFC), but not the ventral tegmental area (VTA) or nucleus accumbens (NAc) shell, attenuated cocaine-primed reinstatement. Combined, these data indicate that α1AR activation in the mPFC is required for cocaine-primed reinstatement, and suggest that α1AR antagonists merit further investigation as pharmacotherapies for cocaine dependence.

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“…Several of these changes in behavior can be mediated by the effect of norepinephrine throughout the brain (e.g. Mitrano et al, 2012Mitrano et al, , 2014. However, many drug-dependent behaviors require activation of the mesolimbic dopamine system (Kalivas, 1995;Kalivas and McFarland, 2003;Zweifel et al, 2008), which indicates that the effect of antagonizing 1 adrenergic signaling on cocaine-elicited behaviors could also be mediated by modulation of the dopamine system.…”

Section: Discussionmentioning

confidence: 99%

Cocaine Increases Dopaminergic Neuron and Motor Activity via Midbrain α1 Adrenergic Signaling

Goertz

Wanat

Gómez

et al. 2014

Neuropsychopharmacol

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Cocaine reinforcement is mediated by increased extracellular dopamine levels in the forebrain. This neurochemical effect was thought to require inhibition of dopamine reuptake, but cocaine is still reinforcing even in the absence of the dopamine transporter. Here, we demonstrate that the rapid elevation in dopamine levels and motor activity elicited by cocaine involves α1 receptor activation within the ventral midbrain. Activation of α1 receptors increases dopaminergic neuron burst firing by decreasing the calcium-activated potassium channel current (SK), as well as elevates dopaminergic neuron pacemaker firing through modulation of both SK and the hyperpolarization-activated cation currents (Ih). Furthermore, we found that cocaine increases both the pacemaker and burst-firing frequency of rat ventral-midbrain dopaminergic neurons through an α1 adrenergic receptor-dependent mechanism within the ventral tegmental area and substantia nigra pars compacta. These results demonstrate the mechanism underlying the critical role of α1 adrenergic receptors in the regulation of dopamine neurotransmission and behavior by cocaine.

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D1-dopamine and α1-adrenergic receptors co-localize in dendrites of the rat prefrontal cortex

Cited by 25 publications

References 49 publications

Phenylephrine enhances glutamate release in the medial prefrontal cortex through interaction with N‐type Ca²⁺ channels and release machinery

Phenylephrine enhances glutamate release in the medial prefrontal cortex through interaction with N‐type Ca²⁺ channels and release machinery

Norepinephrine regulates cocaine-primed reinstatement via α1-adrenergic receptors in the medial prefrontal cortex

Cocaine Increases Dopaminergic Neuron and Motor Activity via Midbrain α1 Adrenergic Signaling

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D1-dopamine and α1-adrenergic receptors co-localize in dendrites of the rat prefrontal cortex

Cited by 25 publications

References 49 publications

Phenylephrine enhances glutamate release in the medial prefrontal cortex through interaction with N‐type Ca2+ channels and release machinery

Phenylephrine enhances glutamate release in the medial prefrontal cortex through interaction with N‐type Ca2+ channels and release machinery

Norepinephrine regulates cocaine-primed reinstatement via α1-adrenergic receptors in the medial prefrontal cortex

Cocaine Increases Dopaminergic Neuron and Motor Activity via Midbrain α1 Adrenergic Signaling

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Phenylephrine enhances glutamate release in the medial prefrontal cortex through interaction with N‐type Ca²⁺ channels and release machinery

Phenylephrine enhances glutamate release in the medial prefrontal cortex through interaction with N‐type Ca²⁺ channels and release machinery