Prazosin modulates the firing pattern of dopamine neurons in rat ventral tegmental area

Grenhoff, J.; Svensson, Torgny H.

doi:10.1016/0014-2999(93)90351-h

Cited by 171 publications

(109 citation statements)

References 31 publications

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“…The selective NE transporter inhibitors nisoxetine (Wong et al 1975) and reboxetine , as well as ␣ 2 -adrenergic antagonists that enhance release of NE (Dennis et al 1987;Thomas and Holman 1991), increase burst firing of ventral tegmental DA neurons which would result in increased DA release in their terminal fields (Linnèr et al 2001;Shi et al 2000;Grenhoff and Svensson 1993).…”

Section: Discussionmentioning

confidence: 99%

Atomoxetine Increases Extracellular Levels of Norepinephrine and Dopamine in Prefrontal Cortex of Rat A Potential Mechanism for Efficacy in Attention Deficit/Hyperactivity Disorder

Bymaster

Katner

Nelson

et al. 2002

Neuropsychopharmacology

1,014

790

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Section: Discussionmentioning

confidence: 99%

Atomoxetine Increases Extracellular Levels of Norepinephrine and Dopamine in Prefrontal Cortex of Rat A Potential Mechanism for Efficacy in Attention Deficit/Hyperactivity Disorder

Bymaster

Katner

Nelson

et al. 2002

Neuropsychopharmacology

1,014

790

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“…Variations of burst firing are reported throughout this study as the percentage of SIB postdrug minus the percentage of SIB predrug. Regularity of firing was measured from the variation coefficient, that is, the standard deviation/mean value of interspike intervals (Grenhoff and Svensson, 1993). Results are expressed throughout as means 7 SEM.…”

Section: Discussionmentioning

confidence: 99%

Prolonged Activation of Mesolimbic Dopaminergic Neurons by Morphine Withdrawal Following Clonidine: Participation of Imidazoline and Norepinephrine Receptors

Georges

Aston‐Jones

2003

Neuropsychopharmacol

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The a2 adrenoceptor (a2R) agonist clonidine is used as a treatment for heroin addiction. Substantial evidence indicates that dopaminergic and noradrenergic systems have key roles in opiate dependence and withdrawal but the possible interactions between these two pathways remain unclear. The objective of this study was to establish the effects of clonidine pretreatment on ventral tegmental area dopaminergic (VTA DA) neuronal activity during morphine withdrawal. Responses of VTA DA neurons to withdrawal precipitated by naltrexone were characterized in anesthetized rats using extracellular recordings. As expected, withdrawal produced a marked inhibition of VTA DA neuronal activity. However, pretreatment with clonidine prevented this inhibition induced by withdrawal, and instead produced a long-lasting activation of firing rate (+50%) and burst firing (+19%). In contrast, pretreatment with a more selective a2R agonist, UK14304, did not prevent the inhibition of VTA DA neuron activity during withdrawal. We tested whether the high affinity of clonidine for imidazoline-1 receptors (I1Rs) was responsible for the difference between these two a2R agonists. In morphine-dependent rats pretreated with rilmenidine (mixed a2R/I1R agonist), precipitation of withdrawal elicited a 22% increase of VTA DA impulse activity. The action of clonidine on I1Rs was studied by coadministering clonidine with RX821002, a specific a2R antagonist. Pretreatment with RX821002 plus clonidine prevented the inhibition of VTA DA activity during withdrawal but failed to produce excitation. These results indicate that the pharmacological effects of clonidine on VTA DA neurons during morphine withdrawal is related to actions on I1Rs as well as a2Rs.

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“…In fact, two decades ago it was shown that stimulation of VTA neurons increases the activity of the LC [45]. Similarly, A1, and A2 NE nuclei were shown to provide excitatory stimulation to VTA DA neurons [53, 54]. Further indirect evidence for NE-DA interaction at the level of the VTA has been provided by autoradiographic and immunohistochemical studies, showing alpha1 and alpha2- adrenergic receptor (AR) expression in most DA neurons of the VTA [55, 56].…”

Section: The Anatomy Of Ne-da Interactionsmentioning

confidence: 99%

“…Regarding mesencephalic DA neurons, NE also modulates VTA DA neurons [53, 54, 119] and there is evidence that NE-containing axons directly project to the VTA and NAc. Thus, it is likely that NE is important for ventral striatal DA release as well.…”

Section: The Role Of Ne In Methamphetamine-induced Behavioural Changesmentioning

confidence: 99%

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

Ferrucci

Giorgi

Bartalucci

et al. 2013

Current Neuropharmacology

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The activity of locus coeruleus (LC) neurons has been extensively investigated in a variety of behavioural states. In fact this norepinephrine (NE)-containing nucleus modulates many physiological and pathological conditions including the sleep-waking cycle, movement disorders, mood alterations, convulsive seizures, and the effects of drugs such as psychostimulants and opioids. This review focuses on the modulation exerted by central NE pathways on the behavioural and neurotoxic effects produced by the psychostimulant methamphetamine, essentially the modulation of the activity of mesencephalic dopamine (DA) neurons. In fact, although NE in itself mediates some behavioural effects induced by methamphetamine, NE modulation of DA release is pivotal for methamphetamine-induced behavioural states and neurotoxicity. These interactions are discussed on the basis of the state of the art of the functional neuroanatomy of central NE- and DA systems. Emphasis is given to those brain sites possessing a remarkable overlapping of both neurotransmitters.

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Prazosin modulates the firing pattern of dopamine neurons in rat ventral tegmental area

Cited by 171 publications

References 31 publications

Atomoxetine Increases Extracellular Levels of Norepinephrine and Dopamine in Prefrontal Cortex of Rat A Potential Mechanism for Efficacy in Attention Deficit/Hyperactivity Disorder

Atomoxetine Increases Extracellular Levels of Norepinephrine and Dopamine in Prefrontal Cortex of Rat A Potential Mechanism for Efficacy in Attention Deficit/Hyperactivity Disorder

Prolonged Activation of Mesolimbic Dopaminergic Neurons by Morphine Withdrawal Following Clonidine: Participation of Imidazoline and Norepinephrine Receptors

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

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