In vivo biogenic amine efflux in medial prefiontal cortex with imipramine, fluoxetine, and fluvoxamine

Jordan, Scott W.; Kramer, Gerald L.; Zukas, Paul K.; Moeller, Melissa; Petty, Frederick

doi:10.1002/syn.890180404

Cited by 128 publications

(76 citation statements)

References 16 publications

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“…Alternatively, an enhanced NE neurotransmission could modulate interactions between MS/DBv and hippocampal oscillators, leading to theta oscillation in both the MS/DBv and hippocampus. In contrast to the NE reuptake inhibitors, our results indicate that fluvoxamine, a selective serotonin reuptake inhibitor (Jordan et al, 1994;Bosker et al, 1995), did not induce or enhance hippocampal theta activity and theta oscillation of MS/DBv neurons. This observation is in agreement with the previous finding demonstrating a permissive role of serotonin system on theta activity: activation of serotonin neurons blocks and inhibition of serotonin neurons activates both septal and hippocampal theta activity either in anesthetized or unanesthetized, behaving animals (Kinney et al, 1996;Marrosu et al, 1996;Vertes and Kocsis, 1997).…”

Section: Controlcontrasting

confidence: 73%

“…Selective actions of fluvoxamine and desipramine on the serotonin and NE transporters, respectively, have been extensively demonstrated using in vivo microdialysis. Thus, acute administration of fluvoxamine, at same doses as tested in the present study, augments extracellular levels of serotonin, but not NE, in various brain regions (Jordan et al, 1994;Bosker et al, 1995;Bymaster et al, 2002). Conversely, the tricyclic antidepressant, desipramine selectively enhances brain extracellular NE, but not serotonin, levels (L'Heureux et al, 1986;Perry and Fuller, 1997;Hajós-Korcsok et al, 2000).…”

Section: Discussionsupporting

confidence: 49%

“…Reboxetine, a racemic mixture of benzyl]-morpholine sulphonate]), synthesized at Pharmacia, Kalamazoo, MI, USA), desipramine hydrochloride (Sigma-Aldrich, St Louis, MO, USA) and fluvoxamine maleate (Solvay Duphar, Weesp, The Netherlands) solutions were made up based upon their salt weights in H 2 O and concentrations adjusted so that injection volumes equalled 1 ml/kg body weight. Desipramine and fluvoxamine were tested at doses that selectively and effectively inhibit NE and serotonin uptake, respectively (L'Heureux et al, 1986;Jordan et al, 1994;Bosker et al, 1995;Perry and Fuller, 1997;Hajós-Korcsok et al, 2000;Bymaster et al, 2002) to inhibit selectively and effectively either NE or serotonin uptake, respectively. After conclusion of experiments, animals were euthanized with an IV bolus of chloral hydrate.…”

Section: Electrophysiological Experimentsmentioning

confidence: 99%

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Norepinephrine but not Serotonin Reuptake Inhibitors Enhance Theta and Gamma Activity of the Septo-Hippocampal System

Hajós¹,

Hoffmann²,

Robinson³

et al. 2002

Neuropsychopharmacol

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Current neurobiological concepts attribute a central role of the hippocampal formation in cognitive and affective processes. Recent studies indicate that the hippocampus is affected in human depression, and antidepressant drugs induce hippocampal adaptive changes that are thought to be associated with their therapeutic action. In the present study, we investigated the action of various antidepressant drugs on the activity of the septo-hippocampal system, its oscillatory activity in particular. The acute effects of the norepinephrine (NE) reuptake inhibitors reboxetine and desipramine, and the selective serotonin reuptake inhibitor fluvoxamine were evaluated. Extracellular single-unit recordings were performed from the medial septum/diagonal band of Broca (MS/DBv), with simultaneous hippocampal EEG recordings of anesthetized rats. Systemic administration of reboxetine synchronized hippocampal EEG, resulting in a significant increase in power at theta frequency, and an increase in frequency and power of gamma-wave activity. Parallel to EEG synchrony, reboxetine induced or enhanced theta oscillation of MS/DBv neurons. Oscillatory frequencies of MS/DBv neurons were identical, and phase locked to the corresponding hippocamapal theta frequencies. Under the same experimental conditions, reboxetine induced a two-fold increase in extracellular NE (but not serotonin) levels in the hippocampus as revealed by microdialysis. Desipramine, but not the serotonin reuptake inhibitor fluvoxamine, evoked responses similar to those of reboxetine regarding septo-hippocampal theta activity. The present findings indicate that even though both NE and serotonin reuptake inhibitors are clinically effective antidepressant drugs, their action on the septo-hippocampal oscillatory behavior is different. It is presumed that selective NE reuptake inhibitors could modulate various cognitive processes associated with hippocampal oscillatory activity.

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Section: Controlcontrasting

confidence: 73%

Section: Discussionsupporting

confidence: 49%

Section: Electrophysiological Experimentsmentioning

confidence: 99%

See 1 more Smart Citation

Norepinephrine but not Serotonin Reuptake Inhibitors Enhance Theta and Gamma Activity of the Septo-Hippocampal System

Hajós¹,

Hoffmann²,

Robinson³

et al. 2002

Neuropsychopharmacol

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“…27 However, in the body, imipramine and amitriptyline are rapidly metabolized into desipramine and nortriptyline, respectively, 28 and rodent microdialysis studies indicate that systemic administration of imipramine boosts brain NE more strongly than it does serotonin. 29 So the principal effect of all tricyclics, in vivo, may actually be boosting the level of NE in the brain, and maybe throughout the rest of the body as well through enhanced release into the bloodstream by the adrenal glands (whose cells also contain a NE transporter 30 ) and enhanced release within other organs by the rest of the sympathetic nervous system.…”

Section: Literature Search Detailsmentioning

confidence: 99%

Is norepinephrine an etiological factor in some types of cancer?

Fitzgerald

2008

Intl Journal of Cancer

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I examine evidence that the signaling molecule norepinephrine (NE) is an etiological factor in some types of cancer. In support of this hypothesis, I cite the following 7 lines of evidence: (i) rodent studies of tumorigenesis in the context of NE manipulation; (ii) human studies of tricyclic antidepressant use and cancer rate; (iii) existence of pheochromocytoma, a cancer of the adrenal glands; (iv) cancer rate in families with individuals who have bipolar disorder; (v) hypertension and cancer risk; (vi) excessive body weight and cancer risk; and (vii) psychological stressors and cancer risk. Three aspects of the body's NE system are consistent with it playing an etiological role in various types of cancer: (i) NE circulates in the blood and can thereby access organ systems throughout the body, in addition to direct peripheral release by the sympathetic nervous system and being released within the brain; (ii) many of the body's organs possess NE receptors on the outer surface of at least some of their cells; (iii) by binding to its extracellular receptors, NE affects intracellular second messenger systems that could influence carcinogenesis. Most importantly, use of existing pharmaceutical drugs that either lower the level of NE (such as clonidine) or block NE receptors may lower the probability of an individual developing cancer, and this hypothesis could be tested immediately by an epidemiologist through examination of existing medical records. ' 2008 Wiley-Liss, Inc.Key words: norepinephrine; pharmacology; clonidine; adrenoceptor; rodent; hypertension; epidemiology; pheochromocytoma I present evidence that the signaling molecule norepinephrine (NE), which is a neurotransmitter and plays various roles in organs other than the brain, is an etiological factor in some types of cancer. In support of this hypothesis, I cite the following 7 lines of evidence: (i) in a series of rodent studies, increasing the level of NE in various organs increases tumorigenesis, whereas decreasing the level decreases tumorigenesis; (ii) in humans, tricyclic antidepressant use, which may boost the level of NE throughout the body, may be associated with increased rates of cancer; (iii) pheochromocytoma, which is a cancer of the adrenal glands, may be an example of NE causing cancer in the organ that releases it into the bloodstream; (iv) families with individuals who have bipolar disorder have elevated cancer rates, where bipolar disorder may be associated with a high level of NE; (v) hypertension is associated with an elevated level of NE in the bloodstream, and may be a cancer risk factor; (vi) excessive body weight is associated with elevated blood NE and is a cancer risk factor; and (vii) psychological stressors are associated with increased release of NE in the brain and bloodstream, and exposure to stress is potentially a cancer risk factor.In addition to the above evidence, including NE's role in the brain, several other aspects of the body's NE system are consistent with an etiological role in cancer: (i) In addition to relea...

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“…Thus, NET plays a role in controlling the intensity and duration of signal transduction (Zahniser et al 2001). NE interacts with many other neurotransmitters both in normal cortical regulation and in the therapeutic response to psychoactive compounds, and one critical interacting neurotransmitter is dopamine (Jordan et al 1994). Dopamine is the NE precursor so that levels of both neurotransmitters are regulated by common factors, for example, tyrosine hydroxylase activity.…”

Section: Introductionmentioning

confidence: 99%

Haplotype architecture of the norepinephrine transporter gene SLC6A2 in four populations

et al. 2004

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The norepinephrine transporter (NET) regulates levels of monoamine neurotransmitters integral to a variety of behaviors and autonomic functions. Two SLC6A2 polymorphisms have been used in genetic association studies, generating intriguing but nondefinitive results on traits such as hypertension and mood. One of these SLC6A2 variants is functional but rare. The other is common but not informative over the entire 48 kb SLC6A2 region and is insufficient to capture the functional diversity potentially contained within any SLC6A2 region. To elucidate SLC6A2 haplotype structure and define markers sufficient to capture haplotype diversity within detected haplotype blocks, 26 single-nucleotide polymorphisms (SNPs) were genotyped in 384 individuals evenly divided across Finnish Caucasian, US Caucasian, Plains American Indian, and African American populations. Three conserved blocks, 13.6, 12.5, and 25 kb in size and showing little evidence for historical recombination were observed in all populations. Haplotype diversity in block 1 and numbers of common haplotypes were highest in African Americans, among whom 5-6 optimal markers were sufficient to maximize diversity of each block. For other populations, 2-3 markers/block sufficed, but the optimal markers differed across populations. The SLC6A2 haplotype map and 25-marker panel (excluding the monomorphic one) is a comprehensive tool for genetic linkage studies on phenotypes related to NET function.

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In vivo biogenic amine efflux in medial prefiontal cortex with imipramine, fluoxetine, and fluvoxamine

Cited by 128 publications

References 16 publications

Norepinephrine but not Serotonin Reuptake Inhibitors Enhance Theta and Gamma Activity of the Septo-Hippocampal System

Norepinephrine but not Serotonin Reuptake Inhibitors Enhance Theta and Gamma Activity of the Septo-Hippocampal System

Is norepinephrine an etiological factor in some types of cancer?

Haplotype architecture of the norepinephrine transporter gene SLC6A2 in four populations

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