Enhanced adrenergic excitation of serotonergic dorsal raphe neurons in genetically obese rats

Ohliger-Frerking, Patricia; Horowitz, J. M.; Horwitz, Barbara A

doi:10.1016/s0304-3940(02)00931-x

Cited by 19 publications

(6 citation statements)

References 10 publications

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“…The dorsal raphe, which contains one of the largest populations of serotonergic neurons in the brain was the only structure activated specifically in sucrose ‘relapse’ mice. There is evidence that serotonergic transmission from the dorsal raphe to the ventromedial hypothalamus contributes to the regulation of feeding (Ohliger‐Frerking et al 2002), and Fos expression in the dorsal raphe is enhanced in response to food anticipation and searching (Takase & Nogueira, 2008). Recently, it has been demonstrated that serotonergic neurons in the dorsal raphe exhibit increased firing when animals are forced to wait for delivery of food and water rewards in response to a conditioned tone (Miyazaki et al 2011).…”

Section: Discussionmentioning

confidence: 99%

Investigation of the neuroanatomical substrates of reward seeking following protracted abstinence in mice

Madsen

Brown

Short³

et al. 2012

The Journal of Physiology

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Key points• Persistent vulnerability to relapse represents a major challenge in the treatment of drug addiction. The brain circuitry that underlies relapse-like behaviour can be investigated using animal models.• This study compared the brains of mice that had relapsed to morphine with mice that had relapsed to sucrose following abstinence. We found that while some brain regions were implicated in both drug and food seeking, other specific parts of the brain were activated for either sucrose or morphine relapse.• Common regions included those with established involvement in reward and relapse-like behaviour. In addition we found some regions not previously linked to these behaviours.• Overall, while our findings support existing literature regarding relapse-like behaviour in rats, we have additionally identified brain regions outside this established circuitry which are worthy of further investigation.Abstract Persistent vulnerability to relapse represents a major challenge in the treatment of drug addiction. The brain circuitry that underlies relapse-like behaviour can be investigated using animal models of drug seeking. As yet there have been no comprehensive brain mapping studies that have specifically examined the neuroanatomical substrates of cue-induced opiate seeking following abstinence in a mouse operant paradigm. The aim of this study was to compare the brain regions involved in sucrose vs. morphine seeking following protracted abstinence in mice. Male CD1 mice were trained to respond for either sucrose (10% w/v) or intravenous morphine (0.1 mg kg −1 per infusion) in an operant paradigm in the presence of a discrete cue. Once stable responding was established, mice were subjected to abstinence in their home cages for 3 weeks and then perfused for tissue collection, or returned to the operant chambers to assess cue-induced reward seeking before being perfused for tissue collection. Brain tissue was processed for Fos immunohistochemistry and Fos expression was quantified in a range of brain nuclei. We identified unique patterns of neuronal activation for sucrose and morphine seeking mice as well as some overlap. Structures activated in both 'relapse' groups included the anterior cingulate and orbitofrontal cortex, nucleus accumbens shell, bed nucleus of the stria terminalis, substantia nigra pars compacta, ventral tegmental area, hippocampus, periaqueductal grey, locus coeruleus and lateral habenula. Structures that were more activated in morphine seeking mice included the nucleus accumbens core, basolateral amygdala, substantia nigra pars reticulata, and the central nucleus of the amygdala. The dorsal raphe was the only structure examined that was specifically activated in sucrose seeking mice. Overall our findings support a cortico-striatal limbic circuit driving opiate seeking, and we have identified some additional circuitry potentially relevant to reward seeking following abstinence. Abbreviations AC, anterior cingulate cortex; BLA, basolateral amygdala; BNST, bed nucleus of the stria terminalis; Ce...

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Section: Discussionmentioning

confidence: 99%

Investigation of the neuroanatomical substrates of reward seeking following protracted abstinence in mice

Madsen

Brown

Short³

et al. 2012

The Journal of Physiology

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“…Stimulation of a 1 -receptors can produce excitation of neurons in the DR (Baraban and Aghajanian, 1980;Menkes et al, 1981;Ohliger-Frerking et al, 2002;Reinhard Jr et al, 1983;Rouqier et al, 1994), the LC (Nakamura et al, 1988;Williams and Marshall, 1987), and the pontine reticular formation (Stevens et al, 1994) and, as discussed above, can facilitate the release of DA in the nucleus accumbens. In addition, neurons in the vermis cortex of the cerebellum are known to send efferent fibers to the LC and ventral tegmental area (Snider et al, 1976) and to the DR (Chan-Palay, 1977), which regulate the activity of these monoaminergic nuclei (Cano et al, 1980;Snider and Snider, 1979).…”

Section: Brain Localizationmentioning

confidence: 99%

Emerging Evidence for a Central Epinephrine-Innervated α1-Adrenergic System that Regulates Behavioral Activation and is Impaired in Depression

Stone

Yang

Rosengarten

et al. 2003

Neuropsychopharmacol

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Currently, most basic and clinical research on depression is focused on either central serotonergic, noradrenergic, or dopaminergic neurotransmission as affected by various etiological and predisposing factors. Recent evidence suggests that there is another system that consists of a subset of brain a 1B -adrenoceptors innervated primarily by brain epinephrine (EPI) that potentially modulates the above three monoamine systems in parallel and plays a critical role in depression. The present review covers the evidence for this system and includes findings that brain a 1 -adrenoceptors are instrumental in behavioral activation, are located near the major monoamine cell groups or target areas, receive EPI as their neurotransmitter, are impaired or inhibited in depressed patients or after stress in animal models, and are restored by a number of antidepressants. This 'EPI-a 1 system' may therefore represent a new target system for this disorder.

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“…Obviously, the administration of yohimbine would act neither at the A6(NA) neurons [154], nor at the C1(Ad) or the DR(5-HT) neurons because all three nuclei are hyper-excited by the CRH released from paraventricular hypothalamic terminals. According to the above, the recovery of the A5(NA) neurons would reduce the C1(Ad) + A6(NA) over-activity, responsible for the hypersecretion of adrenaline plus cortisol [136,[155][156][157][158][159].…”

Section: Therapeutical Evidence Supporting the Postulation That Therementioning

confidence: 99%

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Lechín¹,

Dijs²

2008

TONEURJ

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Abstract:The assessment of circulating neurotransmitters: noradrenaline, adrenaline, dopamine, platelet serotonin, plasma serotonin and plasma tryptophan before and after many types of stressor agents and neuropharmacological drugs carried out over the last thirty years allowed us to accumulate information dealing with the central nervous system (CNS) versus the peripheral autonomic nervous system (ANS) interactions in healthy as well as diseased mammals. Furthermore, the accurate knowledge about the CNS circuitry disorders which underlie both the CNS and peripheral clinical syndromes, has allowed us to prescribe successful neuropharmacological therapeutical strategies for many types of illnesses. In addition, the demonstration that the clinical improvement was always paralleled by the normalization of the neurochemical, hormonal, immunological and clinical profiles affords strong support to our point of view. According to all the above, the authors postulate the existence of two types of diseases: type A and Type N, which are underlain by two opposite CNS + ANS disorders. Type A diseases should be associated with the "uncoping stress" syndrome and are underlain by hyperactivity of the adrenocortical glands plus the CNS disorder characterized by the predominance of the C1(adrenergic) + DR(serotonergic) axis over the A5(noradrenergic) + MR(serotonergic) binomial, whereas the type N diseases depends on the opposite profile: "endogenous depression" syndrome. Finally, we quoted exhaustive evidence showing that the well known fading of both the A6(noradrenergic) + C1(adrenergic) CNS nuclei activity occurring during aging is responsible for the ANS + CNS disorder which is similar to that underlying psychosis, Alzheimer, post-traumatic stress disorder and deficit-attention hyperactive disorder.

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Enhanced adrenergic excitation of serotonergic dorsal raphe neurons in genetically obese rats

Cited by 19 publications

References 10 publications

Investigation of the neuroanatomical substrates of reward seeking following protracted abstinence in mice

Investigation of the neuroanatomical substrates of reward seeking following protracted abstinence in mice

Emerging Evidence for a Central Epinephrine-Innervated α1-Adrenergic System that Regulates Behavioral Activation and is Impaired in Depression

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

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