Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “nucleus accumbens”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2000

Nociceptin differentially affects morphine-induced dopamine release from the nucleus accumbens and nucleus caudate in rats.

The effects induced by nociceptin on morphine-induced release of dopamine (DA), 3,4-dihydroxyphenilacetic acid (DOPAC) and homovanillic acid (HVA) in the nucleus accumbens and nucleus caudate were studied in rats by microdialysis with electrochemical detection. Nociceptin administered intracerebroventricularly (i.c.v.) at doses of 2, 5 and 10 nmol/rat changed neither DA nor metabolites release in the shell of the nucleus accumbens or in the nucleus caudate. Morphine administered intraperitoneally (i.p.) (2, 5, and 10 mg/kg) increased DA and metabolites release more in the shell of the nucleus accumbens than in the nucleus caudate. When nociceptin (5 or 10 nmol) was administered 15 min before morphine (5 or 10 mg/kg), it significantly reduced morphine-induced DA and metabolites release in the shell of the nucleus accumbens, whereas only a slight, nonsignificant reduction was observed in the nucleus caudate. Our data indicate that nociceptin may regulate the stimulating action associated with morphine-induced DA release more in the nucleus accumbens than in the nucleus caudate, and are consistent with recent observations that nociceptin reversed ethanol- and morphine-induced conditioned place preference. Therefore, the nociceptin-induced reduction of DA release stimulated by morphine in the nucleus accumbens, and the results obtained with nociceptin in the conditioned place preference procedure suggest a role for nociceptin in the modulation of the behavioral and neurochemical effects of abuse drugs.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Effects of dopamine depletion on the morphology of medium spiny neurons in the shell and core of the rat nucleus accumbens.

Nucleus accumbens receives a dense dopaminergic innervation which is important in regulating motivated states of behavior such as goal-directed actions, stimulus-reward associations and reinforcement of addictive substances. The shell and core territories of this nucleus each receive functionally and morphologically distinct dopaminergic inputs and lesions of the ascending pathways totally deprive the core but not the shell of dopaminergic fibers. Medium spiny neurons are the principal targets of dopaminergic terminals. The present study explored whether the loss of dopamine inputs can affect these neurons and whether cells in the shell and core would be equally susceptible to such a loss. Intracellular injection in fixed slices and neuronal reconstruction were used to analyze the dendritic trees of 62 neurons in the shell and core of animals that received a unilateral, chronic 6-hydroxydopamine lesion of the medial forebrain bundle. In the dopamine-depleted core, dendrites are significantly shorter (16% decrease) than in the intact core and in both the dopamine-depleted core and lateral shell, dendrites are less spiny than in respective control regions. Dopamine loss in the medial shell is associated with significantly more tortuous dendrites that are lower in spine density. However, the number of spines is not reduced which may mean that the increase recorded for segment length, although insignificant in tests, could be responsible for the change in spine density. These data suggest that the loss of dopamine can affect accumbal neuronal morphology and, moreover, can affect neuronal structures differentially in the shell and core.

Animals↗
PubMed2000

The metabolic rate and vulnerability of dopaminergic neurons, and adenosine dynamics in the cerebral cortex, nucleus accumbens, caudate nucleus, and putamen of the common marmoset.

The pathophysiology of the striatum and cerebral cortex were studied from the pharmacological aspect. Investigation of the dopamine content in the cerebral cortex revealed that the premotor and motor area showed the highest level (61+/-6.2 ng/g). Intravenous injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at a dose of 10 mg/kg reduced the dopamine content in the caudate nucleus and putamen to 2-3% of the control level in common marmosets, while it fell to 60% in the nucleus accumbens. There was no alteration of the dopamine content in the cerebral cortex. Immunohistochemical staining for tyrosine hydroxylase in the midbrains of MPTP-treated marmosets showed almost complete disappearance of dopaminergic cells from the substantia nigra and good preservation of cells in the ventrotegmental area. Dopaminergic cells projecting to the caudate/putamen, nucleus accumbens, and cerebral cortex showed marked, moderate, and no vulnerability to MPTP, respectively. After systemic administration of MPTP, dopaminergic neurons projecting to the caudate nucleus and putamen were damaged equally. However, the compensatory increase of dopamine turnover was more prominent in the putamen than in the caudate nucleus. Thus, nigroputaminal dopaminergic neurons may have a higher level of activity than neurons in the caudate. The neural connections and functions of the caudate nucleus and putamen have already been differentiated anatomically or physiologically. This compensatory increase of the dopamine turnover rate is another aspect of functional differences between the caudate nucleus and putamen. Investigation of the dopamine content in the head, body, and tail of the caudate nucleus showed no differences in the concentration of dopamine. However, a study of the metabolic rate of dopamine using alpha-methyl-p-tyrosine, a tyrosine hydoxylase inhibitor, showed higher metabolism of dopamine in the head of the caudate nucleus in common marmosets. Thus, dopaminergic neurons projecting to the caudate nucleus may show topographical differences in their firing rates. A microdialysis study indicated an increase in the metabolism of adenosine in the striatum of MPTP-treated animals. Cholinergic neurons are interneurons and are one of the main sources of adenosine in the striatum. Dopaminergic input from the substantia nigra acting on cholinergic neurons was decreased following MPTP treatment. The increase of adenosine metabolism suggested that cholinergic neurons in the striatum receive inhibitory inputs from nigrostriatal dopaminergic neurons.

Adenosine↗
PubMed1988

Comparison of the behavioural effects induced by administration in rat nucleus accumbens or nucleus caudatus of selective mu and delta opioid peptides or kelatorphan an inhibitor of enkephalin-degrading-enzymes.

The effects of selective agonists for delta opioid receptors: [D-Thr2, Leu5]-enkephalyl-Thr6 (DTLET) and mu receptors: [D-Ala2, MePhe4, Gly-ol5]-enkephalin (DAGO) and of (R)-3-(N-hydroxyl-carboxamido-2-benzylpropanoyl)-L-alanine (kelatorphan), a complete inhibitor of enkephalin degrading enzymes, on the motor activity of rats was examined after their local administration into the nucleus accumbens (NA) or nucleus caudatus (NC). In both structures DTLET dose dependently enhanced locomotor activity as measured in the open-field test. This strong effect was reversed by the selective delta antagonist: ICI 174,864. Contrastingly, DAGO induced hypoactivity followed by hyperactivity 150 min later. This biphasic effect was blocked by systemic injection of naloxone, but not by ICI 174,864. The physiological relevance of these effects was ascertained by the naloxone-reversible stimulatory responses induced by kelatorphan, supporting a role for endogenous enkephalins in the control of behavior through delta receptor stimulation.

Animals↗
PubMed1992

Increased dopamine release in vivo in nucleus accumbens and caudate nucleus of the rat during drinking: a microdialysis study.

Changes in dopamine release and metabolism during drinking in thirsty rats were studied using in vivo microdialysis. Animals were maintained on controlled water (1 h per day) and trained to lick for water in a behavioural box. Microdialysis probes were then inserted into the left nucleus accumbens and right caudate nucleus through previously implanted guide cannulae, and the following day animals were connected for dialysis perfusion, during which they were allowed 1 h free access to water. Dopamine, and its metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid, increased in both nucleus accumbens and caudate nucleus in association with drinking, but the 5-hydroxytryptamine metabolite, 5-hydroxyindoleacetic acid, only increased in the caudate nucleus. There was a direct correlation between the maximum dopamine release in nucleus accumbens and the maximum licking rate per 10-min period, but the maximum increase in dopamine did not occur until after the period of maximum licking. Increases in 3,4-dihydroxyphenylacetic acid and homovanillic acid were further delayed (by 20 and 30 min, respectively). In the caudate, changes in 5-hydroxyindoleacetic acid showed a very similar time-course to those of 3,4-dihydroxyphenylacetic acid. These data show that dopamine systems in both nucleus accumbens and caudate nucleus are activated in relation to drinking in thirsty rats. In addition, they indicate that 5-hydroxytryptamine systems in the caudate nucleus, but not in nucleus accumbens, may also be involved. The support that the results provide for the hypothesized connection between reward and limbic dopamine is discussed.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Are emotion and motivation localized in the limbic system and nucleus accumbens?

Groups of control rats without surgery or groups of rats prepared with surgical lesions of the septal nuclei, amygdala, cingulate cortex, accumbens nucleus, section of the fornix, or sham surgical operations, were tested in a simple autonomic conditioning situation (conditioned defecation). Control rats and rats with lesions of the accumbens nucleus were also tested in a straight alley maze under varying conditions of water deprivation. In general, the lesions had little effect except that amygdaloid damage impaired acquisition of conditioned defecation. The theory that 'emotion' and 'motivation' can be localized in the 'limbic system' and nucleus accumbens is discussed critically.

Animals↗
PubMed1991

Efferent connections of the striatopallidal and amygdaloid components of the substantia innominata in the cat: projections to the nucleus accumbens and caudate nucleus.

Enkephalin immunoreactivity is used to divide the feline substantia innominata into circumscript subregions, i.e. the "striatopallidal system" and the "extended amygdala". In addition, enkephalin immunoreactivity is used to subdivide the striatopallidal system into two distinct areas, i.e. the subcommissural part of the globus pallidus displaying high enkephalin immunoreactivity and the ventral pallidum displaying moderate enkephalin immunoreactivity. The anterograde axonal transport of Phaseolus vulgaris-leucoagglutinin is used to study the efferents of these areas innervating the caudate nucleus and the nucleus accumbens. It is found that the enkephalin-immunoreactive subcommissural part of the globus pallidus as well as the dorsal enkephalin-immunoreactive regions of the extended amygdala project topographically along a rostrocaudal and mediolateral dimension to the nucleus accumbens. The far rostral parts of the caudate nucleus are found to be innervated by the subcommissural part of the globus pallidus whereas the extended amygdala has no such connection. This pathway is also found to be topographically organized along a mediolateral dimension. The non-enkephalin-immunoreactive area ventral and lateral to the subcommissural part of the globus pallidus is found to have no projections to the nucleus accumbens and caudate nucleus. This region rather innervates the olfactory tubercle. In contrast to the striatopallidal system the sublenticular part of the extended amygdala preferentially projects to the adjoining part of the extended amygdala, i.e. the bed nucleus of the stria terminalis. However, the ventral regions preferentially innervate the medial division of the bed nucleus of the stria terminalis whereas the dorsal regions preferentially innervate the lateral division of the bed nucleus of the stria terminalis. These data indicate that the differential forebrain systems represented in the feline substantia innominata, i.e. the striatopallidal system and extended amygdala have differential output stations. The results are discussed in view of the role of the subcommissural part of the globus pallidus and the nucleus accumbens in orofacial dyskinesia and schizophrenia, respectively.

Amygdala↗
PubMed1990

Effects of locus coeruleus lesions on the release of endogenous dopamine in the rat nucleus accumbens and caudate nucleus as determined by intracerebral microdialysis.

Bilateral 6-hydroxydopamine lesions of the rat locus coeruleus (a) depleted forebrain norepinephrine levels by 67%, (b) reduced the basal release of dopamine in the nucleus accumbens and caudate nucleus by 26% and 19%, respectively, and (c) reduced (+)-amphetamine-induced release in the nucleus accumbens and caudate nucleus. The locus coeruleus appears to exert a tonic excitatory influence on striatal and limbic dopamine release in vivo.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2006

Rapid neuroadaptation in the nucleus accumbens and bed nucleus of the stria terminalis mediates suppression of operant responding during withdrawal from acute opioid dependence.

Single injections of morphine induce a state of acute opioid dependence in humans and animals, measured as precipitated withdrawal when an antagonist is administered 4-24 h after morphine. Additional morphine exposure at daily or weekly intervals results in further increases in withdrawal severity, suggesting that acute opioid dependence reflects the early stages in the development of a chronic state of dependence. The current study evaluated the role of the nucleus accumbens (NAC), bed nucleus of stria terminalis (BNST), interstitial nucleus of posterior limb of the anterior commissure (IPAC), and central amygdala (CeA) in the expression of antagonist-precipitated suppression of operant responding for food as a measure of withdrawal from acute opioid dependence. Rats trained on a fixed-ratio 15 schedule received one or four daily injections of morphine, with the lipophobic opioid antagonist methylnaloxonium (16-2000 ng) infused into one of the brain regions or the lateral ventricle (i.c.v.) 4 h after the final morphine injection. After acute morphine methylnaloxonium was more potent upon infusion into the NAC (17.9-fold potency shift), BNST (6.8-fold) and CeA (5.5-fold) than it was upon i.c.v. administration. Following repeat morphine the NAC and BNST but not CeA continued to show greater sensitivity relative to i.c.v. infusion (12.9-, 8.7-, and 3.2-fold potency shifts, respectively). The IPAC was insensitive to methylnaloxonium after acute or repeat morphine at doses that reliably suppressed responding upon i.c.v. infusion (125-500 ng). Thus, among the components of extended amygdala examined in this study, rapid neuroadaptation within the nucleus accumbens and bed nucleus of the stria terminalis appear to play the most prominent role in antagonist-precipitated suppression of operant responding during the early stages in the development of opioid dependence.

Adaptation, Physiological↗
PubMed1985

The effects of 6-hydroxydopamine lesions of the nucleus accumbens and caudate nucleus of rats on feeding in a novel environment.

Open field activity and feeding behavior were studied in separate groups of rats 1 or 6 weeks after infusions of the neurotoxin, 6-hydroxydopamine (6-OHDA) into the nucleus accumbens or caudate nucleus. These infusions resulted in a specific destruction of the catecholamine innervation of the injected area. When compared with rats which received infusions of vehicle alone, both lesions resulted in a relative reduction in locomotor activity 1 week, but not 6 weeks, after the operation. Both lesions also resulted in a more rapid onset of feeding from wire baskets containing familiar laboratory chow. Rats with lesions of the nucleus accumbens also fed for longer, consumed more food, and fed in longer bouts than did sham-lesioned animals, but rats with lesions of the caudate nucleus did not. These data show changes in feeding behaviour produced by 6-OHDA infusions into the dopamine terminal fields which were long lasting in comparison with the locomotor impairments, and did not arise as a result of locomotor impairment. The differences in feeding behaviour may result from more general changes in behaviour such as an impairment in the reactivity to novel environmental stimuli or switching between types of behaviour.

Animals↗
PubMed1998

Injections of D-amphetamine into the ventral pallidum increase locomotor activity and responding for conditioned reward: a comparison with injections into the nucleus accumbens.

The nucleus accumbens and ventral pallidum receive dopamine (DA) projections from the mesencephalon. Although DA inputs to the nucleus accumbens are implicated in both locomotion and reward processes, little is known of the behavioural significance of DA in the ventral pallidum. These studies examined the effects of D-amphetamine injected into the nucleus accumbens or ventral pallidum on locomotor activity and responding for a conditioned reward (CR). In the nucleus accumbens D-amphetamine dose dependently (1, 3 and 10 microg) increased locomotion within 5-10 min of injection. Intra-ventral pallidum microinjections of D-amphetamine also increased activity in this dose range, but the effect occurred with a longer latency (5-20 min). The magnitude of the response evoked by ventral pallidum injections was lower than that evoked by nucleus accumbens injections. The GABAA antagonist picrotoxin (0.1 microg) stimulated activity when injected into the ventral pallidum but not the nucleus accumbens, providing a pharmacological dissociation between the two injection sites. In the CR studies, D-amphetamine injected into both sites potentiated responding for a CR previously paired with food delivery, without altering responding on an inactive lever. Picrotoxin injected into the ventral pallidum reduced responding and abolished the selectivity of responding for CR. The results show that DA release in the ventral pallidum enhances locomotion and responding for a CR, providing evidence that DA in the ventral pallidum plays a significant role in the mediation of the effects of D-amphetamine. The failure of picrotoxin to elevate responding for CR despite increasing locomotor activity indicates that pharmacologically-induced blockade of GABAA receptors in the ventral pallidum disrupts goal-directed responding.

Animals↗
PubMed2003

Role of muscarinic receptors in the activation of the ventral subiculum and the consequences for dopamine release in the nucleus accumbens.

The nucleus accumbens receives limbic inputs from a number of brain regions, including the ventral subiculum. In rats, activation of the ventral subiculum following microinjection of N-methyl-D-aspartate (NMDA) or carbachol increases locomotor activity, whilst ventral subiculum application of NMDA also increases dopamine efflux in the ipsilateral nucleus accumbens. Microdialysis experiments were therefore conducted to ascertain the consequences for dopamine release in the nucleus accumbens following ventral subiculum administration of carbachol, and to explore the acetylcholine receptor subtype(s) that might be involved. We report that, in anaesthetised rats, ventral subiculum administration of carbachol increased dopamine levels in the nucleus accumbens. The response was attenuated by co-administration with atropine, whilst administration of nicotine and the alpha-7 nicotinic acetylcholine receptor agonist AR-R17779 (spiro[1-azabicyclo[2,2,2]octane-3,5'-oxazolidine]-2'-one monohydrochloride) failed to evoke a response. Oxotremorine-M produced a dose-dependent increase in dopamine efflux confirming sensitivity to muscarinic receptor stimulation. However, the ventral subiculum was insensitive to xanomeline and pilocarpine, muscarinic M(1) receptor-preferring agonists, but sensitive to BuTAC ([5R-[exo]-6-[butylthio]-1,2,5-thiadiazol-3-yl]-1-azabicyclo[3.2.1])octane), a muscarinic M(2)/M(4) receptor agonist. The dopamine response to oxotremorine-M was significantly attenuated, although not abolished by co-administration with the M(2)/M(4) receptor antagonist methoctramine, and studies combining oxotremorine-M with (-)-bicuculline, indicated a dual action in the ventral subiculum that was dependent and independent of reduced GABA neurotransmission. The data presented indicates that activation of the ventral subiculum by carbachol increases dopamine efflux in the nucleus accumbens by stimulation of muscarinic receptors, and that the ventral subiculum-nucleus accumbens projection system is sensitive to muscarinic M(2)/M(4) receptor stimulation.

Animals↗
PubMed2001

Nicotine withdrawal hyperalgesia and opioid-mediated analgesia depend on nicotine receptors in nucleus accumbens.

The nucleus accumbens, as part of the mesolimbic dopaminergic reward pathway, mediates both addiction to and withdrawal from substances of abuse. In addition, activity of substances of abuse such as opioids in the nucleus accumbens has been implicated in pain modulation. Because nucleus accumbens nicotinic receptors are important in nicotine addiction and because nicotinic activity can interact with opioid action, we investigated the contribution of nucleus accumbens nicotinic receptors to opioid-mediated analgesia/antinociception. The response of the nociceptive jaw-opening reflex to opioids was studied in the rat, both before and during chronic nicotine exposure. In nicotine-naive rats, intra-accumbens injection of the nicotinic receptor antagonist mecamylamine blocked antinociception produced by either systemic morphine, intra-accumbens co-administration of a mu- and a delta-opioid receptor agonist, or noxious stimulation (i.e., subdermal capsaicin in the hindpaw); intra-accumbens mecamylamine alone had no effect. The antinociceptive effect of either morphine or noxious stimulation was unchanged during nicotine tolerance; however, intra-accumbens mecamylamine lost its ability to block antinociception produced by either treatment. Intra-accumbens mecamylamine by itself precipitated significant hyperalgesia in nicotine-tolerant rats which could be suppressed by noxious stimulation as well as by morphine. These results indicate that nucleus accumbens nicotinic receptors play an important role in both opioid- and noxious stimulus-induced antinociception in nicotine-naive rats. This role was attenuated in the nicotine-dependent state. The suppression of withdrawal hyperalgesia by noxious stimulation suggests that pain can ameliorate the symptoms of withdrawal, thus suggesting a possible mechanism for pain-seeking behavior.

Analgesia↗
PubMed2004

Quantification of morphological differences in boutons from different afferent populations to the nucleus accumbens.

The nucleus accumbens (Acb) receives convergent glutamatergic inputs from the prefrontal cortex (PFC), central thalamus, basolateral amygdala and the ventral subiculum of the hippocampus. The principal neurons of the nucleus accumbens are modulated by specific sets of convergent afferent inputs, the local circuit neurons also receive a substantial number of glutamatergic inputs, but the full complement of these has yet to be established. The aim of these studies was to define characteristics of the different glutamatergic afferent inputs to the nucleus accumbens that would aid their identification. To enable the characterisation of the glutamatergic inputs to nucleus accumbens neurons we first labelled the four main glutamatergic sources of afferent input to the accumbens with the anterograde tracer biotinylated dextran amine (BDA). Using an unbiased systematic sampling method, the morphological characteristics of their synaptic boutons were measured and assessed at the electron microscopic level. From the criteria assessed, a comparison of the four afferent sources was made, characteristics such as bouton size and vesicle density had significantly different population means, however, the only characteristic that allowed discrimination between the four major glutamatergic afferent to the nucleus accumbens was that of vesicle size. The vesicles in boutons from amygdala were larger than the subiculum which, in turn, were larger than the prefrontal cortex, the thalamus were the smallest in size. The methods used also allow a comparison of the relative frequency of different sized postsynaptic structures targeted, the prefrontal cortex almost exclusively targeted spines whereas the thalamus and the subiculum, in addition to spines, targeted proximal and distal dendrites.

Analysis of Variance↗
PubMed2000

Possible pathways through which neurons of the shell of the nucleus accumbens influence the outflow of the core of the nucleus accumbens.

The nucleus accumbens (Acb), a major sector of the ventral striatum, is considered to be an integral part of the striatal complex. The Acb has been shown to be composed of two subdivisions, core and shell, which are distinguishable in several aspects, suggesting that these two subdivisions play different functional roles. The aim of this study was to identify pathways of the efferents of the shell of the Acb to influence the outflow of the core of the Acb. Potential disynaptic projections of the shell to the core of the Acb were investigated in chloral hydrate-anesthetized male Sprague-Dawley rats. Following ipsilateral injections of biotinylated dextran amine (BDA) into the shell of the Acb and cholera toxin B subunit (CT-B) into the core, strong overlapping distributions of BDA-labeled terminals and CT-B-labeled neuronal cell somata were found in the medial part of the ventral tegmental area, medial part of the lateral hypothalamic area, and dorsolateral part of the basolateral amygdaloid nucleus. The significance of multiple sites of relay between the efferents of the shell and the afferents of the core of the Acb at different levels of the neuraxis may be related to the functional specificity of each relay site.

Animals↗
PubMed1995

Intravenous cocaine, morphine, and amphetamine preferentially increase extracellular dopamine in the "shell" as compared with the "core" of the rat nucleus accumbens.

The nucleus accumbens is considered a critical target of the action of drugs of abuse. In this nucleus a "shell" and a "core" have been distinguished on the basis of anatomical and histochemical criteria. The present study investigated the effect in freely moving rats of intravenous cocaine, amphetamine, and morphine on extracellular dopamine concentrations in the nucleus accumbens shell and core by means of microdialysis with vertically implanted concentric probes. Doses selected were in the range of those known to sustain drug self-administration in rats. Morphine, at 0.2 and 0.4 mg/kg, and cocaine, at 0.5 mg/kg, increased extracellular dopamine selectivity in the shell. Higher doses of cocaine (1.0 mg/kg) and the lowest dose of amphetamine tested (0.125 mg/kg) increased extracellular dopamine both in the shell and in the core, but the effect was significantly more pronounced in the shell compared with the core. Only the highest dose of amphetamine (0.250 mg/kg) increased extracellular dopamine in the shell and in the core to a similar extent. The present results provide in vivo neurochemical evidence for a functional compartmentation within the nucleus accumbens and for a preferential effect of psychostimulants and morphine in the shell of the nucleus accumbens at doses known to sustain intravenous drug self-administration.

Amphetamine↗
PubMed2005

Identification of a noradrenaline-rich subdivision of the human nucleus accumbens.

The nucleus accumbens, situated at the junction between rostral pre-commissural caudate and putamen, is now considered to be critically involved in rewarding and motivational functions mediated by the neurotransmitter dopamine. However, in the human, the precise anatomical boundaries of this nucleus are still undetermined and controversy exists as to the extent to which nucleus accumbens activity is controlled by noradrenaline, a related neurotransmitter now much neglected (in favor of dopamine) by the scientific community. Here we resolve the question of noradrenaline in the human nucleus accumbens and identify, in autopsied brain of normal subjects, a small subdivision of the caudomedial portion of this nucleus that selectively contains strikingly high levels of noradrenaline and thus represents the only area in human brain having equally high levels of both noradrenaline and dopamine. The presence of very high, localized noradrenaline concentrations in the caudomedial nucleus accumbens implies a special biological role for this neurotransmitter in human brain motivational processes.

Aged↗