Nucleus Accumbens Septi

Cross references: 
Amygdaloid Hippocampal Convergence   

    About 15 years ago, while I was volunteering with Food Not Bombs, one of my fellow volunteers was tricked into starting crack cocaine.  As has happened to many others, she became instantly hooked.   Since I wanted to help her, I switched my attention to drugs. 
    It turned out that the part of our nervous systems most involved with addiction is the Nucleus Accumbens Septi (NAC), and I have been interested in the NAC ever since. 
    I eventually found a successful treatment for drugs.  You can read about it at:  
NOTE:  If you get an error message, click the error message. 

    You might ask, "If the stuff works, why is it not more widely known?"   
    Answer:  Perhaps some of the huge profits generated by the illegal drug trade are used to keep the cure hidden. 

The Kolb & Whishaw book gives a very brief discussion of the NAC on
[K&W: 438-441]. 
    See:  Historical Background & Free Book  . 

Nucleus Accumbens Septi (Wiki)   
     "The nucleus accumbens (NAc or NAcc), also known as the accumbens nucleus or as the nucleus accumbens septi
(Latin for nucleus adjacent to the septum) is a region in the basal forebrain rostral to the preoptic area of the hypothalamus.[1] The nucleus accumbens and the olfactory tubercle collectively form the ventral striatum, which is part of the basal ganglia.[2]  

Medial surface, person facing to the left. Nucleus accumbens is very roughly in the area labeled 34.    

    The nucleus accumbens has a significant role in the cognitive processing of motivation, pleasure, and reward and reinforcement learning, and hence has significant role in addiction.[3][4] It plays a lesser role in fear, impulsivity, and the placebo effect.[5][6][7] It is involved in the encoding of new motor programs as well.[3]       
    Each cerebral hemisphere has its own nucleus accumbens. It is located where the head of the caudate and the anterior portion of the putamen meet just lateral to the septum pellucidum. The nucleus accumbens can be divided into two structures—the nucleus accumbens core and the nucleus accumbens shell. These structures have different morphology and function.  

1 Structure
1.1 Input
1.2 Output
1.3 Shell
1.4 Core
2 Cell types
3 Neurotransmitters
4 Function
4.1 Reward and reinforcement
4.2 Maternal behavior
5 Clinical significance
5.1 Addiction
5.2 Depression
5.3 Placebo effect
6 Additional images
7 References
8 External links

My comment:     
    Trust Wikipedia to cut through all the noise.  I've been focused on the  nucleus accumbens (NAC) for at least 15 years.  I have several hundred pages of PubMed printouts and photocopies of textbooks about the NAC, yet this short article did a lot to bring my understanding of it into focus.   
    The most important thing about this article is that it clearly declares that the output from the NAC is GABA ergic.  That means that the axons which leave the NAC use GABA (gamma-aminobutyric acid ) as their neurotransmitter.  This is fortunate for those of us trying to figure out how the brain works.   
    Almost all Neurotransmitters have multiple Receptors, and the effect that a neurotransmitter has depends on with which of its various receptors it is interacting.  Although many neurotransmitters can be either excitatory or inhibitory, depending on with which of their receptors they are interacting, all of GABA's receptors are inhibitory.  Some are fast and some are slow, but all are inhibitory, and this simplifies our analysis considerably since there's never any question about the direction of the effect that the NAC is having on downstream neurons.   
    It means that we can be confident that when the NAC receives excitatory input, it inhibits the neurons to which it transmits, and when the NAC receives inhibitory input, it disinhibits the neurons to which it transmits and that the disinhibited neurons then become more excited.   
    James Olds, who discovered the NAC and spent much of his career studying it, dubbed it the 'Pleasure Center', and, indeed, the greater the level of the transmitter  dopamine (DA) at the D2 receptors in the NAC, the greater the apparent pleasure experienced by the organism.  I say "apparent" because much of the research has been done on mice, and their experience of pleasure is inferred from their behavior.  However, the results with mice generalize completely to humans.  For example, drugs such as heroin and cocaine both increase the level of DA at the D2 receptors in the NAC and also are reported by people who use them as being pleasurable.   
    DA has both excitatory and inhibitory receptors.  The D2 receptor is inhibitory (see:  Dopamine Receptors   ).  That means that as the level of DA at the D2 receptors increases, the output neurons of the NAC are inhibited from transmitting GABA, their inhibitory neurotransmitter.  This in turn disinhibits the neurons to which the NAC projects and allows them to become more excited. 
    Notice that the NAC receives inputs from both the Amygdala (AMG) and the Hippocampus (HIP).  This is important.  The AMG is central to an organism's response to biological needs, including, but not limited to, sex and hunger.  The HIP is central to memory.  The convergence of input from the AMG and the HIP onto the NAC makes the NAC the part of the nervous system where current needs are juxtaposed with the memory of how those needs were satisfied in the past. 
    Because our anthropocentric intellectual tradition makes many researchers reluctant to ascribe 'thinking' to nonhuman animals, when an experimental animal such as a mouse is seen to hesitate between two choices in a maze, starting to take first one path and then the other several times before deciding which way to go , it is said to be engaged in 'vicarious trial and error'.  However, this 'vicarious trial and error' allows for a comparison between current needs, as sensed by the AMG, and memories of how such or similar needs were satisfied in the past, as recorded in the HIP.   
    When the memory of past behavior matches the current need, the level of DA at the D2 receptors increases, the organism has a pleasurable sensation, the tonic inhibition of the neuroaxis by the NAC is released, and the organism behaves in a manner similar to what it remembers as having been a successful way of meeting the need in the past.      
    Most of the above is from memory.  I will search through my voluminous notes and try to provide specific references for the points made, but this will take time. 

comment on references

    Reference [16] is a full length article:

    Neurochemistry of the Nucleus Accumbens and its Relevance to Depression and Antidepressant Action in Rodents   
    "The NAc contains small populations of γ-aminobutylic acid (GABA)-containing and cholinergic interneurons, in addition to a large number of efferent GABAergic medium spiny projecting neurons [102]. The activity of projecting medium spiny neurons is regulated by glutamatergic afferents arising from the prefrontal cortex, hippocampus and amygdala, by dopaminergic afferents from the ventral tegmental area [124], by serotonergic afferents from the raphe nucleus, and by noradrenergic afferents from the locus ceruleus. A schematic diagram is shown in ​Fig.1. These afferents converge primarily on GABA neurons, the main output cells of this region [102]. In addition, GABAergic projection neurons receive inhibitory input, primarily from a small population of GABAergic and cholinergic interneurons [75] but also through feedfoward inhibition [125] and axon collaterals of neighboring
medium spiny neurons [29].  
Medium spiny neurons project to a restricted part of the globus pallidus and the substantia nigra from the core, whereas from the shell, they project not only to the subcommissural part of the ventral pallidum and the ventral tegmental area but also to widespread areas in the hypothalamus and extended amygdala [102]. NAc output is regulated by numerous systems including glutamatergic afferent from the medial prefrontal cortex and hippocampus, both of which differentially regulate activities in the shell and core subregions (Fig.2). Furthermore, various systems such as glutamate, dopamine, GABA, acetylcholine, serotonin and so on regulate each other through pre- and post- receptors (Fig.3). A schematic diagram about the relationships among typical receptors is shown in ​Fig.3. Recently, an emerging body of evidence suggests that the activities of medium spiny projecting neurons, as well as these afferents neurons, are regulated locally by several neuropeptides and transcriptional factors, which are expressed in the NAc, and which are up- or down-regulated by various stressful situations [110]."
It is well recognized that GABAergic neurons function as the main neurons in the NAc, and that the flow of information through the NAc is dependent on the activity of GABAergic spiny projecting neurons. "   
    58 Related citations:$=relatedarticles&logdbfrom=pmc      
    16 Cited by's   

    References [17]  and  [18]  were identical and blank when I first read this article.  However they did have 167 Related citations which I reviewed in place of the missing reference texts:   
After obtaining the list, I reordered it by Pub Date rather than Link Ranking.    

     # 130    1984   
Neurochemically specified subsystems in the basal ganglia.    
    196 Related citations   
    6 Cited by's:      

    #83    1993
Physiological and morphological properties of accumbens core and shell neurons recorded in vitro.   
    172 Related citations  
    26 Cited by's:     

    #68    1994
GABA synapses formed in vitro by local axon collaterals of nucleus accumbens neurons.   
GABAergic medium-spiny neuron axons not only form the principal projections of the nucleus accumbens (nAcc) ..." 
In culture, as in the intact nAcc, medium-spiny neurons account for over 95% of the cells and are GABAergic."   
    137 Related citations  
    7 Cited by's    
Free full text   (PDF)      

The Pleasure Centers  (BTB)   
Beginner-Neurological Level    
"For a species to survive, its members must carry out such vital functions as eating, reproducing, and responding to aggression. Evolution has therefore developed certain areas in our brain whose role is to provide a pleasurable sensation as a “reward” for carrying out these vital functions.
     These areas are interconnected with one another to form what is known as the “reward circuit”.
     The  ventral tegmental area (VTA), a group of neurons at the very centre of the brain, plays an especially important role in this circuit. The VTA receives information from several other regions that tell it how well various fundamental needs, and more specifically human needs, are being satisfied.
     The VTA then forwards this information to another structure further forward in the brain: the  nucleus accumbens (NAC).  To send this information to the  nucleus accumbens  the VTA uses a particular chemical messenger: dopamine  (DA). The increase in the level of dopamine in the  nucleus accumbens, and in other brain regions, reinforces the behaviours by which we satisfy our fundamental needs. "  
My comments
    1.  Although this doesn't mention the receptors, it is consistent with the interpretation given above that increased DA at the D2 receptors relaxes the tonic inhibition exerted by the NACs GABA ergic output and thus facilitates behavior. 
    2.  This is only the  Beginner-Neurological Level .  Click on the link.  On the left side of the page there are links for Intermediate and Advanced, and on the right side of the page there are links for Social, Psychological, Cellular and Molecular.  Each link leads to a different page covering the same topic from a different perspective.  The next two references were links from this page.       

Beginner-Cellular Level    
    Eating, drinking, having sex, and displaying maternal behaviour are all activities that are essential for the survival of the individual and the species. In the course of evolution, natural selection has associated strong feelings of satisfaction with these behaviours that meet such basic needs. A veritable reward circuit evolved to encourage these behaviours. Subsequently, this circuit expanded to encourage us to repeat other pleasurable experiences that we learn in the course of our lives.

    The reward circuit is at the heart of our mental activity and guides all our behaviours. This circuit is complex, (click on the link to see it) but it contains a central link that seems to play a fundamental role.

     This link consists of the nerve connections between two particular small groups of neurons. One of these groups is located in the ventral tegmental area (VTA), and the other in the nucleus accumbens.
    The chemical messenger that makes the connections between these two groups of neurons is dopamine. This is the site where most drugs act and cause dependencies.

Intermediate-Psychological Level

     The brain’s primary role is to maintain equilibrium (homeostasis) in the body’s internal environment. The brain maintains homeostasis by instructing the body to act to correct any imbalances as they arise.     Pleasure is the mechanism that evolution has developed to encourage us to eat, find a sexual partner, take refuge from the cold, etc. When action is possible, pleasure is very often the goal, through the desire-action-satisfaction cycle.

     But action can also be necessary to respond to a threat of danger. When we are confronted with danger, we have two options: flee from it, or render the threat inoperative. In other words, flight or fight! Whether the danger is a hostile person or an inanimate threat such as fire, flight is generally the first option that we consider. But if flight is impossible or would not be effective, we try to confront the danger–in other words, to fight the enemy or fight the flames.
     These active approach and avoidance behaviours are under the control of what is sometimes called the behavioural approach system (BAS). This system comprises two main neural circuits: one corresponding to rewarded action and the other to successful avoidance.

     The reward circuit, or medial forebrain bundle (MFB) is activated in the desire–action–satisfaction cycle. The punishment circuit, or periventricular system (PVS) is activated when you decide whether to fight or flee.

     It should be mentioned in passing that the activation of the PVS in turn activates the sympathetic nervous system and causes ACTH and adrenaline to be released into the body to quickly prepare it for the effort required to fight or flee.

     But sometimes neither gratifying action nor fight or flight is possible. That is when the behavioural inhibition system comes into play.  See:  Stress .     

The Cerebral Hemispheres (Kimball)

Each hemisphere of the cerebrum is subdivided into four lobes visible from the outside:
  • frontal
  • parietal
  • occipital
  • temporal
Hidden beneath these regions of each cerebral cortex is
  • an olfactory bulb; they receive input from the olfactory epithelia.
    Link to discussion of olfaction.
  • a striatum; they receive input from the frontal lobes and also from the limbic system (below). At the base of each striatum is a
  • nucleus accumbens (NA). The pleasurable (and addictive) effects of amphetamines, cocaine, and perhaps other psychoactive drugs seem to depend on their producing increasing levels of dopamine at the synapses in the nucleus accumbens (as well as the VTA).
  • a limbic system; they receives input from various association areas in the cerebral cortex and pass signals on to the  nucleus accumbens.  Each limbic system is made up of a:
Corticotropin-releasing factor in the dorsal raphe nucleus: Linking stress coping and addiction.  (PubMed) - 2010 
    See also:   CRH Receptors   
    Abstract with links.   
    Full length HTML & PDF available online for free.   
from the HTML 
    "Most 5-HT receptor ( Serotonin Receptor ) subtypes including the 5-HT1A, 5-HT1B, 5-HT2A, 5-HT3 and 5-HT4, have excitatory effects on Dopamine release in the nucleus accumbens and/or discharge activity of dopamine neurons in the Ventral Tegmental Area that project to the nucleus accumbens (NAC) (Di Matteo et al., 2008).  
My comments
    There are two problems here:  
    1.  If "excitatory effects on dopamine release in the nucleus accumbens" means an increase in dopamine at the D2 receptors, then this should result in an increase in behavior.   Learned Helplessness  is characterized by a decrease in behavior and is clearly associated with stimulation of serotonergic neurons in the  Dorsal Raphe Nucleus (DRN) which, in turn, increases the transmission of serotonin (5-HT) from the  Dorsal Raphe Nucleus  (DRN) to the NAC.     
    2.  The chart at Serotonin Metabotropic Receptor  says that 5-HT1AR and 5-HT1BR are both inhibitory while 5-HT2AR, 5-HT3R and 5-HT4R are all excitatory.  This appears contradictory. 
    The (Di Matteo et al., 2008)  reference is examined more closely, below. 
more from the HTML         
    Certain drugs of abuse, such as cocaine, increase 5-HT as well as dopamine in the nucleus accumbens (Andrews and Lucki, 2001; Parsons et al., 1995)."    
     "The hyposerotonergic state that results from CRF1 mediated inhibition could contribute to the initiation of substance abuse, perhaps by promoting impulsive behavior.  
My comment
    Just to be totally clear, since "CRF1 mediated inhibition" results in a "hyposerotonergic state", it refers to inhibition of the serotonergic neurons in the DRN.  It's my impression from other references that the "hyposerotonergic state" does indeed lead to impulsive behavior, but it would seem that impulsive behavior can only result from an increase in dopamine at the D2 receptors and a consequent release of the NAC's chronic GABAergic inhibition of the neurons to which it projects.   
    The quotation from the HTML, above, that "Most 5-HT receptor ... subtypes ... have excitatory effects on Dopamine release in the nucleus accumbens ..." would suggest that a  "hyposerotonergic state" would be accompanied by a decrease in dopamine at the D2 receptors.  This decrease in dopamine at the D2 receptors should cause a decrease in impulsive behavior.  So there's a contradiction here.  The article says that  Serotonin  (5HT) increases the release of dopamine in the NAC, which should increase impulsivity, but it also speculates that the "hyposerotonergic state" i.e. low serotonin, may cause a compensatory increase in impulsivity.  This speculation is probably wrong.    
more from the HTML    
    In line with our hypothesis that serotonergic deficits produced by acute stress and CRF1 activation promote active behavior, a hyposerotonergic state has been linked to the increased impulsivity that is a component of drug seeking behavior (Virkkunen and Linnoila, 1990). One may speculate the decreased accumbal 5-HT negatively affects DA release and substance abuse is facilitated in an effort to elevate DA levels."  
My comment
    This runs counter to my expectations.  I was under the impression that behavior was facilitated by decreased, rather than increased, accumbal 5-HT.  Their speculation that "decreased accumbal 5-HT negatively affects DA release" may just be mistaken.  My impression is that "decreased accumbal 5-HT ... affects DA release" positively, rather than negatively.    

Examining the (Di Matteo et al., 2008)  reference more closely,   

Serotonin control of central dopaminergic function: focus on in vivo microdialysis studies. 
    by: Di Matteo V, Di Giovanni G, Pierucci M, Esposito E
Only abstract available online. 
    "In this review, the functional interactions between Serotonin (5-HT) and Dopamine (DA) neuronal systems are discussed with the focus on microdialysis studies in the rodent brain (mainly rats).    
    5-HT by itself is involved both directly and indirectly via actions on complex neuronal circuitry, in the regulation of DA release through multiple 5-HT receptors, playing a critical role in the development of normal and abnormal behaviours.  
    Recent evidence suggests that dysfunction of dopaminergic and serotoninergic Neurotransmitter systems contributes to various disorders including depression, schizophrenia, Parkinson's disease and drug abuse. Here we summarize recent neurochemical works that have extensively explored the role of 5-HT receptors in the control of DA central systems in both basal and drug-induced conditions, using in vivo microdialytic techniques.  
    Several 5-HT receptor subtypes, including the 5-HT(1A), 5-HT(1B), 5-HT(2A), 5-HT(3) and 5-HT(4) receptors, act to facilitate DA release, while the 5-HT(2C) receptor mediates an inhibitory effect of 5-HT on DA release.  
    Taken together, neurochemical approaches using microdialysis can not only contribute to clarification of the physiological role of the serotonergic neuronal systems but may also be a powerful pharmacological approach for the development of therapeutic strategies to the treatment of depression, schizophrenia, Parkinson's disease and drug abuse.     
My comment
    I'm going to need to look at the full paper.   
    One possible resolution of the apparent contradictions noted above would be if the serotonin (5-HT) receptor is the inhibitory 5-HT(2C) receptor.  The relevant parameter seems to be the level of DA at the D2 receptors which are presumably on the postsynaptic membranes of the GABA ergic output neurons.  The DA is provided by neurons located in the Ventral Tegmental Area (VTA).  Therefore, if the 5-HT(2C) receptors are presynaptic on the axons of the dopaminergic neurons from the VTA, they would be in a position to reduce the level of DA at the D2 receptors.     

Glutamatergic input from specific sources influences the nucleus accumbens-ventral pallidum information flow.  - 2011 (PubMed)    
Only abstract available online for free. 
    "The major target of the NAc GABAergic output neurons is the ventral pallidum (VP). VP is part of the reward circuit and controls the ascending mesolimbic dopamine system, as well as the motor output structures and the brainstem.  
    The excitatory inputs governing this system converge in the NAc from the prefrontal cortex (PFC), ventral hippocampus (vHC), midline and intralaminar thalamus (TH) and basolateral nucleus of the amygdala (BLA).  
    It is unclear which if any of these afferents innervate the medium spiny neurons of the NAc, that project to the VP. To identify the source of glutamatergic afferents that innervate neurons projecting to the VP, a dual-labelling method was used: Phaseolus vulgaris leucoagglutinin for anterograde and EGFP-encoded adenovirus for retrograde tract-tracing.  
    Within the NAc, anterogradely labelled BLA terminals formed asymmetric synapses on dendritic spines that belonged to medium spiny neurons retrogradely labelled from the VP.  
    TH terminals also formed synapses on dendritic spines of NAc neurons projecting to the VP.  
    However, dendrites and dendritic spines retrogradely labelled from VP received no direct synaptic contacts from afferents originating from mPFC and vHC in the present material, despite the large number of fibres labelled by the anterograde tracer injections.  
    These findings represent the first experimental evidence for a selective glutamatergic innervation of NAc neurons projecting to the VP. The glutamatergic inputs of different origin (i.e. mPFC, vHC, BLA, TH) to the NAc might thus convey different types of reward-related information during goal-directed behaviour, and thereby contribute to the complex regulation of nucleus accumbens functions."  
My comment
    My long standing hypothesis has been that the NAc was controlled by the BLA and the vHC.  This paper confirms input from the BLA but not from the vHC.       

Related citation from above:
     Biological substrates of reward and aversion: a nucleus accumbens activity hypothesis. - 2009 (PubMed)   
Full length HTML with many active links available online for free. 
From the abstract
    "This basal forebrain structure receives dopamine (DA) input from the ventral tegmental area (VTA) and glutamate (GLU) input from regions including the prefrontal cortex (PFC), amygdala (AMG), and hippocampus (HIP)."  
    "The NAc has a well-established role in mediating the rewarding effects of drugs of abuse and natural rewards such as food and sexual behavior. However, accumulating pharmacological, molecular, and electrophysiological evidence has raised the possibility that it also plays an important (and sometimes underappreciated) role in mediating aversive states.  
    Here we review evidence that rewarding and aversive states are encoded in the activity of NAc medium spiny GABAergic neurons, which account for the vast majority of the neurons in this region."  
My comment
    Contrary to "Glutamatergic input ...", above, this paper confirms input from both the BLA (AMG) and the vHC (HIP).         
From the HTML
    "We propose a simple model of mood in which reward is encoded by reduced activity of NAc MSNs (medium spiny neurons), whereas aversion is encoded by elevated activity of these same cells."  
My comment
    This is a huge article with a long list of active, relevant links.  I only just glanced through it.  The conclusion, above, is enough for now, but the article has a lot more to offer if I feel I need it.       

2000    331<354 
[How does the nucleus accumbens function?].  Spanish   
The nucleus accumbens is made up of an 'electrophysiological coincidence detector' or shell serially connected to a 'motor sequencer' or core, both supporting the role of the nucleus accumbens as a limbic-motor interface."  

Distinct roles of synaptic transmission in direct and indirect striatal pathways to reward and aversive behavior.  
PMID: 20620875  Related citations  

The nucleus accumbens as part of a basal ganglia action selection circuit.  

1609. ?
Dorsal pallidum as a functional motor output of the corpus striatum. Amalric M, Koob GF. "Brain reseach" Brain Res. 1989 Apr 3;483(2):389-94.
[PubMed - indexed for MEDLINE]
Related citations


Come back to: the relationship between the Globus Pallidus  (GP) and the 
Nucleus Accumbens Septi   (NAC).   I'm not sure about this, but it's my impression that both use GABA as an efferent neurotransmitter. 


The nucleus accumbens as a complex of functionally distinct neuronal ensembles: an integration of behavioural, electrophysiological and anatomical data.

1998  60<Mulder AB   
Electrophysiology of the hippocampal and amygdaloid projections to the nucleus accumbens of the rat: convergence, segregation, and interaction of inputs.   
Amygdaloid Hippocampal Convergence   for full Abstract, Similar articles, Cited by's and Free Full Text. 
    Note:  This reference is from a photocopy I made almost 10 years ago.  

Convergence and segregation of ventral striatal inputs and outputs.


    Neurochemistry of the Nucleus Accumbens and its Relevance to Depression and Antidepressant Action in Rodents  

Fig. (1)

An external file that holds a picture, illustration, etc. Object name is CN-4-4-277_F1.jpg

Fig. 3 

An external file that holds a picture, illustration, etc. Object name is CN-4-4-277_F3.jpg

1983   21<22  &  22<23     * *     
Free full text   
Neural projections from nucleus accumbens to globus pallidus, substantia innominata, and lateral preoptic-lateral hypothalamic area    
The anatomical organization and electrophysiological characteristics of a projection from the nucleus accumbens to anteroventral parts of the globus pallidus and to a subpallidal region that includes the substantia innominata (SI), the lateral preoptic area (LPO), and anterior parts of the lateral hypothalamic area (LHA) were investigated in the rat.  
    Autoradiographic experiments, with injections of 3H-proline into different sites in the nucleus accumbens and adjacent caudoputamen, indicate that the descending fibers are organized topographically along both mediolateral and dorsoventral gradients, although labeled fibers from adjacent regions of the nucleus accumbens overlap considerably in the ventral globus pallidus and subpallidal region.  
    Injections confined to the caudoputaman only labeled fibers in the globus pallidus.  
    Retrograde transport experiments with the marker true blue confirmed that only the nucleus accumbens projects to the subpallidal region and that the caudoputamen projects upon the glubus pallidus in a topographically organized manner.  
    In electrophysiological recording experiments single pulse stimulation (0.1 to 0.7 mA; 0.15 msec duration) of the nucleus accumbens changed the discharge rate of single neurons in the ventral globus pallidus and in the SI, LPO, and LHA. Typically, the responses were inhibition of neuronal discharge with latencies of 6 to 18 msec. Single pulse stimulation of the dorsolateral caudoputamen altered the discharge rate of single neurons in dorsal regions of the globus pallidus, with inhibition being the most frequently observed response.  
    The results of these anatomical and electrophysiological experiments are complementary and indicate that fibers from the nucleus accumbens innervate the anteroventral region of the globus pallidus as well as the subpallidal region, while most fibers of the caudoputamen innervate the globus pallidus but not the subpallidal region.  
    It appears, therefore, that these two components of the striatum have different output connections. The possible functional significance of these findings is discussed in relation to the projections of the subpallidal region, which may include an output to the mesencephalic locomotor region, and in relation to the nucleus accumbens afferents from the amygdala and hippocampal formation.
442 Similar articles  

Hippocampal and prefrontal cortical inputs monosynaptically converge with individual projection neurons of the nucleus accumbens.   

Individual nucleus accumbens-projection neurons receive both basolateral amygdala and ventral subicular afferents in rats.    See:  Amygdaloid Hippocampal Convergence   .

2009    14<131 

Cholinergic innervation and thalamic input in rat nucleus accumbens.   

6<131   Free Article   
Glutamate inputs to the nucleus accumbens: does source matter?   

The Nucleus Accumbens: A Comprehensive Review - FullText   

Schematic representation of major afferent (a) and efferent (b) connections of the NAc. SNc = Substantia nigra pars compacta; BNST = bed nucleus of the stria terminalis; GPi = globus pallidus internus; SNr = substantia nigra pars reticulata; ctx = cortex.

Nucleus Accumbens Septi
    160226 - 1236 
    Aug 13, 2019 
    Aug 15, 2019