Accumbens Input

Cross references:    Nucleus Accumbens Septi        Testosterone Accumbens   
Amygdala    Amygdaloid Hippocampal Convergence   

Searching Google for "accumbens input" found  247,000 references:     

Searching PubMed for "Accumbens Input" identified 518 references:   

1975    517<518 
Fimbria input to the nucleus accumbens septi.  
No Abstract. 
    See:  Hippocampus    . 

1980    514<518     126<131 
Convergence of excitatory amygdaloid and hippocampal input in the nucleus accumbens septi.  
No Abstract.  
Amygdaloid Hippocampal Convergence  .      
    See:  Ventral Tegmental Area

1981    508<518  
Inhibition from ventral tegmental area of nucleus accumbens neurons in the rat.  
    See:  Ventral Tegmental Area

1984    493<518 
Microiontophoretic studies of the dopaminergic inhibition from the ventral tegmental area to the nucleus accumbens neurons.  
    See:  Ventral Tegmental Area

1985    490<518  
Inhibition from locus coeruleus of nucleus accumbens neurons activated by hippocampal stimulation.   

    See:  Hippocampus    .   

1985    489<518  
An excitant amino acid projection from the medial prefrontal cortex to the anterior part of nucleus accumbens in the rat.

1985    488<518 
The topographic order of inputs to nucleus accumbens in the rat   
    Only the Abstract available online for free. 
    "Afferents to the nucleus accumbens have been studied with the retrograde transport of unconjugated wheatgerm agglutinin as detected by immunohistochemistry using the peroxidase-antiperoxidase method, in order to define precisely afferent topography from the cortex, thalamus, midbrain and amygdala. 
     Cortical afferent topography was extremely precise. The largest number of cells was found following injections to the anterior accumbens. 
     Anteromedial injections labelled a very large extent of the subiculum and part of the entorhinal cortex.  
    Anterolateral injections produced less subicular and entorhinal label but also labelled the posterior perirhinal cortex.  
    Posteromedial injections labelled only the ventral subiculum and a few cells in the adjacent medial entorhinal cortex.  
    Posterolateral injections labelled few lateral entorhinal neurones but did label a long anteroposterior strip of perirhinal cortex.  
    Prefrontal cortex label was found only after anterior accumbens injections.  
    In the amygdala labelled neurones were found in cortical, central, lateral posterior, anteromedial and basolateral nuclei. Basolateral amygdala projected chiefly to the anteromedial accumbens and central nucleus to anterolateral accumbens. Only a weak amygdala label was found after posterior accumbens injections.  
    In the ventral tegmental area, the midline interfascicular nucleus projected only to medial accumbens. The paranigral ventral tegmentum projected chiefly to the medial accumbens and the parabrachial area chiefly to the lateral accumbens.  
    In the thalamus, heaviest label was found after anterior accumbens injections. Most cells were found in the paraventricular, reuniens and rhomboid nuclei and at posterior thalamic levels lying medial to the fasciculus retroflexus.   There was only restricted topography found from thalamic sites.  
    Retrograde label was also found in the ventral pallidum and lateral hypothalamus. Single small injection sites within accumbens received input from the whole anteroposterior extent of the thalamus and ventral tegmentum. The medial accumbens was found to have a close relationship to habenula, globus pallidus and interfascicular nucleus. It appeared that the heaviest volume of inputs projected to anteromedial accumbens, where output from hippocampus (CAI), subiculum, entorhinal and prefrontal cortices converged with output from amygdala, midline thalamus and ventral tegmentum."  
    My comment
This is far more inputs than I anticipated. 

1985   487<518
A noradrenaline-induced inhibition from locus coeruleus of nucleus accumbens neuron receiving input from hippocampus. 
    See:  Hippocampus    . 

1985    486<518   
Characterization of fimbria input to nucleus accumbens.    
    See:  Hippocampus    . 

1987      472<518 
Inhibitory effects of thyrotropin-releasing hormone on neuronal activity in the nucleus accumbens.  

1988    465<518  
Gamma-aminobutyric acid in the medial rat nucleus accumbens: ultrastructural localization in neurons receiving monosynaptic input from catecholaminergic afferents.   

1989    459<518 
Convergence of hippocampal and dopaminergic input onto identified neurons in the nucleus accumbens of the rat.   
    See:  Hippocampus    . 

1989    458<518      Free PMC Article   
5-Hydroxytryptamine acts at 5-HT2 receptors to decrease potassium conductance in rat nucleus accumbens neurones.   

1989    457<518            
Ventral tegmental area-mediated inhibition of neurons of the nucleus accumbens receiving input from the parafascicular nucleus of the thalamus is mediated by dopamine D1 receptors.   

    See:  Ventral Tegmental Area

1990     453<518      Free PMC Article 
Muscarine reduces inwardly rectifying potassium conductance in rat nucleus accumbens neurones.  

1990    450<518  
Hippocampal fibers make synaptic contacts with glutamate decarboxylase-immunoreactive neurons in the rat nucleus accumbens.   
    See:  Hippocampus    . 

1990    447<518  
Thalamic midline cell populations projecting to the nucleus accumbens, amygdala, and hippocampus in the rat.   

1990    444<518     
In the rat medial nucleus accumbens, hippocampal and catecholaminergic terminals converge on spiny neurons and are in apposition to each other.     

The contribution of basal forebrain to limbic-motor integration and the mediation of motivation to action.   
    See:  Hippocampus    . 

Distribution of amygdala input to the nucleus accumbens septi: An electrophysiological investigation 
    Only Abstract available online for free.     
    "The nucleus accumbens septi (NAS) receives afferent input from the amygdala via the stria terminalis and from the hippocampus via the fimbria."    

Neurons in the ventral subiculum, amygdala and entorhinal cortex which project to the nucleus accumbens: their input from somatostatin-immunoreactive boutons.  

1993    405<518 
In vivo modulation of acetylcholine in the nucleus accumbens of freely moving rats: I. Inhibition by serotonin.  

Tonic D2-mediated attenuation of cortical excitation in nucleus accumbens neurons recorded in vitro.  

Input from the amygdala to the rat nucleus accumbens: its relationship with tyrosine hydroxylase immunoreactivity and identified neurons. 
    See:  Amygdala

377<518    104<131           
Synaptic interactions among excitatory afferents to nucleus accumbens neurons: hippocampal gating of prefrontal cortical input.

    See:    Amygdaloid Hippocampal Convergence  . 

1995   103<131  
Patterns of convergence and segregation in the medial nucleus accumbens of the rat: relationships of prefrontal cortical, midline thalamic, and basal amygdaloid afferents.
    "Compartmentalization is therefore a possible anatomical substrate for condensation or segregation of neuronal signals passing through the nucleus accumbens." 

    See: "Glutamate " . 
    See: Amygdaloid Hippocampal Convergence   .     
    See:   Glutamate Metabotropic Receptor   .   
    See: Amygdaloid Hippocampal Convergence   .     

1998     321<518     Free Article    
Electrophysiological characterization of GABAergic neurons in the ventral tegmental area.    
    See:  Ventral Tegmental Area

317 <518    
Phencyclidine interferes with the hippocampal gating of nucleus accumbens neuronal activity in vivo.   

    See:  Hippocampus    . 

312<518    Free Article  
Cellular sites for dynorphin activation of kappa-opioid receptors in the rat nucleus accumbens shell.  

Direct comparison of projections from the central amygdaloid region and nucleus accumbens shell.   

Modulation of cell firing in the nucleus accumbens.   

Localization of the delta-opioid receptor and dopamine transporter in the nucleus accumbens shell: implications for opiate and psychostimulant cross-sensitization.   

297<518    Free Article  
Dopamine terminals in the rat prefrontal cortex synapse on pyramidal cells that project to the nucleus accumbens.   

The medial prefrontal cortex as a part of the brain reward system.      

The dopaminergic hyper-responsiveness of the shell of the nucleus accumbens is hormone-dependent.   

Presynaptic dopamine D(4) receptor localization in the rat nucleus accumbens shell.   

Direct actions of cannabinoids on synaptic transmission in the nucleus accumbens: a comparison with opioids.   

275<518   &   70<131     Free Article   
Modulation of hippocampal and amygdalar-evoked activity of nucleus accumbens neurons by dopamine: cellular mechanisms of input selection.       
    "Inputs from multiple sites in the telencephalon, including the hippocampus and basolateral amygdala (BLA), converge on neurons in the nucleus accumbens (NAc), and dopamine (DA) is believed to play an essential role in the amplification and gating of these different limbic inputs."  
    "These data suggest that increases in mesoaccumbens DA efflux by hippocampal afferents to the NAc play a critical role in an input selection mechanism, which can ensure preferential responding to the information conveyed from the hippocampus to the ventral striatum."  
    See:  Amygdaloid Hippocampal Convergence  .


Role of glutamate receptors in the nucleus accumbens on behavioural responses to novel conflictive and non-conflictive environments in the rat.  
Note:  At this point PubMed added another reference to the search bringing the total count up to 519 from 518.   

Individual nucleus accumbens-projection neurons receive both basolateral amygdala and ventral subicular afferents in rats.  

    See:  Amygdaloid Hippocampal Convergence  .

    See:   Prefrontal Cortex  . 

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

Dopaminergic Modulation of Prefrontal Cortical Input to Nucleus Accumbens Neurons In Vivo  
    Full-length PDF.
"... converging excitatory inputs from the cortex, hippocampus, and amygdala ..."
    See:   Prefrontal Cortex

Nucleus accumbens dopamine release is necessary and sufficient to promote the behavioral response to reward-predictive cues.

Dopamine-glutamate reciprocal modulation of release and motor responses in the rat caudate-putamen and nucleus accumbens of "intact" animals. 

The mesolimbic dopamine reward circuit in depression.  

Differential involvement of ventral tegmental GABA(A) and GABA(B) receptors in the regulation of the nucleus accumbens dopamine response to stress.    
    See:  Ventral Tegmental Area

Dopaminergic regulation of limbic-striatal interplay.    

156<519    Free PMC Article  
Selective activation of medial prefrontal-to-accumbens projection neurons by amygdala stimulation and Pavlovian conditioned stimuli. 

Basolateral amygdala neurons facilitate reward-seeking behavior by exciting nucleus accumbens neurons.
    See:  Amygdala  

Cholinergic innervation and thalamic input in rat nucleus accumbens.     
Cholinergic interneurons are the only known source of acetylcholine in the rat nucleus accumbens (nAcb); yet there is little anatomical data about their mode of innervation and the origin of their excitatory drive.  
    We characterized the cholinergic and thalamic innervations of nAcb with choline acetyltransferase (ChAT) immunocytochemistry and anterograde transport of Phaseolus vulgaris-leucoagglutinin (PHA-L) from the midline/intralaminar/paraventricular thalamic nuclei.  
    The use of a monoclonal ChAT antiserum against whole rat ChAT protein allowed for an optimal visualization of the small dendritic branches and fine varicose axons of cholinergic interneurons.  
    PHA-L-labeled thalamic afferents were heterogeneously distributed throughout the core and shell regions of nAcb, overlapping regionally with cholinergic somata and dendrites.    
    At the ultrastructural level, several hundred single-section profiles of PHA-L and ChAT-labeled axon terminals were analyzed for morphology, synaptic frequency, and the nature of their synaptic targets.  
    The cholinergic profiles were small and apposed to various neuronal elements, but rarely exhibited a synaptic membrane specialization (5% in single ultrathin sections). Stereological extrapolation indicated that less than 15% of these cholinergic varicosities were synaptic.  
    The PHA-L-labeled profiles were comparatively large and often synaptic (37% in single ultrathin sections), making asymmetrical contacts primarily with dendritic spines (>90%). Stereological extrapolation indicated that all PHA-L-labeled terminals were synaptic.  
    In double-labeled material, some PHA-L-labeled terminals were directly apposed to ChAT-labeled somata or dendrites, but synapses were never seen between the two types of elements. These observations demonstrate that the cholinergic innervation of rat nAcb is largely asynaptic. They confirm that the afferents from midline/intralaminar/paraventricular thalamic nuclei to rat nAcb synapse mostly on dendritic spines, presumably of medium spiny neurons, and suggest that the excitatory drive of nAcb cholinergic interneurons from thalamus is indirect, either via substance P release from recurrent collaterals of medium spiny neurons and/or by extrasynaptic diffusion of glutamate."  

Timing-dependent regulation of evoked spiking in nucleus accumbens neurons by integration of limbic and prefrontal cortical inputs.  
    See:   Prefrontal Cortex        
    "The encoding of reward-predictive stimuli by neurons in the nucleus accumbens (NAcc) depends on integrated synaptic activity from the basolateral amygdala (BLA) and medial prefrontal cortex (mPFC) afferent inputs. In a previous study, we found that single electrical stimulation pulses applied to the BLA facilitate mPFC-evoked spiking in NAcc neurons in a timing-dependent manner, presumably by a fast glutamatergic mechanism. In the present study, the ability of repetitive BLA activation to modulate synaptic inputs to NAcc neurons through dopamine- or N-methyl-D-aspartate (NMDA)-dependent mechanisms is characterized. NAcc neurons receiving excitatory input from both mPFC and BLA were recorded in urethane-anesthetized rats. Train stimulation of the BLA depressed mPFC-evoked spiking in these neurons. This was not attributable to mechanisms involving NMDA or dopamine D1, D2, D3 or D5 receptors, since blockade of these receptors did not affect the BLA-mediated depression. BLA-mediated depression was only evident when the BLA stimulation evoked spikes in the recorded neuron; thus, depolarization of the recorded neuron may be critical for this effect. The ability of the BLA to suppress mPFC-to-NAcc signaling may be a mechanism by which normal or pathologically heightened emotional states disrupt goal-directed behavior in favor of emotionally-driven responses."  
Free PMC Article   

Subregion-Specific Modulation of Excitatory Input and Dopaminergic Output in the Striatum by Tonically Activated Glycine and GABA(A) Receptors.  
    See:  GABA Gate
    See:  Amygdala  

Glutamate Inputs to the Nucleus Accumbens: Does Source Matter?: Neuron 
    Full text available online for free:  
    See:   Glutamate .   
    See:   Glutamate
    See:  Ventral Tegmental Area

The Nucleus Accumbens: Mechanisms of Addiction across Drug Classes Reflect the Importance of Glutamate Homeostasis.    

Morphine treatment enhances glutamatergic input onto neurons of the nucleus accumbens via both disinhibitory and stimulating effect.     

VTA glutamatergic inputs to nucleus accumbens drive aversion by acting on GABAergic interneurons       
    Only Abstract available online for free. 
    "The ventral tegmental area (VTA) is best known for its dopamine neurons, some of which project to nucleus accumbens (nAcc). However, the VTA also has glutamatergic neurons that project to nAcc. The function of the mesoaccumbens glutamatergic pathway remains unknown.  
    Here we report that nAcc photoactivation of mesoaccumbens glutamatergic fibers promotes aversion. Although we found that these mesoaccumbens glutamatergic fibers lack GABA, the aversion evoked by their photoactivation depended on glutamate- and GABA-receptor signaling, and not on dopamine-receptor signaling. We found that mesoaccumbens glutamatergic fibers established multiple asymmetric synapses on single parvalbumin GABAergic interneurons and that nAcc photoactivation of these fibers drove AMPA-mediated cellular firing of parvalbumin GABAergic interneurons.  
    These parvalbumin GABAergic interneurons in turn inhibited nAcc medium spiny output neurons, thereby controlling inhibitory neurotransmission in nAcc. To our knowledge, the mesoaccumbens glutamatergic pathway is the first glutamatergic input to nAcc shown to mediate aversion instead of reward, and the first pathway shown to establish excitatory synapses on nAcc parvalbumin GABAergic interneurons."  

    See:  Ventral Tegmental Area

A thalamic input to the nucleus accumbens mediates opiate dependence : Nature  
    Abstract of Full Length Article online: 
    "Chronic opiate use induces opiate dependence, which is characterized by extremely unpleasant physical and emotional feelings after drug use is terminated. Both the rewarding effects of a drug and the desire to avoid withdrawal symptoms motivate continued drug use1, 2, 3, and the nucleus accumbens is important for orchestrating both processes4, 5.  
    While multiple inputs to the nucleus accumbens regulate reward6, 7, 8, 9, little is known about the nucleus accumbens circuitry underlying withdrawal.  
    Here we identify the paraventricular nucleus of the thalamus as a prominent input to the nucleus accumbens mediating the expression of opiate-withdrawal-induced physical signs and aversive memory. Activity in the paraventricular nucleus of the thalamus to nucleus accumbens pathway is necessary and sufficient to mediate behavioural aversion. Selectively silencing this pathway abolishes aversive symptoms in two different mouse models of opiate withdrawal.  
    Chronic morphine exposure selectively potentiates excitatory transmission between the paraventricular nucleus of the thalamus and D2-receptor-expressing medium spiny neurons via synaptic insertion of GluA2-lacking AMPA receptors.  
    Notably, in vivo optogenetic depotentiation restores normal transmission at these synapses and robustly suppresses morphine withdrawal symptoms. This links morphine-evoked pathway- and cell-type-specific plasticity in the paraventricular nucleus of the thalamus to nucleus accumbens circuit to opiate dependence, and suggests that reprogramming this circuit holds promise for treating opiate addiction." 
    Full length article: 
Many active links and references:  Same link as Abstract.         
    My comment
Since the D2 receptors are inhibitory, "... excitatory transmission between the paraventricular nucleus of the thalamus and D2-receptor-expressing medium spiny neurons" would decrease the GABAergic output of the  Medium Spiny Neurons   and thereby decrease  Tonic Inhibition .   

CotA  Accumbens Input 
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