nucleus accumbens ( NAc or NAcc ), also known as accumbens nucleus , or earlier as nucleus accumbens septi (Latin for the nucleus adjacent to the septum ) is a region in the basal forebral rostral to the preoptic area of ​​the hypothalamus. The nucleus accumbens and the olfactory tubercle collectively form the ventral striatum. Ventral striatum and dorsal striatum together form the striatum, which is a major component of the basal ganglia. Dopaminergic neurons from the mesolimbic pathway project to the medial mid-sponge GABAergic neurons from nucleus accumbens and olfactory tubes. Each hemisphere has its own accumbens nucleus, which can be divided into two nuclei accumbens and the nucleus accumbens nucleus. These substructures have different morphologies and functions.
NACC (subspace vs skin) subregions and different neuron subpopulations in each region (D1-type vs. D2-type D2-type neurons) are responsible for different cognitive functions. Overall, the nucleus accumbens have an important role in the cognitive process of motivation, aversion, reward (ie, the importance of incentives, pleasure, and positive reinforcement), and reinforcement learning (eg, instrumental transfer-Pavlovian); therefore, it has an important role in addiction. In addition, the core nucleus accumbens is centrally involved in slow-wave sleep induction. Nucleus accumbens play a lower role in processing fear (a form of aversion), impulsivity, and placebo effects. It's involved in coding new motor programs as well.
Video Nucleus accumbens
Structure
The nucleus accumbens are aggregates of neurons that are described as having outer shells and nuclei.
Input
Major glutamatergik inputs to the accumbens nucleus include the prefrontal cortex (especially the prelimbic cortex and infralimbic cortex), the basolateral amygdala, the ventral hippocampus, the thalamic nucleus (especially the midline thalamus nucleus and thalamus intalaminar nucleus), and glutamatergic projections of the ventral stands. area. Nucleus accumbens receives dopaminergic input from the ventral tegmental area (VTA), which is connected via the mesolimbic pathway. The nucleus accumbens is often described as one part of the ganglia-thalamo-cortical cortico-basal loop.
The dopaminergic input of the VTA modulates the activity of GABAergic neurons in the nucleus accumbens. These neurons are activated directly or indirectly by euphoriant drugs (eg, amphetamines, opiates, etc.) and by participating in useful experiences (eg, sex, music, sports, etc.).
The other major input source comes from CA1 and the hippocampal ventricular subculum to the dorsomedial area of ​​the nucleus accumbens. The slight depolarization of cells in the accumbens nucleus is correlated with the positivity of the hippocampal neurons, making them more energized. Cells that correlated in excited states of spiny middle-spiked neurons in nucleus accumbens were evenly distributed between the subiculum and CA1. Suburum neurons found hyperpolarize (increase negativity) while CA1 neurons "ripple" (fire & gt; 50 Hz) to achieve this priming.
The nucleus accumbens are one of several regions that receive histaminergic projection from the tuberomammary core (the only source of histamine neurons in the brain).
Output
The output neurons of the nucleus accumbens send axonal projections to the basal ganglia and ventral globus pallidus analogues, known as ventral pallidum (VP). The VP, in turn, projects into the medial dorsal nucleus of the dorsal thalamus, which projects into the prefrontal cortex as well as the striatum. Other afferents of the nucleus accumbens include connections with the tail of the ventral tegmental area, the substantia nigra, and the reticular formation of the pons.
Shell
The nucleus accumbens shell ( NAcc shell ) is a substructure of the nucleus accumbens. Shells and joint nuclei form all nucleus accumbens.
Location: The shell is the outermost region of the nucleus accumbens, and - unlike the nucleus - is considered part of the expanded amygdala, located on its rostral pole.
Cell types: Neurons in the nucleus accumbens are mostly middle-spaced neurons (MSN) containing D1 type (DRD1 and DRD5 type) or D2-type (ie DRD2, DRD3, and DRD4) dopamine receptors. MSN subpopulations contain D1 and D2 type receptors, with about 40% striatal MSN expressing MRD DRD1 and DRD2. This NACC type MSNs mixture with D1 and D2 type receptors is largely confined to NACC skin. Shell-shelled neurons, compared to nuclei, have lower dendritic densities, fewer terminal segments, and fewer branch segments than those in the core. The shell neuron projects a subcommercial part of the ventral pallidum as well as the ventral tegmental area and to a large area in the extended hypothalamus and amygdala.
Function: The shell of the nucleus accumbens is involved in prize cognitive processing, including subjective "liking" reactions to certain fun stimuli, motivational significance, and positive reinforcement. The NACC shell has also been shown to mediate certain Pavlovian instrumental transfers, a phenomenon in which classically conditioned stimuli modify the operant's behavior. A "hedonist hotspot" or pleasure center responsible for fun components or "liking" some intrinsic rewards is also located in a small compartment inside the medial NACC shell. Done-type medium spiny neurons in the Nacc shell mediate cognitive processes that are reward-related, whereas the D2 medium-spaced neurons of D2 type in NACC shells mediate hate-related cognition. Addictive drugs have a greater effect on the release of dopamine in the shell than inside the nucleus.
Core
The core nucleus accumbens ( nucleus NAcc ) is the inner substructure of the nucleus accumbens.
Locations: The nucleus accumbens core is part of the ventral striatum, located within the basal ganglia.
Cell types: The core of the NACC consists primarily of middle-spaced neurons containing D1-type or D2-type dopamine receptors. The neurons in the nucleus, compared to the shell neurons, have increased dendritic dendility, branch segments, and terminal segments. From its core, project neurons to other subcortical areas such as globus pallidus and substansia nigra. GABA is one of the major neurotransmitters in NACC, and GABA receptors are also abundant.
Function: The nucleus accumbens nucleus is involved in the cognitive processing of motor functions associated with appreciation and amplification and slow-wave sleep regulation. In particular, the core encodes new motor programs that facilitate the acquisition of prizes awarded in the future. The indirect path neurons (ie, D2-type) in the NACC nuclei expressing adenosine A 2A receptor-dependence promote slow-wave sleep. The NACC core has also been shown to mediate the general Pavlovian instrumental transfer, a phenomenon in which classically conditioned stimuli modify operant behavior.
Maps Nucleus accumbens
Cell type
Approximately 95% of neurons in NACC are GABAergic medium spiny neurons (MSNs) that primarily express D1 or D2 type receptors; about 1-2% of the remaining neuronal type is a large saline saline interneuron and another 1-2% are GABAergic interneurone. Compared to MSN GABAergic in the shell, those in the core have increased dendritic density of thorns, branch segments, and terminal segments. From its core, project neurons to other subcortical areas such as globus pallidus and substansia nigra. GABA is one of the major neurotransmitters in NACC, and GABA receptors are also abundant. These neurons are also the primary projection or output neurons of the nucleus accumbens.
Neurokimiawi
Some neurotransmitters, neuromodulators, and hormones that signal through receptors in the nucleus accumbens include:
Dopamine: Dopamine is released to the nucleus accumbens after exposure to useful stimuli, including drugs such as substituted amphetamines, cocaine, and morphine.
Phenethylamine and tyramine : Phenethylamine and tyramine are trace amine compounds that are synthesized in some CNS neurone neurons, including all neurons dopamine. In particular, these neurotransmitters act in dopaminergic inputs to NAcc. These substances regulate dopamine presinaptically through their interaction with VMAT2 and TAAR1, analogous to amphetamine.
Glucocorticoids and dopamine: The glucocorticoid receptor is the only corticosteroid receptor in the nucleus accumbens shell. Special L-DOPA, steroids and glucocorticoids are now known to be the only known endogenous compounds that can cause psychotic problems, so understanding the hormonal control of dopaminergic projections associated with glucocorticoid receptors may lead to new treatments for psychotic symptoms. A new study suggests that suppression of glucocorticoid receptors leads to a decrease in dopamine release, which could lead to future studies involving anti-glucocorticoid drugs potentially relieving psychotic symptoms.
A recent study in mice using GABA agonists and antagonists showed that GABA receptors A in the NAc shell have inhibitory controls on altering dopamine-induced behavior, and GABA Receptor B has inhibitory control against altering the behavior mediated by acetylcholine.
Glutamate: Studies have shown that local blockade of NMDA glutamatergic receptors in the spatial learning of CCC interference nuclei. Other studies have shown that both NMDA and AMPA (both glutamate receptors) play an important role in regulating instrumental learning.
Serotonin (5-HT): Overall, 5-HT synapses more and have more synapse contacts in the NAc shell than at the core. They are also larger and thicker, and contain larger solid core vesicles than their counterparts in essence.
Function
Gifts and reinforcement
The nucleus accumbens, being one part of the reward system, plays an important role in the processing of useful stimuli, strengthening stimuli (eg, food and water), and useful and strengthening (addictive, sex and exercise). The dominant response of neurons in the nucleus accumbens to sucrose sucrose is inhibition; the opposite is true in response to quinine aversive administration. Substantial evidence of pharmacological manipulation also suggests that reducing the stimulation of neurons in beneficial nucleus accumbens, such as, for example, would be correct in the case of stimulation of the opioid receptors. Signals dependent on blood oxygen levels (BOLD) in the nucleus accumbens are selectively increased during pleasant image perceptions, evoking emotions and during mental imaging of exciting emotional scenes. However, since BOLD is considered an indirect measure of the regional net excitation against inhibition, the degree to which BOLD measures valence-dependent processing is unknown. Due to the large number of NACC inputs from the limbic region and the strong NACC output to the motor area, the nucleus accumbens has been described by Gordon Mogensen as the interface between the limbic and motor systems.
Nucleus accumbens is causally related to the pleasure experience. Microinjections from agonists -opioids, agonists -opioids or agonists -opioids in the rostrodorsal quadrant of the medial skin increase "liking", while more caudal injection can inhibit disgust reactions, favored reactions, or both. The nucleus accumbens areas can be considered a causal role in the production of limited pleasure both anatomically and chemically, because in addition to opioid agonists only endocannabinoids can increase the feeling of love. In the overall nucleus accumbens, dopamine, GABA receptor agonists or AMPA antagonists merely modify the motivation, while the same applies to opioids and endocannabinoids outside the hotspots in the medial skin. A rostro-caudal gradient exists for an increase in respiratory response versus fear, which is then traditionally considered to require only the function of D1 receptors, and the former requires the functions of D1 and D2. One of the interpretations of this finding, the disinhibition hypothesis, argues that inhibition of accumulators MSNs (the GABAergic) disinhibits downstream structures, allows the expression of appetite or behavioral behavior. The motivational effects of AMPA antagonists, and on lower GABA agonists, are anatomically flexible. Tense conditions can expand the fear-inducing region, while the familiar environment can reduce the size of the area that causes fear. Furthermore, cortical input of the orbitofrontal cortex (OFC) refracts responses to appetite behavior, and infralimbic input, equivalent to the subgenual human cingulate cortex, suppresses response regardless of valence.
Nucleus accumbens is not necessary and not sufficient for instrumental learning, although manipulation may affect performance on instrumental learning tasks. One task in which the effect of NAc lesions is evident is the Pavlovian-instrumental transfer (PIT), in which cues paired with a certain or common reward can increase the instrumental response. Lesions to the nucleus of NAc undermine performance after devaluation and inhibit common PIT effects. On the other hand, lesions in the shell only damage specific PIT effects. This difference is thought to reflect the conditioned response and appetite within the NAc shell and NAc nuclei, respectively.
In the dorsal striatum dichotomy has been observed between D1-MSNs and D2-MSNs, with the first strengthening and increasing movement, and the latter becoming hostile and reducing movement. Such distinctions have traditionally been considered applicable to nucleus accumbens as well, but evidence from pharmacological and optogenetic studies is contradictory. Furthermore, a subset of MSNs NAc express both D1 and D2 MSNs, and pharmacological activation of D1 receptors versus D2 does not need to activate neural populations appropriately. While most studies have not demonstrated the selective optogenetic effects of D1 or MSN D2 on locomotor activity, one study has reported a decrease in basal movement with D2-MSN stimulation. While two studies have reported reduced cocaine reinforcement effect with D2-MSN activation, one study has reported no effect. NAc D2-MSN activation has also been reported to improve motivation, as assessed by PIT, and the activity of D2 receptors is needed to strengthen the VTA stimulation effect. A 2018 study reported that activation of MSN D2 improves motivation through inhibition of the ventral pallidum, thus disabling the VTA.
Mother's behavior
A fMRI study conducted in 2005 found that when rat mothers were in the presence of their children, the areas of the brain involved in reinforcement, including the nucleus accumbens, were highly active. Levels of dopamine increase in nucleus accumbens during mother's behavior, while lesions in this area interfere with maternal behavior. When women are presented with unrelated baby images, fMRI shows an increase in brain activity in the nucleus accumbens and adjacent caudate nuclei, comparable to the extent to which women find these babies "cute".
Inversion
Activation of the D1-type MSN in the nucleus accumbens is involved in the award, whereas the activation of the D2-type MSN in the nucleus accumbens increases reluctance.
Slow-wave sleep
By the end of 2017, research on rodents using optogenetic and chemogenetic methods found that indirect spinal path neurons (ie, D2-type) in nucleus accumbens express adenosine A 2A receptors and ventral projects pallidum is involved in slow wave sleep arrangement. Specifically, the optogenetic activation of the NACC core neurons indirectly induces slow-wave sleep and the chemogenetic activation of the same neuron increases the number and duration of slow-wave sleep episodes. This chemogenetic inhibition of the NACC core neurons suppresses sleep. In contrast, D2-type medium spiny neurons in NACC shells expressing adenosine A 2A receptors have no role in regulating slow-wave sleep.
Clinical interests
Dependency
The current addiction model of chronic drug use involves a change in gene expression in mesocorticolimbic projection. The most important transcription factors that produce this change are Fosb, adenosine monophosphate adenosine (cAMP) adenosine binding (CREB), and nuclear factor kappa B (NF? B). Fosb is the most significant gene transcription factor in addiction because viral or genetic expression in the nucleus accumbens is necessary and sufficient for many nerve adaptations and behavioral effects (eg, increased expression depending on self-administration and reward sensitization). in drug addiction. ? FosB overekspresi has been involved in alcohol addiction (ethanol), cannabinoids, cocaine, methylphenidate, nicotine, opioids, phencyclidine, propofol, and substituted amphetamines, among others. Increased in nucleus accumbens? JunD expressions can reduce or, by large increases, even block most of the nerve changes seen in chronic drug abuse (ie, changes mediated by? FosB).
Fosb also plays an important role in regulating behavioral responses to natural rewards, such as good food, sex, and exercise. Natural rewards, such as abuse drugs, cause? Fosb in the nucleus accumbens, and the achievement of these rewards can chronically produce the same pathological addictive state through FosB's overexpression. Consequently, Fosb is a key transcription factor involved in the addiction of natural gifts as well; in particular, Fosb in the nucleus accumbens is essential for the effect of strengthening sexual rewards. Research on the interaction between natural and drug rewards suggests that psychostimulant and sexual behavior act on the same biomolecular mechanisms to induce? FosB in the nucleus accumbens and has a mediated cross-sensitization effect through? FosB.
Similar to drug awards, non-drug rewards also increase the level of extracellular dopamine in NACC shells. Drug-induced dopamine release in the NACC shell and NAcc nucleus is usually not susceptible to habituation (ie, the development of drug tolerance: decreased dopamine release from future drug exposure as a result of recurrent drug exposure); on the contrary, repeated exposure to drugs inducing dopamine release within the shell and NACC nuclei usually results in sensitization (ie the amount of dopamine released in NACC from future drug exposure increases as a result of recurrent drug exposure). Sensitization of dopamine release in the NACC shell after recurrent drug exposure serves to strengthen drug-induced associations (ie, classical conditioning that occurs when drug use is repeatedly paired with environmental stimuli) and this relationship becomes less susceptible to extinction (ie, "no learning" association this classically conditioned association between drug use and environmental stimulation becomes more difficult). After repeated installs, these classically conditioned environmental stimuli (eg, the context and objects often paired with drug use) often serve as drug cues that serve as a secondary booster of drug use (that is, once the association is formed, exposure to a coupled environmental stimulus triggering a desire or desire to use the drugs that have been associated with them).
Unlike drugs, the release of dopamine in the NACC shell by many types of beneficial non-drug stimuli usually habituates after repeated exposure (ie, the amount of dopamine released from future exposure to beneficial non-drug stimuli usually decreases as a result of repeated exposure against the stimulus).
Depression
In April 2007, two research teams reported having inserted electrodes into the nucleus accumbens to use deep brain stimulation to treat severe depression. In 2010, experiments reported that deep brain stimulation of nucleus accumbens managed to reduce symptoms of depression in 50% of patients who did not respond to other treatments such as electroconvulsive therapy. Nucleus accumbens has also been used as a target to treat small groups of patients with obsessive-compulsive therapy-refractory therapy.
Ablation
To treat addiction and in an attempt to treat mental illness, radio frequency ablation of nucleus accumbens has been done. The results are inconclusive and controversial.
Placebo effect
NACC activation has been shown to occur in anticipation of drug effectiveness when users were given a placebo, demonstrating the contributing role of nucleus accumbens in the placebo effect.
Additional images
See also
- Septal Nucleus
References
External links
- The role of core accumbens in the prize circuit. Part of "Brain from Top to Bottom." on thebrain.mcgill.ca
- Nucleus Accumbens - Mobile Based Database
- Stained slice brain image including "nucleus% 20accumbens" in BrainMaps project
Source of the article : Wikipedia
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