User:Seppi333/sandbox3

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RS lead text in source

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References

^ Renthal W, Carle TL, Maze I, Covington HE, Truong HT, Alibhai I, Kumar A, Montgomery RL, Olson EN, Nestler EJ (2008). "Delta FosB mediates epigenetic desensitization of the c-fos gene after chronic amphetamine exposure". J. Neurosci. 28 (29): 7344–9. doi:10.1523/JNEUROSCI.1043-08.2008. PMC 2610249. PMID 18632938. This study reveals a novel epigenetic pathway through which ΔFosB mediates distinct transcriptional programs and ultimately behavioral plasticity to chronic amphetamine exposure. ... One attractive candidate is c-fos, a gene which is induced dramatically by acute psychostimulants but only weakly after repeated exposure (Hope et al., 1992; Persico et al., 1993; Steiner and Gerfen, 1993), when levels of ΔFosB and ΔFosB-containing AP-1 complexes are high (Hope et al., 1992, 1994). Since the c-fos gene contains an AP-1-like site in its proximal promoter (Morgan and Curran, 1989), it is a plausible candidate for ΔFosB-mediated repression. Induction of c-fos is traditionally viewed as an early marker of neural activation, since it is rapidly and transiently induced in response to a variety of stimuli (Morgan and Curran, 1989). The c-fos gene is also important for behavioral responses to cocaine, as mice lacking c-fos in dopamine D1 receptor-containing neurons, the neuronal cell type where ΔFosB is induced by psychostimulants (McClung et al., 2004), have reduced behavioral sensitization to cocaine (Zhang et al., 2006). These findings led us to investigate whether ΔFosB controls c-fos gene activity after chronic amphetamine exposure. We describe here a novel epigenetic mechanism by which ΔFosB accumulation in response to chronic amphetamine feeds back to desensitize c-fos induction to subsequent drug doses. This novel interplay between ΔFosB and chromatin remodeling events on the c-fos promoter may be an important homeostatic mechanism to regulate an animal's sensitivity to repeated drug exposure.
^ Zlebnik NE, Hedges VL, Carroll ME, Meisel RL (2014). "Chronic wheel running affects cocaine-induced c-Fos expression in brain reward areas in rats". Behav. Brain Res. 261: 71–8. doi:10.1016/j.bbr.2013.12.012. PMC 4067570. PMID 24342748. Emerging evidence from human and animal studies suggests that exercise is a highly effective treatment for drug addiction. ... The mean fold change in cocaine-induced c-Fos cell counts relative to saline-induced c-Fos cell counts was significantly higher in exercising compared to control rats in the NAc core, dorsomedial and dorsolateral CPu, the prelimbic area, and the OFC, indicating differential cocaine-specific cellular activation of brain reward circuitry between exercising and control animals. These results suggest neurobiological mechanisms by which voluntary wheel running attenuates cocaine-motivated behaviors and provide support for exercise as a novel treatment for drug addiction.

Epidemiology refs to add to drug addiction article

SUD epidemiology

I thought these might be interesting content additions, since addiction and ADHD are both manifestations of functional impairments in the mesocorticolimbic projection:

Comorbidity of ADHD in SUD/addiction

Comorbidity of SUD/addiction in ADHD

PMID 23104523

Seppi333 (Insert 2¢ | Maintained) 07:25, 2 November 2014 (UTC)


Brain structure(s)	Regulated cognitive functions	Implicated neuropsychiatric disorders	Refs
Prefrontal cortex and anterior cingulate	cognitive control of behavior attentional control cognitive flexibility decision-making inhibitory control of behavior social cognition working memory	addiction attention deficit hyperactivity disorder (ADHD)	^[1]^[2]
Nucleus accumbens	motivation positive reinforcement reward perception	addiction	^[3]
Hippocampus	declarative memory spatial memory	depression	^[4]^[5]^[6]
Cerebellum	motor coordination motor learning		^[7]
Caudate nucleus	inhibitory control of behavior stimulus-response learning	ADHD Parkinson's disease Huntington's disease	^[1]^[5]
Parietal cortex	attention sensory perception working memory		^[1]^[8]

^ ^a ^b ^c Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 313–321. ISBN 9780071481274. • Executive function, the cognitive control of behavior, depends on the prefrontal cortex, which is highly developed in higher primates and especially humans.
• Working memory is a short-term, capacity-limited cognitive buffer that stores information and permits its manipulation to guide decision-making and behavior. ...
These diverse inputs and back projections to both cortical and subcortical structures put the prefrontal cortex in a position to exert what is often called "top-down" control or cognitive control of behavior. ... The prefrontal cortex receives inputs not only from other cortical regions, including association cortex, but also, via the thalamus, inputs from subcortical structures subserving emotion and motivation, such as the amygdala (Chapter 14) and ventral striatum (or nucleus accumbens; Chapter 15). ...
In conditions in which prepotent responses tend to dominate behavior, such as in drug addiction, where drug cues can elicit drug seeking (Chapter 15), or in attention deficit hyperactivity disorder (ADHD; described below), significant negative consequences can result. ... ADHD can be conceptualized as a disorder of executive function; specifically, ADHD is characterized by reduced ability to exert and maintain cognitive control of behavior. Compared with healthy individuals, those with ADHD have diminished ability to suppress inappropriate prepotent responses to stimuli (impaired response inhibition) and diminished ability to inhibit responses to irrelevant stimuli (impaired interference suppression). ... Functional neuroimaging in humans demonstrates activation of the prefrontal cortex and caudate nucleus (part of the striatum) in tasks that demand inhibitory control of behavior. ... Early results with structural MRI show thinning of the cerebral cortex in ADHD subjects compared with age-matched controls in prefrontal cortex and posterior parietal cortex, areas involved in working memory and attention.{{cite book}}: CS1 maint: multiple names: authors list (link)
^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 315. ISBN 9780071481274. However, damage to the prefrontal cortex has a significant deleterious effect on social behavior, decision making, and adaptive responding to the changing circumstances of life. ... Several subregions of the prefrontal cortex have been implicated in partly distinct aspects of cognitive control, although these distinctions remain somewhat vaguely defined. The anterior cingulate cortex is involved in processes that require correct decision-making, as seen in conflict resolution (eg, the Stroop test, see in Chapter 16), or cortical inhibition (eg, stopping one task and switching to another). The medial prefrontal cortex is involved in supervisory attentional functions (eg, action-outcome rules) and behavioral flexibility (the ability to switch strategies). The dorsolateral prefrontal cortex, the last brain area to undergo myelination during development in late adolescence, is implicated in matching sensory inputs with planned motor responses. The ventromedial prefrontal cortex seems to regulate social cognition, including empathy. The orbitofrontal cortex is involved in social decision making and in representing the valuations assigned to different experiences.{{cite book}}: CS1 maint: multiple names: authors list (link)
^ Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 147, 266, 376. ISBN 9780071481274. VTA DA neurons play a critical role in motivation, reward-related behavior (Chapter 15), attention, and multiple forms of memory. This organization of the DA system, wide projection from a limited number of cell bodies, permits coordinated responses to potent new rewards. Thus, acting in diverse terminal fields, dopamine confers motivational salience ("wanting") on the reward itself or associated cues (nucleus accumbens shell region) ... Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward. ... The NAc and VTA are central components of the circuitry underlying reward and memory of reward. As previously mentioned, the activity of dopaminergic neurons in the VTA appears to be linked to reward prediction. The NAc is involved in learning associated with reinforcement ... The shell of the NAc appears to be particularly important to initial drug actions within reward circuitry; addictive drugs appear to have a greater effect on dopamine release in the shell than in the core of the NAc.{{cite book}}: CS1 maint: multiple names: authors list (link)
^ Cite error: The named reference gray matter was invoked but never defined (see the help page).
^ ^a ^b Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 148, 325–328, 438. ISBN 9780071481274. [dopamine] helps consolidate multiple forms of memory (amygdala and hippocampus) ... the specific crucial structures underlying the ability to store declarative memories are the hippocampus, the subicular complex, and the entorhinal cortex ... These findings strongly suggest that LTP in the hippocampus is required for at least some forms of learning and memory known to be dependent on this brain region. ... Evidence that the caudate nucleus and putamen influence stimulus-response learning comes from lesion studies in rodents and primates and from neuroimaging studies in humans and from studies of human disease. In Parkinson disease, the dopaminergic innervation of the caudate and putamen is severely compromised by the death of dopamine neurons in the substantia nigra pars compacta (Chapter 17). Patients with Parkinson disease have normal declarative memory ... However, they have marked impairments of stimulus-response learning. Patients with Parkinson disease or other basal ganglia disorders such as Huntington disease (in which caudate neurons themselves are damaged) have deficits in other procedural learning tasks, such as the acquisition of new motor programs. ... Huntington disease is associated with degenerative changes that are most apparent in the caudate nucleus and putamen.{{cite book}}: CS1 maint: multiple names: authors list (link)
^ Cite error: The named reference BDNF depression was invoked but never defined (see the help page).
^ Grimaldi G, Argyropoulos GP, Bastian A, Cortes M, Davis NJ, Edwards DJ, Ferrucci R, Fregni F, Galea JM, Hamada M, Manto M, Miall RC, Morales-Quezada L, Pope PA, Priori A, Rothwell J, Tomlinson SP, Celnik P (2014). "Cerebellar Transcranial Direct Current Stimulation (ctDCS): A Novel Approach to Understanding Cerebellar Function in Health and Disease". Neuroscientist. 22 (1): 83–97. doi:10.1177/1073858414559409. PMC 4712385. PMID 25406224.
^ Sereno MI, Huang RS (2014). "Multisensory maps in parietal cortex". Curr. Opin. Neurobiol. 24 (1): 39–46. doi:10.1016/j.conb.2013.08.014. PMC 3969294. PMID 24492077.

This page has been removed from search engines' indexes.

[Chronic_Amphetamine_c-Fos-1] Renthal W, Carle TL, Maze I, Covington HE, Truong HT, Alibhai I, Kumar A, Montgomery RL, Olson EN, Nestler EJ (2008). "Delta FosB mediates epigenetic desensitization of the c-fos gene after chronic amphetamine exposure". J. Neurosci. 28 (29): 7344–9. doi:10.1523/JNEUROSCI.1043-08.2008. PMC 2610249. PMID 18632938. This study reveals a novel epigenetic pathway through which ΔFosB mediates distinct transcriptional programs and ultimately behavioral plasticity to chronic amphetamine exposure. ... One attractive candidate is c-fos, a gene which is induced dramatically by acute psychostimulants but only weakly after repeated exposure (Hope et al., 1992; Persico et al., 1993; Steiner and Gerfen, 1993), when levels of ΔFosB and ΔFosB-containing AP-1 complexes are high (Hope et al., 1992, 1994). Since the c-fos gene contains an AP-1-like site in its proximal promoter (Morgan and Curran, 1989), it is a plausible candidate for ΔFosB-mediated repression. Induction of c-fos is traditionally viewed as an early marker of neural activation, since it is rapidly and transiently induced in response to a variety of stimuli (Morgan and Curran, 1989). The c-fos gene is also important for behavioral responses to cocaine, as mice lacking c-fos in dopamine D1 receptor-containing neurons, the neuronal cell type where ΔFosB is induced by psychostimulants (McClung et al., 2004), have reduced behavioral sensitization to cocaine (Zhang et al., 2006). These findings led us to investigate whether ΔFosB controls c-fos gene activity after chronic amphetamine exposure. We describe here a novel epigenetic mechanism by which ΔFosB accumulation in response to chronic amphetamine feeds back to desensitize c-fos induction to subsequent drug doses. This novel interplay between ΔFosB and chromatin remodeling events on the c-fos promoter may be an important homeostatic mechanism to regulate an animal's sensitivity to repeated drug exposure.

[Chronic_Exercise_c-Fos-2] Zlebnik NE, Hedges VL, Carroll ME, Meisel RL (2014). "Chronic wheel running affects cocaine-induced c-Fos expression in brain reward areas in rats". Behav. Brain Res. 261: 71–8. doi:10.1016/j.bbr.2013.12.012. PMC 4067570. PMID 24342748. Emerging evidence from human and animal studies suggests that exercise is a highly effective treatment for drug addiction. ... The mean fold change in cocaine-induced c-Fos cell counts relative to saline-induced c-Fos cell counts was significantly higher in exercising compared to control rats in the NAc core, dorsomedial and dorsolateral CPu, the prelimbic area, and the OFC, indicating differential cocaine-specific cellular activation of brain reward circuitry between exercising and control animals. These results suggest neurobiological mechanisms by which voluntary wheel running attenuates cocaine-motivated behaviors and provide support for exercise as a novel treatment for drug addiction.

[NHM-Cognitive_Control-3] Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 313–321. ISBN 9780071481274. • Executive function, the cognitive control of behavior, depends on the prefrontal cortex, which is highly developed in higher primates and especially humans.
• Working memory is a short-term, capacity-limited cognitive buffer that stores information and permits its manipulation to guide decision-making and behavior. ...
These diverse inputs and back projections to both cortical and subcortical structures put the prefrontal cortex in a position to exert what is often called "top-down" control or cognitive control of behavior. ... The prefrontal cortex receives inputs not only from other cortical regions, including association cortex, but also, via the thalamus, inputs from subcortical structures subserving emotion and motivation, such as the amygdala (Chapter 14) and ventral striatum (or nucleus accumbens; Chapter 15). ...
In conditions in which prepotent responses tend to dominate behavior, such as in drug addiction, where drug cues can elicit drug seeking (Chapter 15), or in attention deficit hyperactivity disorder (ADHD; described below), significant negative consequences can result. ... ADHD can be conceptualized as a disorder of executive function; specifically, ADHD is characterized by reduced ability to exert and maintain cognitive control of behavior. Compared with healthy individuals, those with ADHD have diminished ability to suppress inappropriate prepotent responses to stimuli (impaired response inhibition) and diminished ability to inhibit responses to irrelevant stimuli (impaired interference suppression). ... Functional neuroimaging in humans demonstrates activation of the prefrontal cortex and caudate nucleus (part of the striatum) in tasks that demand inhibitory control of behavior. ... Early results with structural MRI show thinning of the cerebral cortex in ADHD subjects compared with age-matched controls in prefrontal cortex and posterior parietal cortex, areas involved in working memory and attention.{{cite book}}: CS1 maint: multiple names: authors list (link)

[NHM-PFC_cognitive_processes-4] Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 315. ISBN 9780071481274. However, damage to the prefrontal cortex has a significant deleterious effect on social behavior, decision making, and adaptive responding to the changing circumstances of life. ... Several subregions of the prefrontal cortex have been implicated in partly distinct aspects of cognitive control, although these distinctions remain somewhat vaguely defined. The anterior cingulate cortex is involved in processes that require correct decision-making, as seen in conflict resolution (eg, the Stroop test, see in Chapter 16), or cortical inhibition (eg, stopping one task and switching to another). The medial prefrontal cortex is involved in supervisory attentional functions (eg, action-outcome rules) and behavioral flexibility (the ability to switch strategies). The dorsolateral prefrontal cortex, the last brain area to undergo myelination during development in late adolescence, is implicated in matching sensory inputs with planned motor responses. The ventromedial prefrontal cortex seems to regulate social cognition, including empathy. The orbitofrontal cortex is involved in social decision making and in representing the valuations assigned to different experiences.{{cite book}}: CS1 maint: multiple names: authors list (link)

[NAcc_function-5] Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 147, 266, 376. ISBN 9780071481274. VTA DA neurons play a critical role in motivation, reward-related behavior (Chapter 15), attention, and multiple forms of memory. This organization of the DA system, wide projection from a limited number of cell bodies, permits coordinated responses to potent new rewards. Thus, acting in diverse terminal fields, dopamine confers motivational salience ("wanting") on the reward itself or associated cues (nucleus accumbens shell region) ... Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward. ... The NAc and VTA are central components of the circuitry underlying reward and memory of reward. As previously mentioned, the activity of dopaminergic neurons in the VTA appears to be linked to reward prediction. The NAc is involved in learning associated with reinforcement ... The shell of the NAc appears to be particularly important to initial drug actions within reward circuitry; addictive drugs appear to have a greater effect on dopamine release in the shell than in the core of the NAc.{{cite book}}: CS1 maint: multiple names: authors list (link)

[gray_matter-6] Cite error: The named reference gray matter was invoked but never defined (see the help page).

[NHM-Caudate_Hippocampus-7] Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 148, 325–328, 438. ISBN 9780071481274. [dopamine] helps consolidate multiple forms of memory (amygdala and hippocampus) ... the specific crucial structures underlying the ability to store declarative memories are the hippocampus, the subicular complex, and the entorhinal cortex ... These findings strongly suggest that LTP in the hippocampus is required for at least some forms of learning and memory known to be dependent on this brain region. ... Evidence that the caudate nucleus and putamen influence stimulus-response learning comes from lesion studies in rodents and primates and from neuroimaging studies in humans and from studies of human disease. In Parkinson disease, the dopaminergic innervation of the caudate and putamen is severely compromised by the death of dopamine neurons in the substantia nigra pars compacta (Chapter 17). Patients with Parkinson disease have normal declarative memory ... However, they have marked impairments of stimulus-response learning. Patients with Parkinson disease or other basal ganglia disorders such as Huntington disease (in which caudate neurons themselves are damaged) have deficits in other procedural learning tasks, such as the acquisition of new motor programs. ... Huntington disease is associated with degenerative changes that are most apparent in the caudate nucleus and putamen.{{cite book}}: CS1 maint: multiple names: authors list (link)

[BDNF_depression-8] Cite error: The named reference BDNF depression was invoked but never defined (see the help page).

[Cerebellum-9] Grimaldi G, Argyropoulos GP, Bastian A, Cortes M, Davis NJ, Edwards DJ, Ferrucci R, Fregni F, Galea JM, Hamada M, Manto M, Miall RC, Morales-Quezada L, Pope PA, Priori A, Rothwell J, Tomlinson SP, Celnik P (2014). "Cerebellar Transcranial Direct Current Stimulation (ctDCS): A Novel Approach to Understanding Cerebellar Function in Health and Disease". Neuroscientist. 22 (1): 83–97. doi:10.1177/1073858414559409. PMC 4712385. PMID 25406224.

[parietal-10] Sereno MI, Huang RS (2014). "Multisensory maps in parietal cortex". Curr. Opin. Neurobiol. 24 (1): 39–46. doi:10.1016/j.conb.2013.08.014. PMC 3969294. PMID 24492077.

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