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Article ; Online: Cognition-enhancing and cognition-impairing doses of psychostimulants exert opposing actions on frontostriatal neural coding of delay in working memory.

Spencer, Robert C / Martin, Andrea J / Devilbiss, David M / Berridge, Craig W

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2023 Volume 49, Issue 5, Page(s) 837–844

Abstract: The prefrontal cortex (PFC) and extended frontostriatal circuitry play a critical role in executive cognitive processes that guide goal-directed behavior. Dysregulation of frontostriatal-dependent cognition is implicated in a variety of cognitive/ ... ...

Abstract	The prefrontal cortex (PFC) and extended frontostriatal circuitry play a critical role in executive cognitive processes that guide goal-directed behavior. Dysregulation of frontostriatal-dependent cognition is implicated in a variety of cognitive/behavioral disorders, including addiction and attention deficit hyperactivity disorder (ADHD). Psychostimulants exert dose-dependent and opposing actions on frontostriatal cognitive function. Specifically, low and clinically-relevant doses improve, while higher doses associated with abuse and addiction impair, frontostriatal-dependent cognitive function. Frontostriatal cognition is supported by the coordinated activity of neurons across this circuit. To date, the neural coding mechanisms that support the diverse cognitive actions of psychostimulants are unclear. This represents a significant deficit in our understanding of the neurobiology of frontostriatal cognition and limits the development of novel treatments for frontostriatal cognitive impairment. The current studies examined the effects of cognition-enhancing and cognition-impairing doses of methylphenidate (MPH) on the spiking activity of dorsomedial PFC (dmPFC) and dorsomedial striatal (dmSTR) neurons in 17 male rats engaged in a working memory task. Across this frontostriatal circuit, we observed opposing actions of low- and high-dose MPH on the population-based representation of delay: low-dose strengthened, while high-dose weakened, representation of this event. MPH elicited a more complex pattern of actions on reward-related signaling, that were highly dose-, region- and neuron-dependent. These observations provide novel insight into the neurophysiological mechanisms that support the cognitive actions of psychostimulants.
MeSH term(s)	Rats ; Male ; Animals ; Memory, Short-Term ; Rats, Sprague-Dawley ; Central Nervous System Stimulants/pharmacology ; Central Nervous System Stimulants/therapeutic use ; Methylphenidate/pharmacology ; Methylphenidate/therapeutic use ; Cognition ; Attention Deficit Disorder with Hyperactivity/drug therapy ; Prefrontal Cortex
Chemical Substances	Central Nervous System Stimulants ; Methylphenidate (207ZZ9QZ49)
Language	English
Publishing date	2023-09-23
Publishing country	England
Document type	Journal Article
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-023-01738-6
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Article ; Online: Stress degrades working memory-related frontostriatal circuit function.

Berridge, Craig W / Devilbiss, David M / Martin, Andrea J / Spencer, Robert C / Jenison, Rick L

Cerebral cortex (New York, N.Y. : 1991)

2023 Volume 33, Issue 12, Page(s) 7857–7869

Abstract: Goal-directed behavior is dependent on neuronal activity in the prefrontal cortex (PFC) and extended frontostriatal circuitry. Stress and stress-related disorders are associated with impaired frontostriatal-dependent cognition. Our understanding of the ... ...

Abstract	Goal-directed behavior is dependent on neuronal activity in the prefrontal cortex (PFC) and extended frontostriatal circuitry. Stress and stress-related disorders are associated with impaired frontostriatal-dependent cognition. Our understanding of the neural mechanisms that underlie stress-related cognitive impairment is limited, with the majority of prior research focused on the PFC. To date, the actions of stress across cognition-related frontostriatal circuitry are unknown. To address this gap, the current studies examined the effects of acute noise-stress on the spiking activity of neurons and local field potential oscillatory activity within the dorsomedial PFC (dmPFC) and dorsomedial striatum (dmSTR) in rats engaged in a test of spatial working memory. Stress robustly suppressed responses of both dmPFC and dmSTR neurons strongly tuned to key task events (delay, reward). Additionally, stress strongly suppressed delay-related, but not reward-related, theta and alpha spectral power within, and synchrony between, the dmPFC and dmSTR. These observations provide the first demonstration that stress disrupts the neural coding and functional connectivity of key task events, particularly delay, within cognition-supporting dorsomedial frontostriatal circuitry. These results suggest that stress-related degradation of neural coding within both the PFC and striatum likely contributes to the cognition-impairing effects of stress.
MeSH term(s)	Rats ; Animals ; Memory, Short-Term/physiology ; Corpus Striatum/physiology ; Neostriatum ; Prefrontal Cortex/physiology ; Neurons/physiology
Language	English
Publishing date	2023-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1077450-6
ISSN	1460-2199 ; 1047-3211
ISSN (online)	1460-2199
ISSN	1047-3211
DOI	10.1093/cercor/bhad084
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Zs.A 3235: Show issues

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Article ; Online: Estrus cycle-dependent working memory effects of prefrontal cortex corticotropin-releasing factor neurotransmission.

Berridge, Craig W / Martin, Andrea J / Hupalo, Sofiya / Nicol, Shannon E

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2022 Volume 47, Issue 12, Page(s) 2016–2023

Abstract: The prefrontal cortex (PFC) supports a diversity of cognitive processes. Impairment in PFC-dependent cognition is associated with multiple psychiatric disorders, including those known to display sex differences. Our ability to treat this impairment is ... ...

Abstract	The prefrontal cortex (PFC) supports a diversity of cognitive processes. Impairment in PFC-dependent cognition is associated with multiple psychiatric disorders, including those known to display sex differences. Our ability to treat this impairment is limited, in part due to an incomplete understanding of the neural mechanisms that support PFC-dependent cognition. In previous studies in male rats, we demonstrated that corticotropin-releasing factor (CRF) receptors and neurons in caudal dorsomedial PFC (dmPFC) regulate PFC-dependent working memory. Subcortically, CRF can exert sex-specific actions, a subset of which are ovarian steroid dependent. To date, the cognitive actions of dmPFC CRF neurotransmission in females are unknown. To address this gap, the current studies examined the effects of chemogenetic and pharmacological manipulations of CRF receptors and neurons within the dmPFC of female rats tested in a spatial working memory task. Outside of proestrus, activation of both CRF receptors and neurons in the caudal, but not rostral, dmPFC impaired working memory. Meanwhile, blockade of CRF receptors in the caudal dmPFC or globally in the brain, improved working memory performance, similar to that seen in males. In contrast, these effects were not observed during proestrus. These observations demonstrate that while CRF neurotransmission in the PFC regulates working memory similarly in males and females, these actions are not observed in females when ovarian steroids are at peak levels.
MeSH term(s)	Animals ; Corticotropin-Releasing Hormone/metabolism ; Estrus ; Female ; Male ; Memory, Short-Term ; Prefrontal Cortex ; Rats ; Receptors, Corticotropin-Releasing Hormone/metabolism ; Synaptic Transmission
Chemical Substances	Receptors, Corticotropin-Releasing Hormone ; Corticotropin-Releasing Hormone (9015-71-8)
Language	English
Publishing date	2022-05-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-022-01349-7
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Article ; Online: Prefrontal corticotropin-releasing factor neurons impair sustained attention via distal transmitter release.

Hupalo, Sofiya / Spencer, Robert C / Berridge, Craig W

The European journal of neuroscience

2021

Abstract: The prefrontal cortex (PFC) supports cognitive processes critical for goal-directed behavior. Although the PFC contains a high density of corticotropin-releasing factor (CRF) neurons, their role in cognition has been largely unexplored. We recently ... ...

Abstract	The prefrontal cortex (PFC) supports cognitive processes critical for goal-directed behavior. Although the PFC contains a high density of corticotropin-releasing factor (CRF) neurons, their role in cognition has been largely unexplored. We recently demonstrated that CRF neurons in the caudal dorsomedial PFC (dmPFC) of rats act to impair working memory via activation of local CRF receptors. However, there is heterogeneity in the neural mechanisms that support the diversity of PFC-dependent cognitive processes. Currently, the degree to which PFC CRF neurons impact other forms of PFC-dependent cognition is unknown. To address this issue, the current studies examined the effects of chemogenetic manipulations of PFC CRF neurons on sustained attention in male rats. Similar to working memory, activation of caudal dmPFC CRF neurons impaired, while inhibition of these neurons or global CRF receptor antagonism improved, sustained attention. However, unlike working memory, the sustained attention-impairing effect of PFC CRF neurons was not dependent on local CRF receptors. Moreover, CRF infusion into the caudal dmPFC or other medial PFC subregions had no effect on task performance. Together, these observations demonstrate that while caudal dmPFC CRF neurons impair both working memory and sustained attention, these actions involve distinct neural circuits (local CRF release for working memory and extra-PFC release for sustained attention). Nonetheless, the procognitive actions of systemically administered CRF antagonists across both tasks are similar to those seen with attention deficit hyperactivity disorder-related treatments. Thus, CRF antagonists may have potential for use in the treatment of PFC cognitive dysfunction.
Language	English
Publishing date	2021-05-05
Publishing country	France
Document type	Journal Article
ZDB-ID	645180-9
ISSN	1460-9568 ; 0953-816X
ISSN (online)	1460-9568
ISSN	0953-816X
DOI	10.1111/ejn.15260
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Zs.A 2548: Show issues

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Article ; Online: Receptor and circuit mechanisms underlying differential procognitive actions of psychostimulants.

Spencer, Robert C / Berridge, Craig W

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2019 Volume 44, Issue 10, Page(s) 1820–1827

Abstract: Psychostimulants, including methylphenidate (MPH), improve cognitive processes dependent on the prefrontal cortex (PFC) and extended frontostriatal circuitry. In both humans and animals, systemic MPH improves certain cognitive processes, such as working ... ...

Abstract	Psychostimulants, including methylphenidate (MPH), improve cognitive processes dependent on the prefrontal cortex (PFC) and extended frontostriatal circuitry. In both humans and animals, systemic MPH improves certain cognitive processes, such as working memory, in a narrow inverted-U-shaped manner. In contrast, other processes, including attention-related, are improved over a broader/right-shifted dose range. The current studies sought to elucidate the potential circuit and receptor mechanisms underlying the divergent dose-dependent procognitive effects of psychostimulants. We first observed that, as with working memory, although sustained attention testing was highly dependent on multiple frontostriatal regions, only MPH infusion into the dorsomedial PFC improved task performance. Importantly, the dose-response curve for this action was right-shifted relative to working memory, as seen with systemic administration. Additional studies examined the receptor mechanisms within the PFC associated with the procognitive actions of MPH across working memory and sustained attention tasks. We observed that PFC α2 and D1 receptors contributed to the beneficial effects of MPH across both cognitive tasks. However, α1 receptors only contributed to MPH-induced improvement in sustained attention. Moreover, activation of PFC α1 receptors was sufficient to improve sustained attention. This latter action contrasts with the impairing actions of PFC α1 receptors reported previously for working memory. These results provide further evidence for a prominent role of the PFC in the procognitive actions of MPH and demonstrate the divergent dose sensitivity across cognitive processes aligns with the differential involvement of PFC α1 receptors.
MeSH term(s)	Adrenergic alpha-2 Receptor Antagonists/pharmacology ; Adrenergic alpha-Antagonists/pharmacology ; Animals ; Attention/drug effects ; Benzazepines ; Central Nervous System Stimulants/pharmacology ; Cognition/drug effects ; Dose-Response Relationship, Drug ; GABA-A Receptor Agonists/pharmacology ; Imidazoles/pharmacology ; Male ; Memory, Short-Term/drug effects ; Methylphenidate/pharmacology ; Muscimol/pharmacology ; Neostriatum/drug effects ; Neostriatum/metabolism ; Neural Pathways/drug effects ; Oxathiins/pharmacology ; Prefrontal Cortex/drug effects ; Prefrontal Cortex/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, alpha-1/metabolism ; Receptors, Adrenergic, alpha-2/metabolism ; Receptors, Dopamine D1/antagonists & inhibitors ; Receptors, Dopamine D1/metabolism
Chemical Substances	Adrenergic alpha-2 Receptor Antagonists ; Adrenergic alpha-Antagonists ; Benzazepines ; Central Nervous System Stimulants ; GABA-A Receptor Agonists ; Imidazoles ; Oxathiins ; Receptors, Adrenergic, alpha-1 ; Receptors, Adrenergic, alpha-2 ; Receptors, Dopamine D1 ; SCH 23390 ; atipamezole (03N9U5JAF6) ; Methylphenidate (207ZZ9QZ49) ; Muscimol (2763-96-4) ; benoxathian (92642-94-9)
Language	English
Publishing date	2019-01-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-019-0314-y
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Article ; Online: New developments and future directions in understanding locus coeruleus - Norepinephrine (LC-NE) function.

Foote, Stephen L / Berridge, Craig W

Brain research

2018 Volume 1709, Page(s) 81–84

Abstract: In this commentary we utilize recent observations regarding the organization and actions of the locus coeruleus-noradrenergic system to identify major issues in need of further study to more fully understand the behavioral actions of this major ... ...

Abstract	In this commentary we utilize recent observations regarding the organization and actions of the locus coeruleus-noradrenergic system to identify major issues in need of further study to more fully understand the behavioral actions of this major neurotransmitter system.
MeSH term(s)	Animals ; Humans ; Locus Coeruleus/metabolism ; Norepinephrine/metabolism
Chemical Substances	Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2018-09-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2018.09.033
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Zs.A 161: Show issues

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Article: Dorsal Raphe to Basolateral Amygdala Corticotropin-Releasing Factor Circuit Regulates Cocaine-Memory Reconsolidation.

Ritchie, Jobe L / Qi, Shuyi / Soto, David A / Swatzell, Sydney E / Grenz, Hope I / Pruitt, Avery Y / Artimenia, Lilia M / Cooke, Spencer K / Berridge, Craig W / Fuchs, Rita A

bioRxiv : the preprint server for biology

2024

Abstract: Environmental stimuli elicit drug craving and relapse in cocaine users by triggering the retrieval of strong cocainerelated contextual memories. Retrieval can also destabilize drug memories, requiring reconsolidation, a protein synthesis-dependent ... ...

Abstract	Environmental stimuli elicit drug craving and relapse in cocaine users by triggering the retrieval of strong cocainerelated contextual memories. Retrieval can also destabilize drug memories, requiring reconsolidation, a protein synthesis-dependent storage process, to maintain memory strength. Corticotropin-releasing factor (CRF) signaling in the basolateral amygdala (BLA) is necessary for cocainememory reconsolidation. We have hypothesized that a critical source of CRF in the BLA is the dorsal raphe nucleus (DR) based on its neurochemistry, anatomical connectivity, and requisite involvement in cocaine-memory reconsolidation. To test this hypothesis, male and female Sprague-Dawley rats received adeno-associated viruses to express Gi-coupled designer receptors exclusively activated by designer drugs (DREADDs) selectively in CRF neurons of the DR and injection cannulae directed at the BLA. The rats were trained to self-administer cocaine in a distinct environmental context then received extinction training in a different context. They were then briefly reexposed to the cocaine-predictive context to destabilize (reactivate) cocaine memories. Intra-BLA infusions of the DREADD agonist deschloroclozapine (DCZ; 0.1 mM, 0.5 μL/hemisphere) after memory reactivation attenuated cocaine-memory strength, relative to vehicle infusion. This was indicated by a selective, DCZ-induced and memory reactivation-dependent decrease in drug-seeking behavior in the cocaine-predictive context in DREADD-expressing males and females at test compared to respective controls. Notably, BLA-projecting DR CRF neurons that exhibited increased c-Fos expression during memory reconsolidation co-expressed glutamatergic and serotonergic neuronal markers. Together, these findings suggest that the DR
Language	English
Publishing date	2024-02-12
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.10.579725
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Article ; Online: Differential cognitive actions of norepinephrine a2 and a1 receptor signaling in the prefrontal cortex.

Berridge, Craig W / Spencer, Robert C

Brain research

2016 Volume 1641, Issue Pt B, Page(s) 189–196

Abstract: The prefrontal cortex (PFC) supports cognitive and behavioral processes that guide goal directed behavior. Moreover, dysregulated prefrontal cognitive dysfunction is associated with multiple psychiatric disorders. Norepinephrine (NE) signaling in the PFC ...

Abstract	The prefrontal cortex (PFC) supports cognitive and behavioral processes that guide goal directed behavior. Moreover, dysregulated prefrontal cognitive dysfunction is associated with multiple psychiatric disorders. Norepinephrine (NE) signaling in the PFC is a critical modulator of prefrontal cognition and is targeted by a variety of drugs used to treat PFC-dependent cognitive dysfunction. Noradrenergic modulation of PFC-dependent cognition is complex, with concentration and receptor-specific actions that are likely dependent on neuronal activity state. Recent studies indicate that within the PFC, noradrenergic α1 and α2 receptors exert unique modulatory actions across distinct cognitive processes that allow for context-dependent modulation of cognition. Specifically, high affinity post-synaptic α2 receptors, engaged at moderate rates of NE release associated with moderate arousal levels, promote working memory. In contrast, lower affinity α1 receptors, engaged at higher rates of release associated with high arousal conditions (e.g. stress), impair working memory performance while promoting flexible attention. While these and other observations were initially interpreted to indicate high rates of NE release promotes the transition from focused to flexible/scanning attention, recent findings indicate that α1 receptors promote both focused and flexible attention. Collectively, these observations indicate that while α2 and α1 receptors in the PFC differentially modulate distinct cognitive processes, this cannot be simply ascribed to differential roles of these receptors in 'focused' vs. 'flexible' cognitive processes. Translationally, this information indicates that: (1) not all tests of prefrontal cognitive function may be appropriate for preclinical programs aimed at specific PFC-dependent disorders and (2) the treatment of specific PFC cognitive deficits may require the differential targeting of noradrenergic receptor subtypes. This article is part of a Special Issue entitled SI: Noradrenergic System.
MeSH term(s)	Animals ; Attention/physiology ; Cognition/physiology ; Humans ; Memory, Short-Term/physiology ; Prefrontal Cortex/metabolism ; Receptors, Adrenergic, alpha-1/metabolism ; Receptors, Adrenergic, alpha-2/metabolism ; Sensory Gating/physiology
Chemical Substances	Receptors, Adrenergic, alpha-1 ; Receptors, Adrenergic, alpha-2
Language	English
Publishing date	2016-06-15
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2015.11.024
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Zs.A 161: Show issues

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Article ; Online: Working Memory Impairing Actions of Corticotropin-Releasing Factor (CRF) Neurotransmission in the Prefrontal Cortex.

Hupalo, Sofiya / Berridge, Craig W

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2016 Volume 41, Issue 11, Page(s) 2733–2740

Abstract: The prefrontal cortex (PFC) regulates cognitive processes critical for goal-directed behavior. PFC cognitive dysfunction is implicated in multiple psychopathologies, including attention deficit hyperactivity disorder (ADHD). Although it has long been ... ...

Abstract	The prefrontal cortex (PFC) regulates cognitive processes critical for goal-directed behavior. PFC cognitive dysfunction is implicated in multiple psychopathologies, including attention deficit hyperactivity disorder (ADHD). Although it has long been known that corticotropin-releasing factor (CRF) and CRF receptors are prominent in the PFC, the cognitive effects of CRF action within the PFC are poorly understood. The current studies examined whether CRF receptor activation in the PFC modulates cognitive function in rats as measured in a delayed response task of spatial working memory. CRF dose-dependently impaired working memory performance when administered either intracerebroventricularly (ICV) or directly into the PFC. The working memory actions of CRF in the PFC were topographically organized, with impairment observed only following CRF infusions into the caudal dorsomedial PFC (dmPFC). Additional studies examined whether endogenous CRF modulates working memory. Both ICV and intra-dmPFC administration of the nonselective CRF antagonist, D-Phe-CRF, dose-dependently improved working memory performance. To better assess the translational potential of CRF antagonists, we examined the cognitive effects of systemic administration of the CRF1 receptor selective antagonist, NBI 35965. Similar procognitive actions were observed in these studies. These results are the first to demonstrate that CRF acts in the PFC to regulate PFC-dependent cognition. Importantly, the ability of CRF antagonists to improve working memory is identical to that seen with all approved treatments for ADHD. These observations suggest that CRF antagonists may represent a novel approach for the treatment of ADHD and other disorders associated with dysregulated prefrontal cognitive function.
MeSH term(s)	Acenaphthenes/pharmacology ; Animals ; Corticotropin-Releasing Hormone/analogs & derivatives ; Corticotropin-Releasing Hormone/antagonists & inhibitors ; Corticotropin-Releasing Hormone/metabolism ; Corticotropin-Releasing Hormone/pharmacology ; Corticotropin-Releasing Hormone/toxicity ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug Administration Routes ; Feeding Behavior/drug effects ; Male ; Maze Learning/drug effects ; Memory Disorders/chemically induced ; Memory Disorders/pathology ; Memory, Short-Term/drug effects ; Prefrontal Cortex/drug effects ; Prefrontal Cortex/physiology ; Rats ; Rats, Sprague-Dawley
Chemical Substances	6-cyclopropylmethyl-2-(2,4-dichlorophenyl)-7-ethyl-4-methyl-7,8-dihydro-6H-1,3,6,8a-tetraazaacenaphthylene ; Acenaphthenes ; phenylalanyl corticotropin-releasing factor (12-41) ; Corticotropin-Releasing Hormone (9015-71-8)
Language	English
Publishing date	2016-10
Publishing country	England
Document type	Journal Article
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/npp.2016.85
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Article: Noradrenergic modulation of arousal.

Berridge, Craig W

Brain research reviews

2007 Volume 58, Issue 1, Page(s) 1–17

Abstract: Through a highly divergent efferent projection system, the locus coeruleus-noradrenergic system supplies norepinephrine throughout the central nervous system. State-dependent neuronal discharge activity of locus coeruleus neurons has long-suggested a ... ...

Abstract	Through a highly divergent efferent projection system, the locus coeruleus-noradrenergic system supplies norepinephrine throughout the central nervous system. State-dependent neuronal discharge activity of locus coeruleus neurons has long-suggested a role of this system in the induction of an alert waking state. More recent work supports this hypothesis, demonstrating robust wake-promoting actions of the locus coeruleus-noradrenergic system. Norepinephrine enhances arousal, in part, via actions of beta- and alpha1-receptors located within multiple subcortical structures, including the general regions of the medial septal area and the medial preoptic areas. Recent anatomical studies suggest that arousal-enhancing actions of norepinephrine are not limited to the locus coeruleus system and likely include the A1 and A2 noradrenergic cell groups. Thus, noradrenergic modulation of arousal state involves multiple noradrenergic systems acting within multiple subcortical regions. Pharmacological studies indicate that the combined actions of these systems are necessary for the sustained maintenance of arousal levels associated with spontaneous waking. Enhanced arousal state is a prominent aspect of both stress and psychostimulant drug action and evidence indicates that noradrenergic systems likely play an important role in both stress-related and psychostimulant-induced arousal. These and other observations suggest that the dysregulation of noradrenergic neurotransmission could well contribute to the dysregulation of arousal associated with a variety of behavioral disorders including insomnia and stress-related disorders.
MeSH term(s)	Animals ; Arousal/physiology ; Humans ; Locus Coeruleus/anatomy & histology ; Locus Coeruleus/physiology ; Models, Anatomic ; Neural Pathways/physiology ; Norepinephrine/physiology ; Preoptic Area/anatomy & histology ; Preoptic Area/physiology ; Receptors, Adrenergic/physiology ; Septum of Brain/anatomy & histology ; Septum of Brain/physiology
Chemical Substances	Receptors, Adrenergic ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2007-12-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	423722-5
ISSN	1872-6321 ; 0165-0173
ISSN (online)	1872-6321
ISSN	0165-0173
DOI	10.1016/j.brainresrev.2007.10.013
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Zs.A 1506: Show issues

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