Same Brain Circuits Linked With Psychosis in Two Disorders

2014 ◽  
Vol 49 (12) ◽  
pp. 1-1
Author(s):  
Joan Arehart-Treichel
Keyword(s):  
Brain Circuits

Alcohol Dependence Conceptualized as a Stress Disorder

2019 ◽  
pp. 198-220
Author(s):  
Leandro F. Vendruscolo ◽  
George F. Koob
Keyword(s):  
Prefrontal Cortex ◽  
Alcohol Use ◽  
Alcohol Dependence ◽  
Glucocorticoid Receptors ◽  
Critical Role ◽  
Emotional States ◽  
Brain Circuits ◽  
Negative Emotional State ◽  
Alcohol Alcohol

Alcohol use disorder is a chronically relapsing disorder that involves (1) compulsivity to seek and take alcohol, (2) difficulty in limiting alcohol intake, and (3) emergence of a negative emotional state (e.g., dysphoria, anxiety, irritability) in the absence of alcohol. Alcohol addiction encompasses a three-stage cycle that becomes more intense as alcohol use progresses: binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation. These stages engage neuroadaptations in brain circuits that involve the basal ganglia (reward hypofunction), extended amygdala (stress sensitization), and prefrontal cortex (executive function disorder). This chapter discusses key neuroadaptations in the hypothalamic and extrahypothalamic stress systems and the critical role of glucocorticoid receptors. These neuroadaptations contribute to negative emotional states that powerfully drive compulsive alcohol drinking and seeking. These changes in association with a disruption of prefrontal cortex function that lead to cognitive deficits and poor decision making contribute to the chronic relapsing nature of alcohol dependence.

scholarly journals The FXG: A Presynaptic Fragile X Granule Expressed in a Subset of Developing Brain Circuits

2009 ◽  
Vol 29 (5) ◽  
pp. 1514-1524 ◽  
Author(s):  
S. B. Christie ◽  
M. R. Akins ◽  
J. E. Schwob ◽  
J. R. Fallon
Keyword(s):  
Fragile X ◽  
Developing Brain ◽  
Brain Circuits

Activity-Induced Amyloid-β Oligomers Drive Compensatory Synaptic Rearrangements in Brain Circuits Controlling Memory of Presymptomatic Alzheimer's Disease Mice

2019 ◽  
Vol 86 (3) ◽  
pp. 185-195 ◽  
Author(s):  
Annabella Pignataro ◽  
Giovanni Meli ◽  
Roberto Pagano ◽  
Veronica Fontebasso ◽  
Roberta Battistella ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Brain Circuits

Comparison between two rat sympathetic pathways activated in cold defense

2006 ◽  
Vol 291 (3) ◽  
pp. R589-R595 ◽  
Author(s):  
Youichirou Ootsuka ◽  
Robin M. McAllen
Keyword(s):  
Cold Water ◽  
Relative Sensitivity ◽  
Sympathetic Nerves ◽  
Defense Responses ◽  
Interscapular Brown Adipose Tissue ◽  
Brain Circuits ◽  
Brown Adipose ◽  
Skin Cooling ◽  
Trunk Skin ◽  
Coherence Spectrum

In cold defense and fever, activity increases in sympathetic nerves supplying both tail vessels and interscapular brown adipose tissue (iBAT). These mediate cutaneous vasoconstrictor and thermogenic responses, respectively, and both depend upon neurons in the rostral medullary raphé. To examine the commonality of brain circuits driving these two outflows, sympathetic nerve activity (SNA) was recorded simultaneously from sympathetic fibers in the ventral tail artery (tail SNA) and the nerve to iBAT (iBAT SNA) in urethane-anesthetized rats. From a warm baseline, cold-defense responses were evoked by intermittently circulating cold water through a water jacket around the animal's shaved trunk. Repeated episodes of trunk skin cooling decreased core (rectal) temperature. The threshold skin temperature to activate iBAT SNA was 37.3 ± 0.5°C ( n = 7), significantly lower than that to activate tail SNA (40.1 ± 0.4°C; P < 0.01, n = 7). A fall in core temperature always strongly activated tail SNA (threshold 38.3 ± 0.2°C, n = 7), but its effect on iBAT SNA was absent (2 of 7 rats) or weak (threshold 36.9 ± 0.1°C, n = 5). The relative sensitivity to core vs. skin cooling (K-ratio) was significantly greater for tail SNA than for iBAT SNA. Spectral analysis of paired recordings showed significant coherence between tail SNA and iBAT SNA only at 1.0 ± 0.1 Hz. The coherence was due entirely to the modulation of both signals by the ventilatory cycle because it disappeared when the coherence spectrum was partialized with respect to airway pressure. These findings indicate that independent central pathways drive cutaneous vasoconstrictor and thermogenic sympathetic pathways during cold defense.

scholarly journals Impaired developmental microglial pruning of excitatory synapses on CRH-expressing hypothalamic neurons exacerbates stress responses throughout life

2021 ◽  
Author(s):  
Jessica L Bolton ◽  
Annabel K Short ◽  
Shivashankar Othy ◽  
Cassandra L Kooiker ◽  
Manlin Shao ◽  
...  
Keyword(s):  
Stress Responses ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Mental Illnesses ◽  
Excitatory Synapses ◽  
Process Dynamics ◽  
Brain Circuits ◽  
Synapse Density ◽  
And Function

The developmental origins of stress-related mental illnesses are well-established, and early-life stress/adversity (ELA) is an important risk factor. However, it is unclear how ELA impacts the maturation of salient brain circuits, provoking enduring vulnerability to stress and stress-related disorders. Here we find that ELA increases the number and function of excitatory synapses onto stress-sensitive hypothalamic corticotropin-releasing hormone (CRH)-expressing neurons, and implicate disrupted synapse pruning by microglia as a key mechanism. Microglial process dynamics on live imaging, and engulfment of synaptic elements by microglia, were both attenuated in ELA mice, associated with deficient signaling of the microglial phagocytic receptor Mer. Accordingly, selective chemogenetic activation of ELA microglia increased microglial process dynamics and reduced excitatory synapse density to control levels. Selective early-life microglial activation also mitigated the adrenal hypertrophy and prolonged stress responses in adult ELA mice, establishing microglial actions during development as powerful contributors to experience-dependent sculpting of stress-related brain circuits.

scholarly journals Cell type-specific pharmacology of NMDA receptors using masked MK801

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Yunlei Yang ◽  
Peter Lee ◽  
Scott M Sternson
Keyword(s):  
Synaptic Plasticity ◽  
Ion Channels ◽  
Signaling Pathways ◽  
Drug Addiction ◽  
Neuronal Population ◽  
Dopamine Neurons ◽  
Synaptic Potentiation ◽  
Cell Type ◽  
Brain Circuits ◽  
Cell Type Specific

N-Methyl-D-aspartate receptors (NMDA-Rs) are ion channels that are important for synaptic plasticity, which is involved in learning and drug addiction. We show enzymatic targeting of an NMDA-R antagonist, MK801, to a molecularly defined neuronal population with the cell-type-selectivity of genetic methods and the temporal control of pharmacology. We find that NMDA-Rs on dopamine neurons are necessary for cocaine-induced synaptic potentiation, demonstrating that cell type-specific pharmacology can be used to dissect signaling pathways within complex brain circuits.

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