Phasic Activity of the Basolateral Amygdala, Cingulate Gyrus, and Hippocampus During REM Sleep in the Cat

Stress-related sleep disturbances are distressing clinical symptoms in posttraumatic stress disorder patients. Intensely stressful events and their memories change rapid eye movement (REM) sleep in animal models. REM sleep varies with individual differences of stress resilience or vulnerability. The basolateral amygdala (BLA) is a primary mediator of the effects of stress and fear memories on sleep. However, the molecular mechanisms in BLA regulating the effects of fear conditioning, shock training (ST) and context re-exposure (CTX) on REM sleep are not well known. MicroRNAs (miRNAs) are small, non-coding RNAs and posttranscriptional gene regulators of diverse biological processes. The aim of this study is to investigate ST- and CTX-altered miRNAs in the BLA of resilience and vulnerable animals and on REM sleep regulation. MiRNAs expression profiles in BLA were generated following ST and CTX using the Taqman Low Density rodent microRNA array. The altered BLA miRNAs expression and REM sleep reduction observed in ST and CTX vulnerable animals. AntagomiR-221 microinjection into BLA for one of the upregulated miRNAs, miR-221 in BLA, attenuated the REM sleep reduction. This study suggests that miRNAs in the BLA may play a significant role in mediating the effects of stress and fear memories on REM sleep.

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Visual cortical units associated with phasic activity in REM sleep and wakefulness

Brain Research ◽

10.1016/0006-8993(73)90298-9 ◽

1973 ◽

Vol 55 (2) ◽

pp. 323-331 ◽

Cited By ~ 15

Author(s):

Takuji Kasamatsu ◽

W. Ross Adey

Keyword(s):

Rem Sleep ◽

Phasic Activity ◽

Visual Cortical

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Fluoxetine-induced recovery of serotonin and norepinephrine projections in a mouse model of post-stroke depression

Translational Psychiatry ◽

10.1038/s41398-020-01008-9 ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Amin Zahrai ◽

Faranak Vahid-Ansari ◽

Mireille Daigle ◽

Paul R. Albert

Keyword(s):

Nucleus Accumbens ◽

Basolateral Amygdala ◽

Chronic Treatment ◽

Memory Deficits ◽

Cingulate Gyrus ◽

Axonal Plasticity ◽

Post Stroke ◽

Antidepressant Effects ◽

Post Stroke Depression

Abstract Chronic treatment with fluoxetine (FLX) is required for its antidepressant effects, but the role of serotonin (5-HT) axonal plasticity in FLX action is unknown. To address this, we examined mice with a stroke in the left medial prefrontal cortex (mPFC) resulting in persistent anxiety-like and depression-like behaviors and memory deficits as a model of post-stroke depression. Chronic treatment with FLX (but not exercise) completely reversed the behavioral phenotype and partially reversed changes in FosB-labeled cells in the mPFC, nucleus accumbens, septum, hippocampus, basolateral amygdala (BLA), and dorsal raphe. In these regions, 5-HT or norepinephrine (NE) innervation was quantified by staining for 5-HT or NE transporters, respectively. 5-HT synapses and synaptic triads were identified as synaptophysin-stained sites on 5-HT axons located proximal to gephyrin-stained or PSD95-stained spines. A week after stroke, 5-HT innervation was greatly reduced at the stroke site (left cingulate gyrus (CG) of the mPFC) and the left BLA. Chronically, 5-HT and NE innervation was reduced at the left CG, nucleus accumbens, and BLA, with no changes in other regions. In these areas, pre-synaptic and post-synaptic 5-HT synapses and triads to inhibitory (gephyrin+) sites were reduced, while 5-HT contacts at excitatory (PSD95+) sites were reduced in the CG and prelimbic mPFC. Chronic FLX, but not exercise, reversed these reductions in 5-HT innervation but incompletely restored NE projections. Changes in 5-HT innervation were verified using YFP staining in mice expressing YFP-tagged channelrhodopsin in 5-HT neurons. Thus, FLX-induced 5-HT axonal neuroplasticity of forebrain projections may help mediate recovery from brain injury.

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Linkage between brain blood flow and respiratory drive during rapid-eye-movement sleep

Journal of Applied Physiology ◽

10.1152/jappl.1988.64.4.1457 ◽

1988 ◽

Vol 64 (4) ◽

pp. 1457-1465 ◽

Cited By ~ 14

Author(s):

R. A. Parisi ◽

J. A. Neubauer ◽

M. M. Frank ◽

T. V. Santiago ◽

N. H. Edelman

Keyword(s):

Blood Flow ◽

Eye Movement ◽

Rem Sleep ◽

Emg Activity ◽

Respiratory Drive ◽

Brain Blood Flow ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep ◽

Inspiratory Time ◽

Phasic Activity

The correlation between brain blood flow (BBF) and respiratory neuromotor output, as reflected by diaphragmatic electromyogram (EMG) activity (EMGdi), was studied during wakefulness, rapid-eye-movement (REM) sleep, and non-REM sleep (NREM). Compared with the awake state, mean BBF increased by 4.7% during NREM and by 32.6% during REM (P less than 0.001). Also, surges of BBF during REM occurred during periods of intense phasic activity. EMGdi [peak and peak/inspiratory time (TI)] was highly variable within REM periods but fluctuated as a reciprocal function of simultaneously measured BBf (r = -0.49, P less than 0.001). Furthermore, mean EMGdipeak decreased from NREM to REM in a manner reciprocally related to the corresponding change in BBF (r = -0.77, P = 0.015). These findings suggest that a component of the reduction of respiratory neuromotor output during REM is attributable to increased BBF with consequent relative hypocapnia in the central chemoreceptor environment.

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