Selective Rapid Eye Movement Sleep Deprivation Affects Cell Size and Number in Kitten Locus Coeruleus

Abstract

Cells in the locus coeruleus (LC) constitute the sole source of norepinephrine (NE) in the brain and change their discharge rates according to vigilance state. In addition to its well established role in vigilance, NE affects synaptic plasticity in the postnatal critical period (CP) of development. One form of CP synaptic plasticity affected by NE results from monocular occlusion, which leads to physiological and cytoarchitectural alterations in central visual areas. Selective suppression of rapid eye movement sleep (REMS) in the CP kitten enhances the central effects of monocular occlusion. The mechanisms responsible for heightened cortical plasticity following REMS deprivation (REMSD) remain undetermined. One possible mediator of an increase in plasticity is continuous NE outflow, which presumably persists during extended periods of REMSD. Tyrosine hydroxylase (TH) is the rate-limiting enzyme in the synthesis of NE and serves as a marker for NE-producing cells. We selectively suppressed REMS in kittens for 1 week during the CP. The number and size of LC cells expressing immunoreactivity to tyrosine hydroxylase (TH-ir) was assessed in age-matched REMS-deprived (RD)-, treatment–control (TXC)-, and home cage-reared (HCC) animals. Sleep amounts and slow wave activity (SWA) were also examined relative to baseline. Time spent in REMS during the study was lower in RD compared to TXC animals, and RD kittens increased SWA delta power in the latter half of the REMSD period. The estimated total number of TH-ir cells in LC was significantly lower in the RD than in the TXC kittens and numerically lower than in the HCC animals. The size of LC cells expressing TH-ir was greatest in the HCC group. HCC cells were significantly larger than TH-ir cells in the RD kittens. These data are consistent with presumed reduction in NE in forebrain areas, including visual cortex, caused by 1 week of REMSD.

Sleep-Dependent Oscillatory Synchronization: A Role in Fear Memory Consolidation

“…More specifically, phasic activity during REM sleep and spindle activity during non-REM sleep has been heavily implicated in successful memory consolidation (Datta, 2000 ; Datta et al, 2004 ; Girardeau et al, 2009 ; Fogel and Smith, 2011 ). These effects on memory have been largely attributed to changes in neuronal plasticity, such as long-term potentiation (LTP), long-term depression (LTD), and other cellular modifications (Bramham et al, 1994 ; Datta et al, 2008 ; Shaffery et al, 2012 ; Dumoulin Bridi et al, 2015 ; Frank, 2015 ; Hennies et al, 2016 ; Ravassard et al, 2016 ; Li et al, 2017 ). Despite this knowledge, the mechanisms by which sleep facilitates memory consolidation remains to be completely understood.…”

Activation of brain‐derived neurotrophic factor‐tropomyosin receptor kinase B signaling in the pedunculopontine tegmental nucleus: a novel mechanism for the homeostatic regulation of rapid eye movement sleep

“…; Shaffery et al . ; Kocsis ). In addition, REM sleep homeostatic regulation has been linked to emotional regulation, memory consolidation, and cognitive function (Smith ; Datta ; Poe et al .…”

Effects of Estradiol Valerate and Remifemin on Norepinephrine Signaling in the Brain of Ovariectomized Rats

“…Low estrogen levels reduced the AOD of noradrenergic fibers and the expressions of α 1 -adrenoreceptor and ERα in the POAH, which might cause abnormal thermoregulation in OVX rats. Noradrenergic neurons located in the LC and A1/A2 were the sources of norepinephrine in the brain [15,33], and they projected ascending afferent norepinephrine fibers to the hypothalamus. In order to further confirm the projection to the POAH, CTB retrograde tracer was injected into the VMPO, and the CTB-labeled neurons in the LC were adrenergic neurons.…”