scholarly journals Chronic methamphetamine uncovers a circadian rhythm in multiple-unit neural activity in the dorsal striatum which is independent of the suprachiasmatic nucleus

2021 ◽  
pp. 100070
Author(s):  
Shota Miyazaki ◽  
Yu Tahara ◽  
Christopher S. Colwell ◽  
Gene D. Block ◽  
Wataru Nakamura ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Suprachiasmatic Nucleus ◽  
Neural Activity ◽  
Dorsal Striatum ◽  
Multiple Unit

Neural activity in the dorsal striatum during cognitive decision making

2010 ◽  
Vol 68 ◽  
pp. e299
Author(s):  
Satoshi Nonomura ◽  
Kazuyuki Samejima ◽  
Kenji Doya ◽  
Jun Tanji
Keyword(s):  
Decision Making ◽  
Neural Activity ◽  
Dorsal Striatum ◽  
Cognitive Decision

Circadian rhythm and response to light of extracellular glutamate and aspartate in rat suprachiasmatic nucleus

1996 ◽  
Vol 271 (3) ◽  
pp. R579-R585 ◽  
Author(s):  
S. Honma ◽  
Y. Katsuno ◽  
K. Shinohara ◽  
H. Abe ◽  
K. Honma
Keyword(s):  
Circadian Rhythm ◽  
Suprachiasmatic Nucleus ◽  
Light Pulse ◽  
Continuous Light ◽  
In Vivo Microdialysis ◽  
Dark Phase ◽  
Dark Cycle ◽  
Complete Darkness ◽  
Endogenous Circadian Rhythm

Extracellular concentrations of glutamate and aspartate were measured in the vicinity of rat suprachiasmatic nucleus (SCN) by means of in vivo microdialysis. The concentrations of both excitatory amino acids (EAAs) were higher during the dark phase than during the light under the light-dark cycle, showing pulsatile fluctuations throughout the day. When rats were released into the complete darkness, the 24-h pattern in the aspartate continued for at least one cycle, whereas that in the glutamate disappeared. The nocturnal increases in the EAA levels were not due to the increase of locomotor activity during the nighttime, because the 24-h rhythms were also detected in animals under urethan anesthesia. The patterns of extracellular EAA levels were changed when rats were released into the continuous light. Circadian rhythm was not detected in the glutamate, whereas the 24-h pattern was maintained in the aspartate with the levels increased to various extents. A 30-min light pulse given either at zeitgber time (ZT) 1 or ZT 13 elevated the EAA levels during the latter half of the light pulse, except glutamate by a pulse at ZT 1. The extracellular EAA levels in the vicinity of the rat SCN showed the circadian rhythm with a nocturnal peak and increased in response to the continuous light and a brief light pulse. The aspartate level is considered to be regulated by the endogenous circadian rhythm, but the glutamate levels seems to be modified by the light-dark cycle.

scholarly journals Forebrain NgR1 Overexpression Impairs DA Release Suggesting Synergy of Local and Global Synaptic Plasticity Mechanisms

2020 ◽  
Vol 12 ◽  
Author(s):  
Emma Arvidsson ◽  
Sarolta Gabulya ◽  
Alvin Tore Brodin ◽  
Tobias Erik Karlsson ◽  
Lars Olson
Keyword(s):  
Synaptic Plasticity ◽  
Potassium Chloride ◽  
Neural Activity ◽  
Dorsal Striatum ◽  
Inverse Correlation ◽  
Long Term Memory ◽  
The Status ◽  
Global Systems ◽  
Da Release

Structural synaptic reorganizations needed to permanently embed novel memories in the brain involve complex plasticity-enhancing and plasticity-inhibiting systems. Increased neural activity is linked to rapid downregulation of Nogo receptor 1 (NgR1), needed to allow local structural synaptic plasticity. This local regulation of plasticity is thought to be moderated by global systems, such as the ascending cholinergic and monoaminergic systems, adding significance to locally increased neural activity. Here we address the reverse possibility that the global systems may also be influenced by the status of local plasticity. Using NgR1-overexpressing mice, with impaired plasticity and long-term memory, we measured the ability to release dopamine (DA), implicated in regulating plasticity and memory. In vivo chronoamperometric recording with high temporal and spatial resolution revealed severe impairment of potassium chloride (KCl)-induced increase of extracellular DA in the dorsal striatum of mice overexpressing NgR1 in forebrain neurons. A similar, but lesser, impairment of DA release was seen following amphetamine delivery. In contrast, potassium chloride-evoked DA release in NgR1 knockout (KO) mice led to increased levels of extracellular DA. That NgR1 can impair DA signaling, thereby further dampening synaptic plasticity, suggests a new role for NgR1 signaling, acting in synergy with DA signaling to control synaptic plasticity.Significance Statement:The inverse correlation between local NgR1 levels and magnitude of KCl-inducible amounts of DA release in the striatum reinforces the rule of NgR1 as a regulator of structural synaptic plasticity and suggests synergy between local and global plasticity regulating systems.

scholarly journals Astrocytic Modulation of Neuronal Activity in the Suprachiasmatic Nucleus: Insights from Mathematical Modeling

2020 ◽  
Vol 35 (3) ◽  
pp. 287-301
Author(s):  
Natthapong Sueviriyapan ◽  
Chak Foon Tso ◽  
Erik D. Herzog ◽  
Michael A. Henson
Keyword(s):  
Circadian Rhythm ◽  
Suprachiasmatic Nucleus ◽  
Neuronal Activity ◽  
Clock Genes ◽  
Rhythmic Activity ◽  
Neuronal Population ◽  
Circadian Period ◽  
Circadian Oscillators ◽  
Bidirectional Interactions ◽  
The Impact

The suprachiasmatic nucleus (SCN) of the hypothalamus consists of a highly heterogeneous neuronal population networked together to allow precise and robust circadian timekeeping in mammals. While the critical importance of SCN neurons in regulating circadian rhythms has been extensively studied, the roles of SCN astrocytes in circadian system function are not well understood. Recent experiments have demonstrated that SCN astrocytes are circadian oscillators with the same functional clock genes as SCN neurons. Astrocytes generate rhythmic outputs that are thought to modulate neuronal activity through pre- and postsynaptic interactions. In this study, we developed an in silico multicellular model of the SCN clock to investigate the impact of astrocytes in modulating neuronal activity and affecting key clock properties such as circadian rhythmicity, period, and synchronization. The model predicted that astrocytes could alter the rhythmic activity of neurons via bidirectional interactions at tripartite synapses. Specifically, astrocyte-regulated extracellular glutamate was predicted to increase neuropeptide signaling from neurons. Consistent with experimental results, we found that astrocytes could increase the circadian period and enhance neural synchronization according to their endogenous circadian period. The impact of astrocytic modulation of circadian rhythm amplitude, period, and synchronization was predicted to be strongest when astrocytes had periods between 0 and 2 h longer than neurons. Increasing the number of neurons coupled to the astrocyte also increased its impact on period modulation and synchrony. These computational results suggest that signals that modulate astrocytic rhythms or signaling (e.g., as a function of season, age, or treatment) could cause disruptions in circadian rhythm or serve as putative therapeutic targets.

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