Local Stress-Limiting Systems and their Cardioprotective Effects
Felix Z. Meerson, Alexander V. Galkin in Adaptive Protection of The Heart: Protecting Against Stress and Ischemic Damage, 2019
At the same time it is important to remember that adenosine not only modulates the regulation of the executive organs, but is also active in the central nervous system as well, where it is present at high concentrations and its receptors and binding sites are abundant in various brain regions: hippocampus, cerebellum, hypothalamus, etc.114,115,134 At present the adenosinergic system is regarded as a chief modulator of neuronal function. It mainly acts to impede neurotransmission by suppressing the release of neuromediators through the A1 and A2 receptors located on the axonal presynaptic membrane.113,114,127,140 Besides, neuronal inhibition by adenosine has also been observed at the postsynaptic membrane level.127,140 These data come from experiments with exogenous adenosine and its receptor agonists; however, convincing evidence is available that the same holds true for the endogenous mechanism (see Jackisch113 for references).
Overview of Neurotransmission: Relationship to the Action of Antiepileptic Drugs
Carl L. Faingold, Gerhard H. Fromm in Drugs for Control of Epilepsy:, 2019
Although adenosine can be taken up by synaptosomes and released following depolarization, there is no evidence that adenosine is stored in synaptic vesicles like the neurotransmitters we have considered above. Moreover, the release of adenosine appears to be calcium independent,120 although both calcium-dependent and calcium-independent release have apparently been reported.141 Unlike most established neurotransmitters, adenosine is apparently released from postsynaptic membranes, axons, and glial cells, in addition to nerve terminals.120 No clearcut adenosinergic pathways have been established in brain, although there is a regional variation in the concentration of adenosine and some adenosine-deaminase-rich neurons have been found in the basal hypothalamus.120 The pool from which adenosine is released on stimulation has not been identified.
Conducting the Investigative Interview
Darrell L. Ross, Gary M. Vilke in Guidelines for Investigating Officer-Involved Shootings, Arrest-Related Deaths, and Deaths in Custody, 2018
How might rest contribute to more complete and accurate eyewitness recall? One hypothesis is that REM (rapid eye movement) sleep plays an important role in the consolidation of memories (see Stickgold, 2005 for a review) and therefore recall should be more complete following sleep. It is well known that stress can typically cause an increase in cortisol (hormone) and while it is thought that cortisol may sometimes enhance the formation of memories, it has been found that the remaining presence of increased cortisol can impair memory retrieval (Ackerman et al., 2013). Recent research also suggests that sleep deprivation may contribute to the generation of false memories (Fenn et al., 2009). Interestingly, the generation of false memories caused by sleep deprivation has been found to be largely reversed with the administration of caffeine, “indicating that adenosinergic mechanisms can contribute to the generation of false memories associated with sleep loss” (Diekelmann et al., 2008).
Amyloid beta (1–42) downregulates adenosine-2b receptors in addition to mitochondrial impairment and cholinergic dysfunction in memory-sensitive mouse brain regions
Published in Journal of Receptors and Signal Transduction, 2020
Bhupesh Chandra Semwal, Debapriya Garabadu
Adenosine is an endogenous purine nucleoside, formed from the metabolism of adenosine triphosphate (ATP) and exerts several functions in the brain through adenosinergic receptors [13]. Recently, caffeine, a nonselective adenosinergic drug, is reported to improve the cognitive function and reduce the Aβ aggregation in the AD-like animals [14,15]. It has also been documented that the adenosine receptor agonist exerts neuroprotection [16] and attenuates the mitochondrial oxidative stress by decreasing superoxide generation in experimental animals [17]. Additionally, it is reported that the activation of the A2b receptor exerts anti-inflammatory effect in the central nervous system of the animals [18,19]. However, there is no report about the involvement of A2b receptors in the pathophysiology of Aβ-induced AD-like manifestations.
The synchrony effect revisited: chronotype, time of day and cognitive performance in a semantic analogy task
Published in Chronobiology International, 2018
Kati Nowack, Elke Van Der Meer
Here, further research is necessary to investigate the cognitive effects of chronic sleep deprivation as well as associated biological factors such as the role of adenosinergic mechanisms thought to be involved in regulating the sleep-wake cycle, arousal, vigilance and attention (e.g. Urry & Landolt, 2014). Serotonic functioning has not only been associated with wakefulness, fluid intelligence and executive functioning necessary for analogic reasoning (Oishi & Lazarus,2017; Payton et al. 2005). Evidence also links eveningness to more aggressive and impulsive behavioural tendencies associated with lower serotonin levels (e.g. Brunner and Hen 1997; Goldstein et al. 2007; Pattij and Vanderschuren 2008). However, biological factors linked to time of day and social jetlag were not assessed in the current study. Likewise, investigating the impact of chronotype on the synchrony effect with university students only as well as the small sample size limits the generalisability of our results. Hypotheses arising from the current findings should (and will) be tested in a representative sample involving independent populations of all ages and educational backgrounds.
Optimizing sleep across the menopausal transition
Published in Climacteric, 2023
Work in animal models shows that ovarian hormones, including estradiol, regulate female sleep [70]. However, the underlying neurobiological substrates, mechanisms and pathways remain unknown [71], and further work is needed to define the neural circuits involved [72], considering circadian timing and reproductive stage, especially given some of the paradoxical effects [73] of estradiol on sleep–wake behavior in rodents versus women. Estradiol is a neuroactive steroid and there are estrogen receptors in sleep and arousal-regulating nuclei, including the preoptic area of the hypothalamus, suprachiasmatic nucleus and locus coeruleus [71]. Estradiol (and other hormones of the hypothalamic pituitary ovarian axis), therefore, may influence sleep–wake regulation directly, for example by influencing adenosinergic actions in the preoptic area (a sleep-promoting nucleus) to affect sleep homeostasis [73] or by influencing arousal systems in the lateral hypothalamus (rich in hypocretin-releasing neurons, which promote wakefulness) [71], or the locus coeruleus (primary site of norepinephrine, involved in arousal) [71]. Estradiol could also act indirectly to influence sleep via other systems, including thermosensory and thermoregulatory sites in the hypothalamus, which overlap with sleep-active sites [74].
Related Knowledge Centers
- Adenosine
- Adenosine Receptor Agonist
- Adenosine Receptor Antagonist
- Caffeine
- Dopaminergic
- Gabaergic
- Adenosine Reuptake Inhibitor
- Cannabinoidergic
- Cholinergic
- Glycinergic