scholarly journals A Runner’s High for New Neurons? Potential Role for Endorphins in Exercise Effects on Adult Neurogenesis

Biomolecules ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1077
Author(s):  
Timothy J. Schoenfeld ◽  
Chance Swanson
Keyword(s):  
Adult Neurogenesis ◽  
Potential Role ◽  
Peptide Hormone ◽  
Hippocampal Neurogenesis ◽  
Behavioral Effects ◽  
Direct Effects ◽  
Brain Health ◽  
Endogenous Opioid ◽  
Beta Endorphin ◽  
Beta Endorphins

Physical exercise has wide-ranging benefits to cognitive functioning and mental state, effects very closely resembling enhancements to hippocampal functioning. Hippocampal neurogenesis has been implicated in many of these mental benefits of exercise. However, precise mechanisms behind these effects are not well known. Released peripherally during exercise, beta-endorphins are an intriguing candidate for moderating increases in neurogenesis and the related behavioral benefits of exercise. Although historically ignored due to their peripheral release and status as a peptide hormone, this review highlights reasons for further exploring beta-endorphin as a key mediator of hippocampal neurogenesis. This includes possible routes for beta-endorphin signaling into the hippocampus during exercise, direct effects of beta-endorphin on cell proliferation and neurogenesis, and behavioral effects of manipulating endogenous opioid signaling. Together, beta-endorphin appears to be a promising mechanism for understanding the specific ways that exercise promotes adult neurogenesis specifically and brain health broadly.

scholarly journals The Entorhinal Cortex and Adult Neurogenesis in Major Depression

2021 ◽  
Vol 22 (21) ◽  
pp. 11725
Author(s):  
Il Bin Kim ◽  
Seon-Cheol Park
Keyword(s):  
Entorhinal Cortex ◽  
Adult Neurogenesis ◽  
Potential Role ◽  
Neural Circuitry ◽  
Hippocampal Neurogenesis ◽  
Dependent Manner ◽  
Hippocampal Function ◽  
Comprehensive Understanding ◽  
Activity Dependent

Depression is characterized by impairments in adult neurogenesis. Reduced hippocampal function, which is suggestive of neurogenesis impairments, is associated with depression-related phenotypes. As adult neurogenesis operates in an activity-dependent manner, disruption of hippocampal neurogenesis in depression may be a consequence of neural circuitry impairments. In particular, the entorhinal cortex is known to have a regulatory effect on the neural circuitry related to hippocampal function and adult neurogenesis. However, a comprehensive understanding of how disruption of the neural circuitry can lead to neurogenesis impairments in depression remains unclear with respect to the regulatory role of the entorhinal cortex. This review highlights recent findings suggesting neural circuitry-regulated neurogenesis, with a focus on the potential role of the entorhinal cortex in hippocampal neurogenesis in depression-related cognitive and emotional phenotypes. Taken together, these findings may provide a better understanding of the entorhinal cortex-regulated hippocampal neurogenesis model of depression.

scholarly journals Stress-Related Dysfunction of Adult Hippocampal Neurogenesis—An Attempt for Understanding Resilience?

2021 ◽  
Vol 22 (14) ◽  
pp. 7339
Author(s):  
Julia Leschik ◽  
Beat Lutz ◽  
Antonietta Gentile
Keyword(s):  
Major Depression ◽  
Adult Neurogenesis ◽  
Current Knowledge ◽  
Functional Relation ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Special Focus ◽  
Extrinsic Cues ◽  
Health And Disease ◽  
Newborn Neurons

Newborn neurons in the adult hippocampus are regulated by many intrinsic and extrinsic cues. It is well accepted that elevated glucocorticoid levels lead to downregulation of adult neurogenesis, which this review discusses as one reason why psychiatric diseases, such as major depression, develop after long-term stress exposure. In reverse, adult neurogenesis has been suggested to protect against stress-induced major depression, and hence, could serve as a resilience mechanism. In this review, we will summarize current knowledge about the functional relation of adult neurogenesis and stress in health and disease. A special focus will lie on the mechanisms underlying the cascades of events from prolonged high glucocorticoid concentrations to reduced numbers of newborn neurons. In addition to neurotransmitter and neurotrophic factor dysregulation, these mechanisms include immunomodulatory pathways, as well as microbiota changes influencing the gut-brain axis. Finally, we discuss recent findings delineating the role of adult neurogenesis in stress resilience.

scholarly journals Does Impairment of Adult Neurogenesis Contribute to Pathophysiology of Alzheimer's Disease? A Still Open Question

2021 ◽  
Vol 13 ◽  
Author(s):  
Domenica Donatella Li Puma ◽  
Roberto Piacentini ◽  
Claudio Grassi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Adult Neurogenesis ◽  
Memory Formation ◽  
Hippocampal Neurogenesis ◽  
Synaptic Function ◽  
Adult Hippocampal Neurogenesis ◽  
Amyloid Β Protein

Adult hippocampal neurogenesis is a physiological mechanism contributing to hippocampal memory formation. Several studies associated altered hippocampal neurogenesis with aging and Alzheimer's disease (AD). However, whether amyloid-β protein (Aβ)/tau accumulation impairs adult hippocampal neurogenesis and, consequently, the hippocampal circuitry, involved in memory formation, or altered neurogenesis is an epiphenomenon of AD neuropathology contributing negligibly to the AD phenotype, is, especially in humans, still debated. The detrimental effects of Aβ/tau on synaptic function and neuronal viability have been clearly addressed both in in vitro and in vivo experimental models. Until some years ago, studies carried out on in vitro models investigating the action of Aβ/tau on proliferation and differentiation of hippocampal neural stem cells led to contrasting results, mainly due to discrepancies arising from different experimental conditions (e.g., different cellular/animal models, different Aβ and/or tau isoforms, concentrations, and/or aggregation profiles). To date, studies investigating in situ adult hippocampal neurogenesis indicate severe impairment in most of transgenic AD mice; this impairment precedes by several months cognitive dysfunction. Using experimental tools, which only became available in the last few years, research in humans indicated that hippocampal neurogenesis is altered in cognitive declined individuals affected by either mild cognitive impairment or AD as well as in normal cognitive elderly with a significant inverse relationship between the number of newly formed neurons and cognitive impairment. However, despite that such information is available, the question whether impaired neurogenesis contributes to AD pathogenesis or is a mere consequence of Aβ/pTau accumulation is not definitively answered. Herein, we attempted to shed light on this complex and very intriguing topic by reviewing relevant literature on impairment of adult neurogenesis in mouse models of AD and in AD patients analyzing the temporal relationship between the occurrence of altered neurogenesis and the appearance of AD hallmarks and cognitive dysfunctions.

scholarly journals Adult neurogenesis in natural populations

2001 ◽  
Vol 79 (4) ◽  
pp. 297-302 ◽  
Author(s):  
R Boonstra ◽  
L Galea ◽  
S Matthews ◽  
J M Wojtowicz
Keyword(s):  
Adult Neurogenesis ◽  
Mammalian Species ◽  
Natural Populations ◽  
Hippocampal Neurogenesis ◽  
Adult Brain ◽  
Biologically Relevant ◽  
Evolutionarily Conserved ◽  
Functional Consequences ◽  
Song Production ◽  
And Function

The dogma that the adult brain produces no new neurons has been overturned, but the critics are still asking, so what? Is adult neurogenesis a biologically relevant phenomenon, or is it perhaps harmful because it disrupts the existing neuronal circuitry? Considering that the phenomenon is evolutionarily conserved in all mammalian species examined to date and that its relevance has been well documented in non-mammalian species, it seems self-evident that neurogenesis in adult mammals must have a role. In birds, it has been established that neurogenesis varies dramatically with seasonal changes in song production. In chickadees, the learning behaviour related to finding stored food is also correlated with seasonal adult neurogenesis. Such studies are still nonexistent in mammals, but the related evidence suggests that neurogenesis does vary seasonally in hamsters and shows sexual differences in meadow voles. To promote studies on natural populations asking fundamental questions of the purpose and function of neurogenesis, we organized a Workshop on "Hippocampal Neurogenesis in Natural Populations" in Toronto in May 2000. The Workshop highlighted recent discoveries in neurogenesis from the lab, and focused on its functional consequences. The consensus at the Workshop was that demonstration of a role for neurogenesis in natural behaviours will ultimately be essential if we are to understand the purpose and function of neurogenesis in humans.Key words: neurogenesis, hippocampus, dentate gyrus, learning, memory, wild population.

Differential Behavioral Effects of Peripheral and Systemic Morphine and Naloxone in a Rat Model of Repeated Acute Inflammation

2001 ◽  
Vol 94 (5) ◽  
pp. 870-875 ◽  
Author(s):  
Serge Perrot ◽  
Gisèle Guilbaud ◽  
Valérie Kayser
Keyword(s):  
Rat Model ◽  
Behavioral Effects ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Peripheral Tissues ◽  
Carrageenan Injection ◽  
Antinociceptive Effects ◽  
Intravenous Morphine ◽  
System Activation ◽  
Sites Of Action

Background It has been reported that opioid antinociceptive effects are enhanced in animal models of inflammation, but it remains unclear whether this sensitization to morphine is related to predominant central or peripheral increased effects. Methods The authors compared the behavioral effects of intraplantar and intravenous morphine and naloxone in a rat model of repeated acute carrageenan-induced inflammation in which enhanced responses to noxious stimuli result from sensitization in peripheral tissues or central sensitization. The antinociceptive effects of intraplantar morphine (50, 75, 100, 150, and 200 microg), intravenous morphine (0.3, 0.6, and 1 mg/kg), and the pronociceptive effects of intraplantar naloxone methiodide (150 microg) and intravenous naloxone (1 mg/kg) against noxious pressure (vocalization thresholds to paw pressure) in rats were assessed 3 h after one or two carrageenan plantar injections performed 7 days apart. Results After the first carrageenan injection, intraplantar and intravenous morphine produced significant increase of vocalization thresholds to paw pressure in inflamed but not in noninflamed paws. After the second carrageenan injection, the antinociceptive effects of intraplantar morphine were significantly reduced compared with those obtained after the first carrageenan injection, whereas effects of intravenous morphine were significantly enhanced and present in both hind paws. Intravenous naloxone demonstrated similar pronociceptive patterns after the first and second carrageenan injection. Intraplantar naloxone methiodide produced pronociceptive effects in inflamed hind paw that were significantly enhanced after the second carrageenan injection. Conclusions When inflammation is enhanced by recurrent stimulations, the antinociceptive effects of systemic morphine are enhanced. This increase is more likely related to central than peripheral sites of action, beyond endogenous opioid system activation.

scholarly journals Developmental exposure to diesel exhaust upregulates transcription factor expression, decreases hippocampal neurogenesis, and alters cortical lamina organization: relevance to neurodevelopmental disorders

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Toby B. Cole ◽  
Yu-Chi Chang ◽  
Khoi Dao ◽  
Ray Daza ◽  
Robert Hevner ◽  
...  
Keyword(s):  
Adult Neurogenesis ◽  
Diesel Exhaust ◽  
Neurodevelopmental Disorders ◽  
Autism Spectrum ◽  
Hippocampal Neurogenesis ◽  
Behavioral Alterations ◽  
Developmental Exposure ◽  
Males And Females ◽  
Male Specific ◽  
Transcription Factor Expression

Abstract Background Exposure to traffic-related air pollution (TRAP) during development and/or in adulthood has been associated in many human studies with both neurodevelopmental and neurodegenerative diseases, such as autism spectrum disorder (ASD) and Alzheimer’s disease (AD) or Parkinson’s disease (PD). Methods In the present study, C57BL/6 J mice were exposed to environmentally relevant levels (250+/−50 μg/m3) of diesel exhaust (DE) or filtered air (FA) during development (E0 to PND21). The expression of several transcription factors relevant for CNS development was assessed on PND3. To address possible mechanistic underpinnings of previously observed behavioral effects of DE exposure, adult neurogenesis in the hippocampus and laminar organization of neurons in the somatosensory cortex were analyzed on PND60. Results were analyzed separately for male and female mice. Results Developmental DE exposure caused a male-specific upregulation of Pax6, Tbr1, Tbr2, Sp1, and Creb1 on PND3. In contrast, in both males and females, Tbr2+ intermediate progenitor cells in the PND60 hippocampal dentate gyrus were decreased, as an indication of reduced adult neurogenesis. In the somatosensory region of the cerebral cortex, laminar distribution of Trb1, calbindin, and parvalbumin (but not of Ctip2 or Cux1) was altered by developmental DE exposure. Conclusions These results provide additional evidence to previous findings indicating the ability of developmental DE exposure to cause biochemical/molecular and behavioral alterations that may be involved in neurodevelopmental disorders such as ASD.

Preliminary Studies on Bemitradine-Induced Cardiotoxicity in Female Rats

1991 ◽  
Vol 10 (5) ◽  
pp. 511-523 ◽  
Author(s):  
S. Levin ◽  
D. Semler ◽  
S. Gad ◽  
E. Burton ◽  
G. Walsh ◽  
...  
Keyword(s):  
Potential Role ◽  
The Other ◽  
Female Rats ◽  
Separate Experiment ◽  
Direct Effects ◽  
Primary Metabolite ◽  
T Wave ◽  
Mixed Function Oxidases ◽  
Circulating Levels

The mechanism of bemitradine (SC-33643) cardiotoxicity in female rats was investigated in the set of preliminary experiments reported here. Specifically, the involvement of bemitradine metabolites and the potential role of adrenal epinephrine release were examined. Desethylbemi-tradine (the primary metabolite of bemitradine) was shown to be cardiotoxic at oral dosages greater than 300 mg/kg for 7 days. In a separate experiment, a major metabolite (bemitradine glycol) unique to the rat was not cardiotoxic at dosages up to 600 mg/kg for 7 days. Treatment of rats with SKF 525-A enhanced the lethality and the cardiotoxicity of bemitradine. In contrast, prior treatments of rats with phenobarbital resulted in decreased cardiotoxicity of both bemitradine and desethylbemitradine (a bemitradine metabolite presumably further metabolized by the microsomal mixed function oxidases). In other independent experiments, bemitradine-induced cardiotoxicity was shown to be accompanied by adrenal damage and decreases in adrenal epinephrine. Propranolol (a β-antagonist) treatment protected rats against cardiotoxicity. Bemitradine also had a direct effect on the heart, as evidenced in an experiment in which bemitradine caused dose-related increases in the T-wave of the rat ECG complex. These data suggest that (1) both bemitradine and desethylbemitradine may be responsible for the cardiotoxicity, and the other downstream metabolites are not and (2) cardiotoxicity may be due to the combination of direct effects of bemitradine on the rat heart and the bemitradine-mediated release of adrenal epinephrine (a known cardiotoxin at high circulating levels).

Plasma Beta-Endorphin Concentrations in People with Learning Disability and Self-Injurious and/or Autistic Behaviour

1996 ◽  
Vol 168 (1) ◽  
pp. 105-109 ◽  
Author(s):  
Sophie H. N. Willemsen-Swinkels ◽  
Jan K. Buitelaar ◽  
Florence G. Weijnen ◽  
Jos H. H. Thijssen ◽  
Herman Van Engeland
Keyword(s):  
Learning Disability ◽  
Learning Disabled ◽  
Opioid System ◽  
Disabled People ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Beta Endorphin ◽  
Functional Disturbances ◽  
Autistic Behaviour ◽  
Opioid Systems

BackgroundIt has been suggested that the key variable in reduced plasma immunoreactive β-endorphin concentrations in autistic subjects may be concomitant self-injurious behaviour.MethodWe studied morning levels of plasma β-endorphin in 33 learning disabled people with self-injurious and/or autistic behaviour.ResultsThe β-endorphin level of the subjects with severe self-injurious behaviour proved to be significantly lower than that of autistic subjects without severe self-injurious behaviour (3.6 (1.4) pmol/l v. 5.8 (4.3) pmol/l; t-test: P = 0.045. Replication: 3.7 (1.1) pmol/l v. 5.7 (3.8) pmol/l; t-test P = 0.043). Individuals with mild and occasional self-injurious behaviour were found to have β-endorphin levels comparable to those without self-injurious behaviour. Further, subjects being treated with neuroleptics had lower β-endorphin levels than untreated subjects.ConclusionsThese results stress that in any study of opioid systems of learning disabled people, it is very important to differentiate between people with and without severe self-injurious behaviour. The results support the idea that severe self-injurious behaviour may be related to functional disturbances in the endogenous opioid system.

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