Female sexual behaviors in rodents (lordosis and appetitive or "proceptive" behaviors) are induced through a genomic mechanism by the sequential actions of estradiol (E2) and progesterone (P), or E2 and testosterone (T) at their respective receptors. However, non-steroidal agents, such as gonadotropin-releasing hormone (GnRH), Prostaglandin E2 (PGE2), noradrenaline, dopamine, oxytocin, α-melanocyte stimulating hormone, nitric oxide, leptin, apelin, and others, facilitate different aspects of female sexual behavior through their cellular and intracellular effects at the membrane and genomic levels in ovariectomized rats primed with E2. These neurotransmitters often act as intermediaries of E2 and P (or T). The classical model of steroid hormone action through intracellular receptor binding has been complemented by an alternative scenario wherein the steroid functions as a transcription factor after binding the receptor protein to DNA. Another possible mechanism occurs through the activation of second messenger systems (cyclic AMP, cyclic GMP, calcium), which subsequently initiate phosphorylation events via diverse kinase systems (protein kinases A, G, or C). These kinases target the progesterone receptor (PR) or associated effector proteins that connect the PR to the trans-activation machinery. This may also happen to the androgen receptor (AR). In addition, other cellular mechanisms could be involved since the chemical structure of these non-steroidal agents causes a change in their lipophobicity that prevents them from penetrating the cell and exerting direct transcriptional effects; however, they can exert effects on different components of the cell membrane activating a cross-talk between the cell membrane and the regulation of the transcriptional mechanisms.
BACKGROUND: Subjective cognitive decline (SCD) is a risk factor for future cognitive impairment and dementia. It is uncertain whether the neurodegeneration of the cholinergic system is already present in SCD individuals. We aimed to review the current evidence about the association between SCD and biomarkers of degeneration in the cholinergic system. METHOD: Original articles were extracted from three databases: Pubmed, Web of Sciences, and Scopus, in January 2023. Two researchers screened the studies independently. RESULTS: A total of 11 research articles were selected. SCD was mostly based on amnestic cognitive complaints. Cholinergic system biomarkers included neuroimaging markers of basal forebrain volume, functional connectivity, transcranial magnetic stimulation, or biofluid. The evidence showed associations between basal forebrain atrophy, poorer connectivity of the cholinergic system, and SCD CONCLUSIONS: Degenerative changes in the cholinergic system can be present in SCD. Subjective complaints may help when identifying individuals with brain changes that are associated with cognitive impairment. These findings may have important implications in targeting individuals that may benefit from cholinergic-target treatments at very early stages of neurodegenerative diseases.
- MeSH
- Alzheimerova nemoc * MeSH
- biologické markery MeSH
- cholinergní látky MeSH
- kognitivní dysfunkce * diagnostické zobrazování MeSH
- lidé MeSH
- magnetická rezonanční tomografie MeSH
- neurozobrazování metody MeSH
- pars basalis telencephali * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- systematický přehled MeSH
Apart from its role in motor coordination, the importance of the cerebellum in cognitive and affective processes has been recognized in the past few decades. Spinocerebellar ataxias (SCA) and Friedreich ataxia (FRDA) are rare neurodegenerative diseases of the cerebellum presenting mainly with a progressive loss of gait and limb coordination, dysarthria, and other motor disturbances, but also a range of cognitive and neuropsychiatric symptoms. This narrative review summarizes the current knowledge on neuropsychiatric impairment in SCA and FRDA. We discuss the prevalence, clinical features and treatment approaches in the most commonly reported domains of depression, anxiety, apathy, agitation and impulse dyscontrol, and psychosis. Since these symptoms have a considerable impact on patients' quality of life, we argue that further research is mandated to improve the detection and treatment options of neuropsychiatric co-morbidities in ataxia patients.
- MeSH
- Friedreichova ataxie * komplikace MeSH
- komorbidita MeSH
- kvalita života MeSH
- lidé MeSH
- mozeček MeSH
- spinocerebelární ataxie * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
Habituation is the most fundamental form of learning. As a firewall that protects our brain from sensory overload, it is indispensable for cognitive processes. Studies in humans and animal models provide increasing evidence that habituation is affected in autism and related monogenic neurodevelopmental disorders (NDDs). An integrated application of habituation assessment in NDDs and their animal models has unexploited potential for neuroscience and medical care. With the aim to gain mechanistic insights, we systematically retrieved genes that have been demonstrated in the literature to underlie habituation. We identified 258 evolutionarily conserved genes across species, describe the biological processes they converge on, and highlight regulatory pathways and drugs that may alleviate habituation deficits. We also summarize current habituation paradigms and extract the most decisive arguments that support the crucial role of habituation for cognition in health and disease. We conclude that habituation is a conserved, quantitative, cognition- and disease-relevant process that can connect preclinical and clinical work, and hence is a powerful tool to advance research, diagnostics, and treatment of NDDs.
Animals and humans share similar reactions to the effects of addictive substances, including those of their brain networks to drugs. Our review focuses on simple invertebrate models, particularly the honeybee (Apis mellifera), and on the effects of drugs on bee behaviour and brain functions. The drug effects in bees are very similar to those described in humans. Furthermore, the honeybee community is a superorganism in which many collective functions outperform the simple sum of individual functions. The distribution of reward functions in this superorganism is unique - although sublimated at the individual level, community reward functions are of higher quality. This phenomenon of collective reward may be extrapolated to other animal species living in close and strictly organised societies, i.e. humans. The relationship between sociality and reward, based on use of similar parts of the neural network (social decision-making network in mammals, mushroom body in bees), suggests a functional continuum of reward and sociality in animals.
In classical neuroscience, Dale ́s principle postulates that neuronal identity is conferred by the specific neurotransmitter that it releases. However, the brain might be more tractable to specific situations regardless of specific specialisation which may contradict this principle. Hence, this constrained approach of how we perceive and study the nervous system must be revisited and revised, specifically by studying the dopaminergic system. We presume a relatively flexible change in the dopaminergic system due to neuronal activity or environmental changes. While the parallel between the reward system of mammals and insects is generally well accepted, herein, we extend the idea that the insect nervous system might also possess incredible plasticity, similar to the mammalian system. In this review, we critically evaluate the available information about the reward system in vertebrates and invertebrates, emphasising the dopaminergic neuronal plasticity, a challenge to the classical Dale's principle. Thus, neurotransmitter switching significantly disrupts the static idea of neural network organisation and suggests greater possibilities for a dynamic response to the current life context of organisms.
- MeSH
- dopamin MeSH
- dopaminergní neurony fyziologie MeSH
- Drosophila melanogaster fyziologie MeSH
- Drosophila * fyziologie MeSH
- houbová tělesa * fyziologie MeSH
- lidé MeSH
- neurotransmiterové látky fyziologie MeSH
- savci MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
The fruit fly Drosophila melanogaster brain is the most extensively investigated model of a reward system in insects. Drosophila can discriminate between rewarding and punishing environmental stimuli and consequently undergo associative learning. Functional models, especially those modelling mushroom bodies, are constantly being developed using newly discovered information, adding to the complexity of creating a simple model of the reward system. This review aims to clarify whether its reward system also includes a hedonic component. Neurochemical systems that mediate the 'wanting' component of reward in the Drosophila brain are well documented, however, the systems that mediate the pleasure component of reward in mammals, including those involving the endogenous opioid and endocannabinoid systems, are unlikely to be present in insects. The mushroom body components exhibit differential developmental age and different functional processes. We propose a hypothetical hierarchy of the levels of reinforcement processing in response to particular stimuli, and the parallel processes that take place concurrently. The possible presence of activity-silencing and meta-satiety inducing levels in Drosophila should be further investigated.
- MeSH
- Drosophila melanogaster * MeSH
- Drosophila * MeSH
- houbová tělesa MeSH
- odměna MeSH
- posilování (psychologie) MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
There has been an accumulation of knowledge about the human microbiome, some detailed investigations of the gastrointestinal microbiota and its functions, and the highlighting of complex interactions between the gut, the gut microbiota, and the central nervous system. That assumes the involvement of the microbiome in the pathogenesis of various CNS diseases, including schizophrenia. Given this information and the fact, that the gut microbiota is sensitive to internal and environmental influences, we have speculated that among the factors that influence the formation and composition of gut microbiota during life, possible key elements in the schizophrenia development chain are hidden where gut microbiota is a linking component. This article aims to describe and understand the developmental relationships between intestinal microbiota and the risk of developing schizophrenia.
- MeSH
- císařský řez škodlivé účinky MeSH
- dysbióza * etiologie imunologie mikrobiologie MeSH
- lidé MeSH
- mikrobiota * imunologie MeSH
- probiotika terapeutické užití MeSH
- schizofrenie * dietoterapie imunologie mikrobiologie MeSH
- těhotenství MeSH
- zánět * dietoterapie imunologie mikrobiologie MeSH
- zpožděný efekt prenatální expozice * imunologie mikrobiologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
Sleep deprivation (SD) has become a relevant health problem in modern societies. We can be sleep deprived due to lifestyle habits or due to sleep disorders, such as insomnia, obstructive sleep apnea (OSA) and neurological disorders. One of the common element of sleep disorders is the condition of chronic SD, which has complex biological consequences. SD is capable of inducing different biological effects, such as neural autonomic control changes, increased oxidative stress, altered inflammatory and coagulatory responses and accelerated atherosclerosis. All these mechanisms links SD and cardiovascular and metabolic disorders. Epidemiological studies have shown that short sleep duration is associated with increased incidence of cardiovascular diseases, such as coronary artery disease, hypertension, arrhythmias, diabetes and obesity, after adjustment for socioeconomic and demographic risk factors and comorbidities. Thus, an early assessment of a condition of SD and its treatment is clinically relevant to prevent the harmful consequences of a very common condition in adult population.
- MeSH
- autonomní nervový systém * MeSH
- kardiovaskulární nemoci * MeSH
- lidé MeSH
- obstrukční spánková apnoe MeSH
- rizikové faktory MeSH
- spánková deprivace * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
The research of the glutamatergic system in schizophrenia has advanced with the use of non-competitive antagonists of glutamate NMDA receptors (phencyclidine, ketamine, and dizocilpine), which change both human and animal behaviour and induce schizophrenia-like manifestations. Models based on both acute and chronic administration of these substances in humans and rats show phenomenological validity and are suitable for searching for new substances with antipsychotic effects. Nevertheless, pathophysiology of schizophrenia remains unexplained. In the light of the neurodevelopmental model of schizophrenia based on early administration of NMDA receptor antagonists it seems that increased cellular destruction by apoptosis or changes in function of glutamatergic NMDA receptors in the early development of central nervous system are decisive for subsequent development of psychosis, which often does not manifest itself until adulthood. Chronic administration of antagonists initializes a number of adaptation mechanisms, which correlate with findings obtained in patients with schizophrenia; therefore, this model is also suitable for research into pathophysiology of this disease.
- MeSH
- antagonisté excitačních aminokyselin farmakologie MeSH
- financování organizované MeSH
- fyziologická adaptace MeSH
- ketamin farmakologie MeSH
- lidé MeSH
- modely nemocí na zvířatech MeSH
- modely neurologické MeSH
- receptory N-methyl-D-aspartátu antagonisté a inhibitory metabolismus MeSH
- schizofrenie metabolismus patofyziologie MeSH
- toxické psychózy metabolismus patofyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- přehledy MeSH
