Critical reviews in neurobiology最新文献

{"title":"Pharmacology of endogenous neuroactive steroids.","authors":"Doodipala Samba Reddy","doi":"10.1615/critrevneurobiol.v15.i34.20","DOIUrl":"https://doi.org/10.1615/critrevneurobiol.v15.i34.20","url":null,"abstract":"<p><p>Neuroactive steroids are potent endogenous neuromodulators with rapid actions in the central nervous system. Neuroactive steroids have been claimed to have specific physiological roles in normal or pathological brain function. This article reviews the emerging evidence that progesterone-, deoxycorticosterone-, and testosterone-derived endogenous neuroactive steroids play an important role in the modulation of neural excitability and brain function. Neuroactive steroids such as allopregnanolone and allotetrahydrodeoxycorticosterone (THDOC) are extremely potent positive allosteric modulators of GABAA receptors with sedative, anxiolytic, and anticonvulsant properties. The sulfated neuroactive steroids pregnenolone sulfate (PS) and dehydroepiandrosterone sulfate (DHEAS), which are negative GABAA receptor modulators, induce anxiogenic and proconvulsant effects. Thus, natural fluctuations in neuroactive steroid levels during the menstrual cycle and stress could affect several nervous system functions. There is strong evidence that allopregnanolone and THDOC are involved in the pathophysiology of premenstrual syndrome, catamenial epilepsy, major depression, and stress-sensitive brain disorders. Neuroactive steroids PS and DHEAS have been shown to modulate memory functions. However, the significance of the testosterone-derived neuroactive steroid 3alpha-androstanediol is not well understood. Like naturally occurring neuroactive steroids, synthetic derivatives such as ganaxolone have been proven in preclinical and clinical studies to be effective anticonvulsants with great potential for human use. Future research on inhibition or stimulation of specific neuroactive steroid synthesizing enzymes could provide an improved understanding and novel approaches for the treatment of anxiety, epilepsy, and depression.</p>","PeriodicalId":10778,"journal":{"name":"Critical reviews in neurobiology","volume":"15 3-4","pages":"197-234"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24610440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Botulinum neurotoxin: the neuromuscular junction revisited.","authors":"Julie A Coffield","doi":"10.1615/critrevneurobiol.v15.i34.10","DOIUrl":"https://doi.org/10.1615/critrevneurobiol.v15.i34.10","url":null,"abstract":"<p><p>Botulinum neurotoxin is the neuromuscular poison that is responsible for the fatal disease botulism. This toxin is also a valued therapeutic agent in the treatment of an increasing number of neuromuscular disorders. Unfortunately, in the wrong hands, botulinum neurotoxin is also a deadly biological \"weapon. The diverse health consequences of botulinum neurotoxin combined with the increased threat of bioterrorism underscore the profound importance of understanding exactly how this toxin exerts its effects on the clinically relevant mammalian target site, the neuromuscular junction. Despite the fact that a great deal has been learned about the cellular actions of botulinum neurotoxin during the past three decades, questions still remain. For example, what protein or proteins mediate transport of the toxin into the cholinergic nerve terminal? What factors control the duration of toxin action in the nerve terminal? Until recently, scholarly pursuit of such questions was technically challenging in neuromuscular tissues. Recent advancements in biotechnology have now made it feasible to pursue these important issues at the neuromuscular junction and to correlate biochemical studies in nontarget tissues with clinically relevant functional outcomes. This narrative reviews our current understanding of the actions of botulinum neurotoxin at the neuromuscular junction, presents recent findings from our own work in neuromuscular tissues, and encourages future studies regarding botulinum neurotoxin at its target site.</p>","PeriodicalId":10778,"journal":{"name":"Critical reviews in neurobiology","volume":"15 3-4","pages":"175-96"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24610439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rodent models of depression: reexamining validity without anthropomorphic inference.","authors":"Philip V Holmes","doi":"10.1615/critrevneurobiol.v15.i2.30","DOIUrl":"https://doi.org/10.1615/critrevneurobiol.v15.i2.30","url":null,"abstract":"<p><p>This review aims to stimulate new ways of thinking about how to model depression in rats and mice. The article is founded on the premise that anthropomorphic inferences should be removed entirely from research involving rodents. The application of animal models to study depression over the past 30 years has been based largely on nonempirical and hence nonscientific assumptions about psychological states that probably do not exist and certainly cannot be measured in rodents. Such assumptions may have led to the misinterpretation of some behaviors, such as decreased locomotor activity or decreased sucrose consumption, as symptoms of depression in rats. Previous research has also overemphasized the causal role of stress in depression. After reviewing major features of several commonly employed models, this article challenges traditional concepts about validity. Models are first evaluated based on the goals of the research. Screening for potential antidepressant compounds requires little or no consideration of the validity of the model. Issues of validity become more critical when attempting to study the neurobiological basis of depression. The primary importance of face validity is emphasized, and the value of various behavioral measures is assessed based on how directly they resemble discrete behavioral symptoms seen in depressed humans. A \"neurobehaviorally mechanistic\" approach is described. This approach relies on formulating discrete, neurobiological hypotheses to explain individual symptoms rather than to explain collections of symptoms or the entire disorder. The approach thus relies on pragmatic measures of operationally well-defined behavioral variables. The review concludes with the proposal that understanding the neurobiological basis for individual symptoms will ultimately yield a better understanding of depression.</p>","PeriodicalId":10778,"journal":{"name":"Critical reviews in neurobiology","volume":"15 2","pages":"143-74"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24405620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex differences in the central nervous system actions of ethanol.","authors":"Leslie L Devaud,&nbsp;Paul Alele,&nbsp;Chadda Ritu","doi":"10.1615/critrevneurobiol.v15.i1.20","DOIUrl":"https://doi.org/10.1615/critrevneurobiol.v15.i1.20","url":null,"abstract":"<p><p>For many years, researchers have avoided including females in their research because of the poorly understood influences of cycling hormones. However, we are becoming increasingly aware that sex matters, showing that it is important to conduct studies in females as well as males. This review will focus on the central nervous system (CNS) actions of alcohol (ethanol) because we have found significant sex differences in ethanol actions at the molecular as well as the behavioral level. Most recently, in our studies of ethanol dependence and withdrawal, we found that female rats displayed a shorter time for recovery from ethanol withdrawal, assessed by measuring seizure susceptibility. We now report that this finding was confirmed with a second convulsant agent. Moreover, GABAA receptor function was differentially altered in ethanol-withdrawn female compared to male rats. Studies by other investigators have reported additional significant sex differences in ethanol seeking and drinking behaviors and across several measures of ethanol dependence and withdrawal. We are gaining a better understanding of how the actions of ethanol in the CNS overlay sex differences in brain architecture and the hormonal milieu. Therefore, it is not surprising to observe sex-selective effects on cellular and behavioral outcomes from ethanol consumption. While current research is focused on characterizing sex differences in the actions of ethanol, it has not yet reached the point where we can integrate our findings into a unifying concept of how being female differentially regulates CNS responses to ethanol. This is likely a result of the complexity of ethanol actions, involving multiple neurotransmitter systems and responses covering the spectrum from drug seeking behaviors to neuropathological consequences of ethanol misuse. Regardless, the observed sex differences in ethanol withdrawal are noteworthy because they suggest that treatment of alcoholism should be managed differently in women than in men. Finally, it remains important to compare and contrast responses in males and females because recent studies of sex differences in basic physiology have made it clear that being female impacts health and disease.</p>","PeriodicalId":10778,"journal":{"name":"Critical reviews in neurobiology","volume":"15 1","pages":"41-59"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40827893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Herpes simplex virus-mediated gene transfer as a tool for neuropsychiatric research.","authors":"W. Carlezon, E. Nestler, R. Neve","doi":"10.1615/CRITREVNEUROBIOL.V14.I1.30","DOIUrl":"https://doi.org/10.1615/CRITREVNEUROBIOL.V14.I1.30","url":null,"abstract":"There is an enormous initiative to establish causal relationships between brain biology (including patterns of gene expression) and behavior. Unfortunately, genetic intervention is not accomplished easily in the brain. One strategy is to engineer and deliver to the brain specialized viral vectors that carry a gene (or genes) of interest, thereby exploiting the natural ability of viruses to insert genetic information into cells. When delivered to the brain, these vectors cause infected cells to increase expression of the genes of interest. Viral vectors are particularly useful when the goal is to manipulate expression of a single gene in a specific brain region, at a specific time, and in animals that developed normally. There are several types of virus that can be adapted for use as viral vectors, including those based on herpes simplex virus (HSV-1), adenovirus (AV), adeno-associated virus (AAV), and lentivirus. Although each vector has its own unique advantages and disadvantages, this rapidly evolving technology has the potential to revolutionize neuropsychiatric research by offering the opportunity to establish, with anatomical and temporal specificity, causal relations between altered expression of individual gene products and alterations in complex behavior.","PeriodicalId":10778,"journal":{"name":"Critical reviews in neurobiology","volume":"16 1","pages":"47-67"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81587100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep after immobilization stress and sleep deprivation: common features and theoretical integration.","authors":"V S Rotenberg","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The goal of the present paper is to elucidate and to resolve contradictions in the relationships among different forms of stress, sleep deprivation, and paradoxical sleep (PS) functions. Acute immobilization stress and the stress of learned helplessness are accompanied by an increase of PS, whereas the stress of defense behavior and the stress of self-stimulation cause PS reduction. Recovery sleep after total sleep deprivation performed on the rotating platform is marked by a dramatic rebound of PS although NREM (non-rapid eye movement) sleep deprivation is more prominent than PS deprivation. This PS rebound leads to a quick reversal of the pathology caused by prolonged sleep deprivation. The search activity (SA) concept presents an explanation for these contradictions. SA increases body resistance to stress and diseases, whereas renunciation of search (giving up, helplessness) decreases body resistance. PS and dreams contain covert SA, which compensates for the lack of the overt SA in the preceding period of wakefulness. The requirement for PS increases after giving up and decreases after active defense behavior and self-stimulation. Immobilization stress prevents SA in waking behavior and increases the need in PS. Sleep deprivation on the rotating platform, like immobilization stress, prevents SA, produces conditions for learned helplessness and, suppresses PS. Such a combination increases PS pressure and decreases body resistance.</p>","PeriodicalId":10778,"journal":{"name":"Critical reviews in neurobiology","volume":"14 3-4","pages":"225-31"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22296106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural origins of the P300.","authors":"M. Soltani, Robert T. Knight","doi":"10.1615/CRITREVNEUROBIOL.V14.I3-4.20","DOIUrl":"https://doi.org/10.1615/CRITREVNEUROBIOL.V14.I3-4.20","url":null,"abstract":"A review of the literature investigating the neural origins of detection behavior in humans reveals two event-related potential components, P3a and P3b, each with a distinct neural organization and cognitive function.The P3a is involved in automatic novelty detection and characterized by a more anterior cortical distribution, whereas the P3b is concerned with volitional target detection and has a more posterior cortical distribution. Intracranial investigation, studies with patients with focal brain lesions, and functional neuroimaging (fMRI) studies converge with scalp-recorded event-related potential (ERP) data in suggesting that a widespread cortical network gives rise to both automatic and controlled detection behavior. The main regions consistently attributed to generating detection-related brain activation include the temporal-parietal junction, medial temporal complex, and the lateral prefrontal cortex. The extant human and animal literature addressing the neural networks, neuropharmacological underpinnings, and behavioral significance of the P300 potential will be reviewed.","PeriodicalId":10778,"journal":{"name":"Critical reviews in neurobiology","volume":"2 1","pages":"199-224"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90634255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Episodic memory meets working memory in the frontal lobe: functional neuroimaging studies of encoding and retrieval.","authors":"Andy C. H. Lee, Trevor W. Robbins, Adrian M. Owen","doi":"10.1615/CRITREVNEUROBIOL.V14.I3-4.10","DOIUrl":"https://doi.org/10.1615/CRITREVNEUROBIOL.V14.I3-4.10","url":null,"abstract":"Recent functional-neuroimaging studies have provided a wealth of new information suggesting that regions of the prefrontal cortex play a role in episodic memory encoding and retrieval. This review seeks to evaluate the results of these studies in the context of one general model that has proposed that the left prefrontal cortex is preferentially involved in episodic memory encoding, whereas the right prefrontal cortex is preferentially involved in episodic memory retrieval, irrespective of the type (e.g., modality) of information being remembered. The origins of this framework are considered in some detail and then all relevant functional-neuroimaging studies are critically reviewed. The results of this review fail to provide support for the functional-asymmetry model, suggesting instead that episodic memory encoding and retrieval may actually involve similar regions of the lateral prefrontal cortex when all factors relating to the type of stimulus material (i.e., modality), are appropriately controlled.","PeriodicalId":10778,"journal":{"name":"Critical reviews in neurobiology","volume":"40 1","pages":"165-97"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77081283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Episodic memory meets working memory in the frontal lobe: functional neuroimaging studies of encoding and retrieval.","authors":"A C Lee,&nbsp;T W Robbins,&nbsp;A M Owen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Recent functional-neuroimaging studies have provided a wealth of new information suggesting that regions of the prefrontal cortex play a role in episodic memory encoding and retrieval. This review seeks to evaluate the results of these studies in the context of one general model that has proposed that the left prefrontal cortex is preferentially involved in episodic memory encoding, whereas the right prefrontal cortex is preferentially involved in episodic memory retrieval, irrespective of the type (e.g., modality) of information being remembered. The origins of this framework are considered in some detail and then all relevant functional-neuroimaging studies are critically reviewed. The results of this review fail to provide support for the functional-asymmetry model, suggesting instead that episodic memory encoding and retrieval may actually involve similar regions of the lateral prefrontal cortex when all factors relating to the type of stimulus material (i.e., modality), are appropriately controlled.</p>","PeriodicalId":10778,"journal":{"name":"Critical reviews in neurobiology","volume":"14 3-4","pages":"165-97"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22296104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep after immobilization stress and sleep deprivation: common features and theoretical integration.","authors":"V. Rotenberg","doi":"10.1615/CRITREVNEUROBIOL.V14.I3-4.30","DOIUrl":"https://doi.org/10.1615/CRITREVNEUROBIOL.V14.I3-4.30","url":null,"abstract":"The goal of the present paper is to elucidate and to resolve contradictions in the relationships among different forms of stress, sleep deprivation, and paradoxical sleep (PS) functions. Acute immobilization stress and the stress of learned helplessness are accompanied by an increase of PS, whereas the stress of defense behavior and the stress of self-stimulation cause PS reduction. Recovery sleep after total sleep deprivation performed on the rotating platform is marked by a dramatic rebound of PS although NREM (non-rapid eye movement) sleep deprivation is more prominent than PS deprivation. This PS rebound leads to a quick reversal of the pathology caused by prolonged sleep deprivation. The search activity (SA) concept presents an explanation for these contradictions. SA increases body resistance to stress and diseases, whereas renunciation of search (giving up, helplessness) decreases body resistance. PS and dreams contain covert SA, which compensates for the lack of the overt SA in the preceding period of wakefulness. The requirement for PS increases after giving up and decreases after active defense behavior and self-stimulation. Immobilization stress prevents SA in waking behavior and increases the need in PS. Sleep deprivation on the rotating platform, like immobilization stress, prevents SA, produces conditions for learned helplessness and, suppresses PS. Such a combination increases PS pressure and decreases body resistance.","PeriodicalId":10778,"journal":{"name":"Critical reviews in neurobiology","volume":"37 1","pages":"225-31"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90938028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}