Neuroplasticity

2019 ◽  
pp. 230-260
Author(s):  
Judy S. Reilly ◽  
Lara R. Polse
Keyword(s):  
Neural Plasticity ◽  
Late Onset ◽  
Neural Substrates ◽  
Brain Regions ◽  
Developing Brain ◽  
Perinatal Stroke ◽  
Alternative Pathways ◽  
Affective Expression ◽  
Unilateral Brain ◽  
Irreparable Damage

With respect to language, it has long been observed that children who experience early unilateral brain injury do not show the same irreparable damage as do adults with homologous late-onset strokes. Neural plasticity has been proposed as the explanation for such differential linguistic profiles; that is, the plasticity of the young, developing brain allows the possibility for extensive adaptation and organization following a neural insult. Recent research, however, suggests that there are limits to this ability to adapt and organize. Results from a another communicative system, affect, suggest that children with unilateral pre- or perinatal stroke show similar (albeit subtler) effects to adults with homologous late-onset injuries. This chapter presents findings on language development in children who sustained a pre- or perinatal unilateral stroke, and complements these studies with a discussion of affective expression in these same children. These prospective studies of children with perinatal stroke provide a unique window into the development of the neural substrates for language and affect. Specifically, they afford a context to investigate the degree to which particular brain regions may be privileged for specific behavioral functions, as well as how the developing brain adapts to organize alternative pathways in the wake of an early insult.

scholarly journals Neural substrates of propranolol-induced impairments in the reconsolidation of nicotine-associated memories in smokers

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiao Lin ◽  
Jiahui Deng ◽  
Kai Yuan ◽  
Qiandong Wang ◽  
Lin Liu ◽  
...  
Keyword(s):  
Neural Activity ◽  
Neural Substrates ◽  
Brain Regions ◽  
Reward Processing ◽  
Memory Reconsolidation ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging ◽  
Postcentral Gyrus ◽  
Propranolol Group ◽  
Propranolol Administration

AbstractThe majority of smokers relapse even after successfully quitting because of the craving to smoking after unexpectedly re-exposed to smoking-related cues. This conditioned craving is mediated by reward memories that are frequently experienced and stubbornly resistant to treatment. Reconsolidation theory posits that well-consolidated memories are destabilized after retrieval, and this process renders memories labile and vulnerable to amnestic intervention. This study tests the retrieval reconsolidation procedure to decrease nicotine craving among people who smoke. In this study, 52 male smokers received a single dose of propranolol (n = 27) or placebo (n = 25) before the reactivation of nicotine-associated memories to impair the reconsolidation process. Craving for smoking and neural activity in response to smoking-related cues served as primary outcomes. Functional magnetic resonance imaging was performed during the memory reconsolidation process. The disruption of reconsolidation by propranolol decreased craving for smoking. Reactivity of the postcentral gyrus in response to smoking-related cues also decreased in the propranolol group after the reconsolidation manipulation. Functional connectivity between the hippocampus and striatum was higher during memory reconsolidation in the propranolol group. Furthermore, the increase in coupling between the hippocampus and striatum positively correlated with the decrease in craving after the reconsolidation manipulation in the propranolol group. Propranolol administration before memory reactivation disrupted the reconsolidation of smoking-related memories in smokers by mediating brain regions that are involved in memory and reward processing. These findings demonstrate the noradrenergic regulation of memory reconsolidation in humans and suggest that adjunct propranolol administration can facilitate the treatment of nicotine dependence. The present study was pre-registered at ClinicalTrials.gov (registration no. ChiCTR1900024412).

scholarly journals Cannabinoids, reward processing, and psychosis

2021 ◽  
Author(s):  
Brandon Gunasekera ◽  
Kelly Diederen ◽  
Sagnik Bhattacharyya
Keyword(s):  
Psychotic Disorders ◽  
Neural Substrates ◽  
Brain Regions ◽  
Reward Processing ◽  
Anterior Cingulate ◽  
Psychotic Symptoms ◽  
Dopamine Synthesis ◽  
Future Research ◽  
Drug Challenge ◽  
Psychotomimetic Effects

Abstract Background Evidence suggests that an overlap exists between the neurobiology of psychotic disorders and the effects of cannabinoids on neurocognitive and neurochemical substrates involved in reward processing. Aims We investigate whether the psychotomimetic effects of delta-9-tetrahydrocannabinol (THC) and the antipsychotic potential of cannabidiol (CBD) are underpinned by their effects on the reward system and dopamine. Methods This narrative review focuses on the overlap between altered dopamine signalling and reward processing induced by cannabinoids, pre-clinically and in humans. A systematic search was conducted of acute cannabinoid drug-challenge studies using neuroimaging in healthy subjects and those with psychosis Results There is evidence of increased striatal presynaptic dopamine synthesis and release in psychosis, as well as abnormal engagement of the striatum during reward processing. Although, acute THC challenges have elicited a modest effect on striatal dopamine, cannabis users generally indicate impaired presynaptic dopaminergic function. Functional MRI studies have identified that a single dose of THC may modulate regions involved in reward and salience processing such as the striatum, midbrain, insular, and anterior cingulate, with some effects correlating with the severity of THC-induced psychotic symptoms. CBD may modulate brain regions involved in reward/salience processing in an opposite direction to that of THC. Conclusions There is evidence to suggest modulation of reward processing and its neural substrates by THC and CBD. Whether such effects underlie the psychotomimetic/antipsychotic effects of these cannabinoids remains unclear. Future research should address these unanswered questions to understand the relationship between endocannabinoid dysfunction, reward processing abnormalities, and psychosis.

scholarly journals Npas4a expression in the teleost forebrain is associated with stress coping style differences in fear learning

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Matthew R. Baker ◽  
Ryan Y. Wong
Keyword(s):  
Neural Plasticity ◽  
Coping Style ◽  
Molecular Mechanisms ◽  
Conditioned Fear ◽  
Coping Styles ◽  
Brain Regions ◽  
Contextual Fear Conditioning ◽  
Fear Learning ◽  
Stress Coping ◽  
Contextual Fear

AbstractLearning to anticipate potentially dangerous contexts is an adaptive behavioral response to coping with stressors. An animal’s stress coping style (e.g. proactive–reactive axis) is known to influence how it encodes salient events. However, the neural and molecular mechanisms underlying these stress coping style differences in learning are unknown. Further, while a number of neuroplasticity-related genes have been associated with alternative stress coping styles, it is unclear if these genes may bias the development of conditioned behavioral responses to stressful stimuli, and if so, which brain regions are involved. Here, we trained adult zebrafish to associate a naturally aversive olfactory cue with a given context. Next, we investigated if expression of two neural plasticity and neurotransmission-related genes (npas4a and gabbr1a) were associated with the contextual fear conditioning differences between proactive and reactive stress coping styles. Reactive zebrafish developed a stronger conditioned fear response and showed significantly higher npas4a expression in the medial and lateral zones of the dorsal telencephalon (Dm, Dl), and the supracommissural nucleus of the ventral telencephalon (Vs). Our findings suggest that the expression of activity-dependent genes like npas4a may be differentially expressed across several interconnected forebrain regions in response to fearful stimuli and promote biases in fear learning among different stress coping styles.

APOE ɛ4 Allele Moderates the Association Between Basal Forebrain Nuclei Volumes and Allocentric Navigation in Older Adults Without Dementia

2022 ◽  
pp. 1-17
Author(s):  
Ondrej Lerch ◽  
Martina Pařízková ◽  
Martin Vyhnálek ◽  
Zuzana Nedelská ◽  
Jakub Hort ◽  
...  
Keyword(s):  
Older Adults ◽  
Basal Forebrain ◽  
Medial Temporal Lobe ◽  
Structural Equation ◽  
Brain Aging ◽  
Late Onset ◽  
Brain Regions ◽  
Real Space ◽  
Complex Model ◽  
E4 Allele

Background: Cholinergic deficit and medial temporal lobe (MTL) atrophy are hallmarks of Alzheimer’s disease (AD) leading to early allocentric spatial navigation (aSN) impairment. APOE ɛ4 allele (E4) is a major genetic risk factor for late-onset AD and contributes to cholinergic dysfunction. Basal forebrain (BF) nuclei, the major source of acetylcholine, project into multiple brain regions and, along with MTL and prefrontal cortex (PFC), are involved in aSN processing. Objective: We aimed to determine different contributions of individual BF nuclei atrophy to aSN in E4 positive and E4 negative older adults without dementia and assess whether they operate on aSN through MTL and PFC or independently from these structures. Methods: 120 participants (60 E4 positive, 60 E4 negative) from the Czech Brain Aging Study underwent structural MRI and aSN testing in real-space arena setting. Hippocampal and BF nuclei volumes and entorhinal cortex and PFC thickness were obtained. Associations between brain regions involved in aSN were assessed using MANOVA and complex model of mutual relationships was built using structural equation modelling (SEM). Results: Path analysis based on SEM modeling revealed that BF Ch1-2, Ch4p, and Ch4ai nuclei volumes were indirectly associated with aSN performance through MTL (pch1 - 2 = 0.039; pch4p = 0.042) and PFC (pch4ai = 0.044). In the E4 negative group, aSN was indirectly associated with Ch1-2 nuclei volumes (p = 0.015), while in the E4 positive group, there was indirect effect of Ch4p nucleus (p = 0.035). Conclusion: Our findings suggest that in older adults without dementia, BF nuclei affect aSN processing indirectly, through MTL and PFC, and that APOE E4 moderates these associations.

scholarly journals Reported Hearing Loss in Alzheimer’s Disease Is Associated With Loss of Brainstem and Cerebellar Volume

2021 ◽  
Vol 15 ◽  
Author(s):  
Daniel A. Llano ◽  
Susanna S. Kwok ◽  
Viswanath Devanarayan ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hearing Loss ◽  
Normal Subjects ◽  
Neural Substrates ◽  
Epidemiological Studies ◽  
Brain Regions ◽  
Pathological State ◽  
Brain Volumes ◽  
The Relationship

Multiple epidemiological studies have revealed an association between presbycusis and Alzheimer’s Disease (AD). Unfortunately, the neurobiological underpinnings of this relationship are not clear. It is possible that the two disorders share a common, as yet unidentified, risk factor, or that hearing loss may independently accelerate AD pathology. Here, we examined the relationship between reported hearing loss and brain volumes in normal, mild cognitive impairment (MCI) and AD subjects using a publicly available database. We found that among subjects with AD, individuals that reported hearing loss had smaller brainstem and cerebellar volumes in both hemispheres than individuals without hearing loss. In addition, we found that these brain volumes diminish in size more rapidly among normal subjects with reported hearing loss and that there was a significant interaction between cognitive diagnosis and the relationship between reported hearing loss and these brain volumes. These data suggest that hearing loss is linked to brainstem and cerebellar pathology, but only in the context of the pathological state of AD. We hypothesize that the presence of AD-related pathology in both the brainstem and cerebellum creates vulnerabilities in these brain regions to auditory deafferentation-related atrophy. These data have implications for our understanding of the potential neural substrates for interactions between hearing loss and AD.

scholarly journals Neurotoxic astrocytic glypican-4 drives APOE4-dependent tau pathology

2021 ◽  
Author(s):  
Sivaprakasam Ramamoorthy ◽  
Kirill Gorbachev ◽  
Ana Pereira
Keyword(s):  
Late Onset ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Brain Regions ◽  
Tau Proteins ◽  
Tau Pathology ◽  
Density Lipoprotein Receptor ◽  
Apoe Receptor ◽  
The Brain

Apolipoprotein E4 (APOE4) is the crucial genetic risk factor of late-onset Alzheimer disease (AD). Aggregation of tau proteins into insoluble filaments and their spreading across the brain regions are major drivers of neurodegeneration in tauopathies, including in AD. However, the exact mechanisms through which APOE4 induces tau pathology remains unknown. Here, we report that the astrocyte-secreted protein glypican-4 (GPC-4), a novel binding partner of APOE4, drives tau pathology. GPC-4 preferentially interacts with APOE4 in comparison to other APOE isoforms and post-mortem APOE4-carrying AD brains highly express GPC-4 in neurotoxic astrocytes. The astrocyte-secreted GPC-4 induced both tau accumulation and propagation in vitro. CRISPR/dCas9 mediated activation of GPC-4 in a tauopathy animal model robustly induced tau pathology. Further, APOE4-induced tau pathology was greatly diminished in the absence of GPC-4. We found that GPC-4 promoted the stabilization of the APOE receptor low-density lipoprotein receptor-related protein 1 (LRP1) on the cellular surface, which effectively facilitates endocytosis of tau protein. Together, our data comprehensively demonstrate that one of the key APOE4-induced tau pathologies is directly mediated by GPC-4.

scholarly journals Placental, Matrilineal, and Epigenetic Mechanisms Promoting Environmentally Adaptive Development of the Mammalian Brain

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Kevin D. Broad ◽  
Eridan Rocha-Ferreira ◽  
Mariya Hristova
Keyword(s):  
Genomic Imprinting ◽  
Neural Plasticity ◽  
Information Transfer ◽  
Developing Brain ◽  
Mammalian Brain ◽  
Neural Function ◽  
Mammalian Development ◽  
Intrauterine Development ◽  
Epigenetic Information ◽  
Ultimate Control

The evolution of intrauterine development, vivipary, and placentation in eutherian mammals has introduced new possibilities and constraints in the regulation of neural plasticity and development which promote neural function that is adaptive to the environment that a developing brain is likely to encounter in the future. A range of evolutionary adaptations associated with placentation transfers disproportionate control of this process to the matriline, a period unique in mammalian development in that there are three matrilineal genomes interacting in the same organism at the same time (maternal, foetal, and postmeiotic oocytes). The interactions between the maternal and developing foetal hypothalamus and placenta can provide a template by which a mother can transmit potentially adaptive information concerning potential future environmental conditions to the developing brain. In conjunction with genomic imprinting, it also provides a template to integrate epigenetic information from both maternal and paternal lineages. Placentation also hands ultimate control of genomic imprinting and intergenerational epigenetic information transfer to the matriline as epigenetic markers undergo erasure and reprogramming in the developing oocyte. These developments, in conjunction with an expanded neocortex, provide a unique evolutionary template by which matrilineal transfer of maternal care, resources, and culture can be used to promote brain development and infant survival.

Understanding risk and resilience in maltreated children

2019 ◽  
pp. 304-323
Author(s):  
Joan Kaufman ◽  
Janitza L Montalvo-Ortiz ◽  
Richard S Lee
Keyword(s):  
Child Abuse ◽  
Psychiatric Disorders ◽  
Neural Plasticity ◽  
Genetic Factors ◽  
Strong Predictor ◽  
Empirical Work ◽  
Brain Regions ◽  
Risk And Resilience ◽  
Poor Treatment ◽  
History Of

Individuals with a history of child abuse are at high risk for a broad range of psychiatric and substance use disorders. This chapter reviews key findings from research on the genetics of child abuse-related psychiatric disorders, neuroimaging investigations with maltreated youth, and resiliency studies. Relevant empirical work in the field was reviewed, with an emphasis on prior reviews, meta-analytic studies, and recent publications. Genetic factors are not associated with distinct psychiatric disorders but rather diverse clinical phenotypes, and a history of abuse is frequently associated with alterations in structural and functional brain changes across multiple brain regions and circuits that mediate a wide variety of emotional and cognitive processes. Heterogeneity in clinical outcome and brain measures varies as a function of a wide range of factors, and emerging findings on genetic and neural plasticity offers significant promise in understanding risk and resilience in maltreated youth. Child maltreatment is a strong predictor of early onset of psychiatric illness, increased comorbidity, and poor treatment response; however, a history of abuse need not lead to the development of psychiatric problems. Risk is altered by genetic factors, and can be ameliorated by positive factors in the environment—including the availability of positive support, enrichment experiences, and the delivery of evidence-based psychotherapeutic clinical interventions. Future multidisciplinary and translational studies will help to further delineate the mechanisms by which experiences of maltreatment confers risk for psychopathology, as well as help to further delineate factors associated with resiliency.

scholarly journals The Cross-Modal Effects of Sensory Deprivation on Spatial and Temporal Processes in Vision and Audition: A Systematic Review on Behavioral and Neuroimaging Research since 2000

2019 ◽  
Vol 2019 ◽  
pp. 1-21 ◽  
Author(s):  
Laura Bell ◽  
Lisa Wagels ◽  
Christiane Neuschaefer-Rube ◽  
Janina Fels ◽  
Raquel E. Gur ◽  
...  
Keyword(s):  
Systematic Review ◽  
Temporal Processing ◽  
Neural Plasticity ◽  
Sensory Deprivation ◽  
Brain Regions ◽  
Behavioral Performance ◽  
Brain Organization ◽  
Processing Resources ◽  
The Cross ◽  
The Brain

One of the most significant effects of neural plasticity manifests in the case of sensory deprivation when cortical areas that were originally specialized for the functions of the deprived sense take over the processing of another modality. Vision and audition represent two important senses needed to navigate through space and time. Therefore, the current systematic review discusses the cross-modal behavioral and neural consequences of deafness and blindness by focusing on spatial and temporal processing abilities, respectively. In addition, movement processing is evaluated as compiling both spatial and temporal information. We examine whether the sense that is not primarily affected changes in its own properties or in the properties of the deprived modality (i.e., temporal processing as the main specialization of audition and spatial processing as the main specialization of vision). References to the metamodal organization, supramodal functioning, and the revised neural recycling theory are made to address global brain organization and plasticity principles. Generally, according to the reviewed studies, behavioral performance is enhanced in those aspects for which both the deprived and the overtaking senses provide adequate processing resources. Furthermore, the behavioral enhancements observed in the overtaking sense (i.e., vision in the case of deafness and audition in the case of blindness) are clearly limited by the processing resources of the overtaking modality. Thus, the brain regions that were previously recruited during the behavioral performance of the deprived sense now support a similar behavioral performance for the overtaking sense. This finding suggests a more input-unspecific and processing principle-based organization of the brain. Finally, we highlight the importance of controlling for and stating factors that might impact neural plasticity and the need for further research into visual temporal processing in deaf subjects.

scholarly journals Sense of Agency Beyond Sensorimotor Process: Decoding Self-Other Action Attribution in the Human Brain

2020 ◽  
Vol 30 (7) ◽  
pp. 4076-4091
Author(s):  
Ryu Ohata ◽  
Tomohisa Asai ◽  
Hiroshi Kadota ◽  
Hiroaki Shigemasu ◽  
Kenji Ogawa ◽  
...  
Keyword(s):  
Subjective Experience ◽  
Parietal Lobe ◽  
Neural Substrates ◽  
Brain Regions ◽  
Sense Of Agency ◽  
Posterior Parietal ◽  
Sensorimotor Information ◽  
The One ◽  
The Right ◽  
Different Levels

Abstract The sense of agency is defined as the subjective experience that “I” am the one who is causing the action. Theoretical studies postulate that this subjective experience is developed through multistep processes extending from the sensorimotor to the cognitive level. However, it remains unclear how the brain processes such different levels of information and constitutes the neural substrates for the sense of agency. To answer this question, we combined two strategies: an experimental paradigm, in which self-agency gradually evolves according to sensorimotor experience, and a multivoxel pattern analysis. The combined strategies revealed that the sensorimotor, posterior parietal, anterior insula, and higher visual cortices contained information on self-other attribution during movement. In addition, we investigated whether the found regions showed a preference for self-other attribution or for sensorimotor information. As a result, the right supramarginal gyrus, a portion of the inferior parietal lobe (IPL), was found to be the most sensitive to self-other attribution among the found regions, while the bilateral precentral gyri and left IPL dominantly reflected sensorimotor information. Our results demonstrate that multiple brain regions are involved in the development of the sense of agency and that these show specific preferences for different levels of information.

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