Aspects of Neuroplasticity

2021 ◽  
pp. 9-23
Author(s):  
John Zerilli

The brain exhibits an impressive degree of plasticity, even as it ages. Plasticity is really an intrinsic feature of the nervous system, not an exceptional or occasional state. Neuroplasticity comprises a family of different types of plasticity. Of these, synaptic plasticity is perhaps the best-understood variety, and it plays an important role in cortical map reorganization and memory consolidation. Cortical map plasticity is of direct relevance to any discussion of modularity. There are two types of cortical map plasticity: intramodal (within a modality) and crossmodal. Crossmodal plasticity is likely to arise from the underlying supramodal (or “metamodal”) organization of the brain.

Author(s):  
Patricia S. Churchland ◽  
Terrence J. Sejnowski

This chapter examines the physical mechanisms in nervous systems in order to elucidate the structural bases and functional principles of synaptic plasticity. Neuroscientific research on plasticity can be divided into four main streams: the neural mechanism for relatively simple kinds of plasticity, such as classical conditioning or habituation; anatomical and physiological studies of temporal lobe structures, including the hippocampus and the amygdala; study of the development of the visual system; and the relation between the animal's genes and the development of its nervous system. The chapter first considers the role of the mammalian hippocampus in learning and memory before discussing Donald Hebb's views on synaptic plasticity. It then explores the mechanisms underlying neuronal plasticity and those that decrease synaptic strength, the relevance of time with respect to plasticity, and the occurrence of plasticity during the development of the nervous system. It also describes modules, modularity, and networks in the brain.


2006 ◽  
Vol 18 (5) ◽  
pp. 793-802 ◽  
Author(s):  
Björn H. Rasch ◽  
Jan Born ◽  
Steffen Gais

High central nervous system levels of acetylcholine (ACh) are commonly regarded as crucial for learning and memory, and a decline in cholinergic neurotransmission is associated with Alzheimer's dementia. However, recent findings revealed exceptions to this rule: The low ACh tone characterizing slowwave sleep (SWS) has proven necessary for consolidation of hippocampus-dependent declarative memories during this sleep stage. Such observations, together with recent models of a hippocampal-neocortical dialogue underlying systems memory consolidation, suggest that high levels of ACh support memory encoding, whereas low levels facilitate consolidation. We tested this hypothesis in human subjects by blocking cholinergic neurotransmission during wakefulness, starting 30 min after learning. Subjects received the muscarinic antagonist scopolamine (4 µg/kg bodyweight intravenously) and the nicotinic antagonist mecamylamine (5 mg orally). Compared to placebo, combined muscarinic and nicotinic receptor blockade significantly improved consolidation of declarative memories tested 10 hr later, but simultaneously impaired acquisition of similar material. Consolidation of procedural memories, which are not dependent on hippocampal functioning, was unaffected. Neither scopolamine nor mecamylamine alone enhanced declarative memory consolidation. Our findings support the notion that ACh acts as a switch between modes of acquisition and consolidation. We propose that the natural shift in central nervous system cholinergic tone from high levels during wakefulness to minimal levels during SWS optimizes declarative memory consolidation during a period with no need for new memory encoding.


BIOspektrum ◽  
2021 ◽  
Vol 27 (6) ◽  
pp. 588-590
Author(s):  
Zeeshan Mushtaq ◽  
Jan Pielage

AbstractThe precise regulation of synaptic connectivity is essential for the processing of information in the brain. Any aberrant loss of synaptic connectivity due to genetic mutations will disrupt information flow in the nervous system and may represent the underlying cause of psychiatric or neurodegenerative diseases. Therefore, identification of the molecular mechanisms controlling synaptic plasticity and maintenance is essential for our understanding of neuronal circuits in development and disease.


2020 ◽  
Vol 21 (4) ◽  
pp. 1538 ◽  
Author(s):  
Luca Franchini ◽  
Nicolò Carrano ◽  
Monica Di Luca ◽  
Fabrizio Gardoni

N-Methyl-d-Aspartate Receptors (NMDARs) are ionotropic glutamate-gated receptors. NMDARs are tetramers composed by several homologous subunits of GluN1-, GluN2-, or GluN3-type, leading to the existence in the central nervous system of a high variety of receptor subtypes with different pharmacological and signaling properties. NMDAR subunit composition is strictly regulated during development and by activity-dependent synaptic plasticity. Given the differences between GluN2 regulatory subunits of NMDAR in several functions, here we will focus on the synaptic pool of NMDARs containing the GluN2A subunit, addressing its role in both physiology and pathological synaptic plasticity as well as the contribution in these events of different types of GluN2A-interacting proteins.


2004 ◽  
Vol 91 (03) ◽  
pp. 457-464 ◽  
Author(s):  
Manuel Yepes ◽  
Daniel Lawrence

SummaryNeuroserpin is a member of the serine proteinase inhibitor (serpin) gene family that reacts preferentially with tissue-type plasminogen activator (tPA) and is primarily localized to neurons in regions of the brain where tPA is also found. Outside of the central nervous system (CNS) tPA is predominantly found in the blood where its primary function is as a thrombolytic enzyme. However, tPA is also expressed within the CNS where it has a very different function, promoting events associated not only with synaptic plasticity but also with cell death in a number of settings, such as cerebral ischemia and seizures. Neuroserpin is released from neurons in response to neuronal depolarization and plays an important role in the development of synaptic plasticity. Following the onset of cerebral ischemia there is an increase in both tPA activity and neuroserpin expression in the area surrounding the necrotic core (ischemic penumbra), and treatment with neuroserpin following ischemic stroke or overexpression of the neuroserpin gene results in a significant decrease in the volume of the ischemic area as well as in the number of apoptotic cells. TPA activity and neuroserpin expression are also increased in specific areas of the brain by seizures, and treatment with neuroserpin slows the progression of seizure activity throughout the CNS and results in significant neuronal survival in the hippocampus. Mutations in human neuroserpin result in a form of autosomal dominant inherited dementia which is characterized by the presence of intraneuronal inclusion bodies and is known as Familial Encephalopathy with Neuroserpin Inclusion Bodies.


2000 ◽  
Vol 23 (6) ◽  
pp. 996-999 ◽  
Author(s):  
V. S. Rotenberg

The target articles on sleep and dreaming are discussed in terms of the concept of search activity integrating different types of behavior, body resistance, REM sleep/dream functions, and the brain catecholamine system. REM sleep may be functionally sufficient or insufficient, depending on the dream scenario, the latter being more important than the physiological manifestation of REM sleep. REM sleep contributes to memory consolidation in the indirect way.[Nielsen; Revonsuo; Solms; Vertes & Eastman]


2021 ◽  
Vol 15 ◽  
Author(s):  
Mark D. Namba ◽  
Jonna M. Leyrer-Jackson ◽  
Erin K. Nagy ◽  
M. Foster Olive ◽  
Janet L. Neisewander

Recent studies examining the neurobiology of substance abuse have revealed a significant role of neuroimmune signaling as a mechanism through which drugs of abuse induce aberrant changes in synaptic plasticity and contribute to substance abuse-related behaviors. Immune signaling within the brain and the periphery critically regulates homeostasis of the nervous system. Perturbations in immune signaling can induce neuroinflammation or immunosuppression, which dysregulate nervous system function including neural processes associated with substance use disorders (SUDs). In this review, we discuss the literature that demonstrates a role of neuroimmune signaling in regulating learning, memory, and synaptic plasticity, emphasizing specific cytokine signaling within the central nervous system. We then highlight recent preclinical studies, within the last 5 years when possible, that have identified immune mechanisms within the brain and the periphery associated with addiction-related behaviors. Findings thus far underscore the need for future investigations into the clinical potential of immunopharmacology as a novel approach toward treating SUDs. Considering the high prevalence rate of comorbidities among those with SUDs, we also discuss neuroimmune mechanisms of common comorbidities associated with SUDs and highlight potentially novel treatment targets for these comorbid conditions. We argue that immunopharmacology represents a novel frontier in the development of new pharmacotherapies that promote long-term abstinence from drug use and minimize the detrimental impact of SUD comorbidities on patient health and treatment outcomes.


2018 ◽  
Vol 10 (3) ◽  
pp. 41-44
Author(s):  
N. V. Skripchenko ◽  
S. E. Ukraintsev ◽  
E. G. Makarova ◽  
E. Yu. Skripchenko

The review article presents the scientific substantiation of the prospective direction of research of the intestinal microbiota and its role in the formation of various neurological pathologies. Reflected information about the enteral nervous system, which has direct relevance in the interaction between the brain and intestines. The study of the intestinal microbiota is currently carried out using modern methods of metagenomics, sequencing and bioinformation analysis. Data are presented on the formation of functional digestive disorders in children with altered intestinal microbiota and the ways of correction are determined.


2019 ◽  
Vol 30 (5) ◽  
pp. 485-495 ◽  
Author(s):  
Li-na Sun ◽  
Xiao-li Liu

Abstract Convergent lines of evidence indicate the critical roles of adiponectin in regulating neural functions on different levels. Because of the importance in maintaining neural plasticity including adult neurogenesis and synaptic plasticity, adiponectin has the potential to serve as the treatment targets in therapies of neurological and psychiatric disorders. Hence, systematic review is needed to summarize how adiponectin works in the brain, and how the adiponectin pathway is employed as the treatment method needs to be determined. Moreover, the benefits of adiponectin as the regulator for neural plasticity such as synaptic plasticity and neurogenesis have been supported by many literatures. In the current article, we reviewed the functions of adiponectin in different types of neural plasticity. We also demonstrated the potential value of adiponectin as the treatment target for different types of neurodegenerative and psychiatric disorders. Taken together, this review offers a new insight about adiponectin as the ideal target to develop the new treatment methods against neurodegeneration or psychiatric diseases.


2017 ◽  
Author(s):  
Zachariah R. Cross ◽  
Mark J. Kohler ◽  
Matthias Schlesewsky ◽  
M. Gareth Gaskell ◽  
Ina Bornkessel-Schlesewsky

AbstractWe hypothesise a beneficial influence of sleep on the consolidation of the combinatorial mechanisms underlying incremental sentence comprehension. These predictions are grounded in recent work examining the effect of sleep on the consolidation of linguistic information, which demonstrate that sleep-dependent neurophysiological activity consolidates the meaning of novel words and simple grammatical rules. However, the sleep-dependent consolidation of sentence-level combinatorics has not been studied to date. Here, we propose that dissociable aspects of sleep neurophysiology consolidate two different types of combinatory mechanisms in human language: sequence-based (order-sensitive) and dependency-based (order-insensitive) combinatorics. The distinction between the two types of combinatorics is motivated both by cross-linguistic considerations and the neurobiological underpinnings of human language. Unifying this perspective with principles of sleep-dependent memory consolidation, we posit that a function of sleep is to optimise the consolidation of sequence-based knowledge (the when) and the establishment of semantic schemas of unordered items (the what) that underpin cross-linguistic variations in sentence comprehension. This hypothesis builds on the proposal that sleep is involved in the construction of predictive codes, a unified principle of brain function that supports incremental sentence comprehension. Finally, we discuss neurophysiological measures (EEG/MEG) that could be used to test these claims, such as the quantification of neuronal oscillations, which reflect basic mechanisms of information processing in the brain.


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