Stress, Trauma and Synaptic Plasticity
Autor Maxwell Bennett, Jim Lagopoulosen Limba Engleză Hardback – 28 feb 2019
Neuroștiința contemporană a evoluat de la o descriere generală a stresului către o cartografiere precisă a modificărilor structurale la nivel celular. Observăm că Stress, Trauma and Synaptic Plasticity marchează acest progres, mutând accentul pe degenerarea sinaptică în materia cenușie. Suntem de părere că rigoarea cu care Maxwell Bennett și Jim Lagopoulos analizează mecanismele moleculare oferă o claritate necesară atât cercetătorilor, cât și clinicienilor.
Lucrarea este structurată pentru a ghida cititorul prin rețelele sinaptice complexe afectate de traume, evidențiind rolul neuromodulatorilor precum dopamina și serotonina. Merită menționat modul în care autorii explică influența glucocorticoizilor asupra funcției BDNF, oferind o bază solidă pentru înțelegerea instabilității sinaptice. Această abordare completează perspectiva oferită de Synaptic Stress and Pathogenesis of Neuropsychiatric Disorders, adăugând o analiză detaliată a controlului epigenetic și a geneticii receptorilor NMDA, elemente mai puțin explorate în volumele tehnice generale.
În contextul operei lui Maxwell Bennett, acest volum reprezintă o aplicare empirică a fundamentelor teoretice stabilite în lucrări precum Neuroscience and Philosophy – Brain, Mind and Language. Dacă în scrierile anterioare Bennett se concentra pe dimensiunea conceptuală și filozofică a neuroștiinței, aici adoptă o metodologie strict biologică și clinică, similară cu investigația sa din Virginia Woolf and Neuropsychiatry, dar aplicată la scara microscopică a plasticității creierului. Rezultatul este un text dens, cu un ritm analitic susținut, care transformă datele de laborator în ipoteze viabile despre mecanismele fricii.
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Specificații
ISBN-10: 3319911155
Pagini: 208
Ilustrații: XXXIII, 231 p. 47 illus., 18 illus. in color.
Dimensiuni: 155 x 235 mm
Greutate: 0.68 kg
Ediția:1st ed. 2018
Editura: Springer International Publishing
Colecția Springer
Locul publicării:Cham, Switzerland
De ce să citești această carte
Această lucrare este esențială pentru cei care doresc să înțeleagă biologia traumei dincolo de simptome. Cititorul câștigă o perspectivă detaliată asupra modului în care stresul „reconfigurează” fizic creierul prin pierderea sinaptică. Este un instrument de referință pentru studenții la medicină și cercetătorii care au nevoie de o sinteză actualizată a interacțiunilor dintre epigenetică, hormoni și plasticitatea neuronală.
Despre autor
Maxwell Bennett este un neurocercetător de renume internațional, profesor și director fondator al Brain and Mind Research Institute din cadrul Universității din Sydney. Cariera sa a fost marcată de contribuții fundamentale în înțelegerea funcționării sinaptice, fiind distins cu medalia Macfarlane Burnet. Jim Lagopoulos este expert în neuroimagistică prin rezonanță magnetică și director al Thompson Institute, cu o activitate vastă în cercetarea tulburărilor post-traumatice și a sănătății mintale la tineri. Împreună, cei doi autori combină expertiza în biologie moleculară cu observația clinică de ultimă oră.
Descriere scurtă
The changes to the grey matter in certain areas of the brain are similar in stressed humans and animals, with the most likely basis for these changes being the degeneration of synaptic connections. In the book’s first sections the reader will learn about the core network of synaptic connections that are affected by stress and trauma disorders. These synaptic connections are modulated by dopamine, serotonin and Brain Derived Neurotrophic Factor (BDNF). In subsequent chapters, the NMDA-receptor mediated plasticity of these synapses is discussed, with particular attention given to how glucocorticoids can interfere with the function of BDNF and thereby affect the synapse’s physical stability. Furthermore, the reader will learn about the importance of the genetics of the glucocorticoid gene and the epigenetic control of BDNF in connection with synaptic plasticity. The authors conclude by integrating the observations summarized in the previous sections so as to present plausible hypotheses regarding the identity of the networks, synapses and molecular pathways that support fear and extinction.
Providing an up-to-date overview of the mechanisms of synaptic plasticity and physiological changes in the stressed and traumatized brain, this book will appeal to researchers, clinicians and students in the neurosciences.
M. R. Bennett AO is an internationally renowned neuroscientist. He is a professor of Neuroscience & University Chair at the University of Sydney, the founding director of the ‘Brain and Mind Research Institute’ and has been the president and organizer of many societies and symposia. His research has led to groundbreaking revelations in understanding synaptic functioning. He is the author of numerous papers and books, including ‘Philosophical Foundations of Neuroscience’ (2003 with Peter Hacker) and the recent works ‘Virginia Woolf and Neuropsychiatry’ (2013), ‘History of Cognitive Neuroscience (2008 with Peter Hacker) and ‘Neuroscience and Philosophy: Brain, Mind and Language (2006 with Daniel Dennett, John Searle and Peter Hacker). Prof. Bennett has received the leading award in biology and medicine in Australia (the Macfarlane Burnet Medal) as well as being made an ‘Office of the Order of Australia’ for his outstanding ‘service to the biological sciences, particularly in the field of neurosciences’.
Professor J. Lagopoulos is the inaugural director of the Sunshine Coast Mind and Neuroscience – Thompson Institute, which focuses on mental health and neurological research, clinical services and teaching. He is an expert in magnetic resonance imaging (MRI) and has been involved in neuroimaging for over 20 years. His work focuses on youth mental health, post-traumatic stress disorders, traumatic brain injury and healthy brain ageing and dementia. Prof. Lagopoulos is a leading academic and medical specialist who has published more than 170 peer-reviewed papers and contributed to several books. He is member of numerous international societies, including the ‘International Society for Magnetic Resonance in Medicine’ and the ‘Organization of Human Brain Mapping’. He has received several awards, including the ‘Westmead Foundation Prize’.
Cuprins
1. Grey matter changes in the brain following stress and trauma
1.1 During maturity
1.2 During Childhood
1.3 Animal Models
2. Synaptic changes responsible for grey matter changes in the brain of animal models following stress
2.1 Changes in the number of neurons, astrocytes and oligodendrocytes following stress
2.2 Changes in the length and volume of dendrites following stress
2.3 Discussion
2.4 The relation between stress-induced decreases in synapses/dendrites and grey matter loss
3. Identification of the core neural network subserving PTSD in animal models and their modulation
3.1 Animal models of PTSD
3.2 Neural circuitry subserving animal models of PTSD
3.3 Transmitters and growth factors mediating modulation of the core synaptic circuit in PTSD animal models
3.4 Conclusion
4. Modulation of the core neural network in stress: the role of Brain Derived Neurotrophic Factor & LTP
4.1 BDNF gene transcription controlled by glucocorticoid and mineralocorticoid receptors
4.2 Evidence that BDNF gene transcription controlled by epigenetic changes
4.3 BDNF control of dendritic spines
4.4 BDNF/TrkB control of dendritic spines modulated by glucocorticoid and mineralocorticoid receptors
4.5 BDNF/TrkB control of dendritic spines modulated by corticotropin releasing factor (hormone)
4.6 Cannabinoid (receptor CB1) modulation of BDNF gene transcription and BDNF/TrkB control of dendritic spines
4.7 Serotonin transporter (SERT) modulation of BDNF gene transcription and BDNF/TrkB control of dendritic spines
4.8 Conclusion
5. Modulation of the core neural network in stress: the role of Endocannabinoids & LTD
5.1 The role of endocannabinoids
5.2 Functional amygdala networks in acquisition and extinction
5.3 Classical LTP and LTD in the functional networks mediating acquisition and
5.4 Endocannabinoids in functioning networks in the basolateral amygdala
5.5 Functional amygdala networks that mediate extinction: the roles of LTDi and endocannabinoids at extinction neurons in the basolateral amygdala
5.6 Conclusion
6. Functioning of the core neural network in fear and extinction
6.1 Fear
6.2 Extinction
6.3 Synaptic plasticity
6.4 Modelling the amygdala in fear and extinction
6.5 Identifying the site of extinction failure in the amygdala
6.6 BDNF function at synapses in the core neural network for extinction
6.7 The role of the MeCP2 complex in extinction
6.8 Hypotheses concerning mechanisms for extending periods of extinction
Appendix 1: F-actin determination of dendritic spine integrity
Appendix 2: Regulation of NMDA receptors
Caracteristici
comprehensive overview on the role of synaptic plasticity in induction of fear and fear extinction
discusses the impact of stress and trauma on structure and cellular basis of grey matter
describes neuronal networks of fear systems
elaborates on BDNF and Endocannabinoids