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Kog.Neuro. (Fach) / Neuroplasticity (Lektion)

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• Neuroplasticity -capability of the nervous system to reorganize its function and structure to adapt to current requirements Sale et al., 2014: "...brain plasticity is defined as the capacity of neurons or neural circuits to adapt structurally and functionally in response to experience. This is fundamental for the adaptability of our behaviour, for learning, for memory processes, for brain development and brain repair." -quantitatively and qualitatively different during development and in adult life.
• What does neuroplasticity mean for us psychologists? -environment matters for brain development -behaviour is not entirely innate, but interaction between genotype and environmental factors -neuroplasticity is the prerequisite for any type of learning -as psychologists: brain plasticity mediates any type of intervention! 
• At what kind of level can neuroplasticity be studied? all kinds of levels, which are mutually dependent. E.g.: molecular, neural, synaptic, system behavioural level Molecular level: Neuromodulators and neurotropic factors (production and signaling) Synaptic level: efficiency of synaptic contact, elimination or formation
• How to study neuroplasticity? Experience must be systematically manipulated by... 1) intervention or training studies (cognitive interventions, motor training, perceptual training...) 2) direct or indirect injuries of the central nervous system (direct: lesions to the CNS, due to stress, neurodegenerative diseases, aging...; indirect: sensory deprivation, either partial or total deprivation, e.g. monocular blindness vs total blindness, deafness...) 3) development
• Hubel und Wiesel, 1964 -Demonstrated sensitive phases in the development of neural functioning by manipulating visual input after birth (monocular deprivation during the critical period leads to loss of binocular neurons in visual cortex!)
• Ocular Dominance Plasticity -induced by monocular deprivation -characterized by three temporally and mechanistically different phases: 1. 2-3 days after MD, Hebbian-dependent dramatic loss of response to the deprived eye 2. 5 days after MD, Hebbian and homeostatic-dependent increase in the open eye together with smaller increases to the deprived eye 3. after reopening the deprived eye and restoring binocular vision, neurotropic signaling-dependent return of respones to baseline
• MD in mice during critical period vs MD in adult mice -in adult mice, there are NO changes for the deprived eye, while the connections for the non deprived eye get stronger. After MD, connections return to baseline level for all cortical layers -during critical period, the connections for the non-deprived eye get stronger, while connections for the deprived eye get lost. Already after short 2-day deprivation, the lost connections of the deprived eye for layer 4 do not return to baseline!
• Rose et al, 2016; MD in adults -after adult MD, OD is restored at neural level -neurons that change strongly, but recover precisely (together with strong synapses who do not change "BACKBONE TUNING") may mediate the plasticity of the visual cortex
• sensitive phase, Knudsen 2004 -limited epoch during development, when experience has a larger impact on brain development
• critical period, Knudsen 2004 specific kind of sensitive phase -specific time frame, in which experience is crucial for brain development, experience results in IRREVERSIBLE CHANGE of brain function
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• Amblyopia -neurodevelopmental disorder of spatial vision -typically associated with strabism, mon(ocular) cataracts, anisometropia
• Anisometropia refractory power of two eyes differ (due to different size of eyeballs eg)
• Strabism non-aligned eyes due to muscle dysfunction
• characteristics of amblyopia (Levi, 2015) -starts before age 3 usually -changes at level of V1, V2 -treatment has to start early -sensory deficits including loss of visual acuity, contrast sensitivity, position acuity, impaires contour integration...
• Interventions to enhance adult plasticity (mice) Sale et al., 2014 -environmental enrichment -dark exposure -caloric restriction -exercise -perceptual learning   --> increase of serotoning, increase of BDNF, increase of IGF/I --> abruptly increase adult plasticity!
• dark exposure mice and mice with enriched environment prior to MD; recovery? Huebener & Bonhöffner, 2014 dark exposure mice and mice with enriched environment prior to MD -->changes the ipsi/contralateral ration of visual evoked potentials (VEP)  --> recovery from MD is facilitated by running in mice during presentation of visual stimuli --> visual stimulation during MD changes the Ocular Dominance (ODI Ocular Dominance Index) ALSO!--> experience during critical period influences plasticity in adulthood! During brain development a scaffold is elaborated (!), which sets limits of later plasticity!
• Physical exercise in amblyops Lunghi et al. -amblyopic eye patched -exercise and movie -controls only movie -->visual acuity of amblyopic eye improved for a year --> eye dominance shifted towards amblyopic eye
• Enhancing adult plasticity Bavelier et al., 2010 -removing structural brakes (=perineural nets, myelin) -resetting functional brakes (=inhibitory-excitatory circuits) -interventions push the system into plastic state (genetic, pharmacological, environmental: attentional demanding,high rewarding,extensive and diverse sensory stimulation)
• Adult Plasticity: Gamification Levi, 2015 Interventions in form of video games, movies improve stereovision in amblyopic patients (strabismic amblyopia)
• Crossmodal palsticity On a behavioural level can be observed: eg Blind Humans shos better performance at a range of auditory and tactile tasks, while deaf humans better visual and spatial skills have
• Crossmodal plasticity, deaf individuals Lomber, Meredith, Krall, 2010 -deaf cats show better peripheral vision and better detection of visual motion -researchers deactivated specific brain areas by cooling --> compensation of visual localisation was deactivated when specific brain area was deactivated, which is known to be important for auditory spatial processing in hearing cats!
• Lomber et al. hypothesis to cross modal plasticity -cortical modules might change in response to deafness their input modality, while maintaining their output functions -modality-specific features might have less potential for cross-modal reorganisation
• "voices for faces"- voice identity processing in congenital blinds and late blindness -congenital blindness: learn voices quicker and better generalize to new voice probes -late blindness: learn voices quicker --> fMRI: compared to healthy controls: both blindness types have higher activation in occipital areas, task-specific (voice-identity processing) activation can be observed in fusiform area  --> ERP:crossmodal activation of fusiform gyrus is faster activated in congenitally blind than in late blinds. Congenitally blind do seem to have an additional compensatory mechanism!
• sensory map - plasticity just some EXAMPLES: somatosensory - auditory - visual -syndactly connecting two fingers (surgically connected) lead to receptive field which can be activated by either of both fingers -behavioural training for specific frequency in owl monkeys lead to overrepresentation of specific frequencies -retinal lesion in cats : the lesion projectino zone in visual cortex is activated by adjacent input 
• musicians and piano tones Pantev et al, 1998 -tones elicit higher activation in auditory cortex of musicians -the earlier the musician started with his instrument, the bigger is the effect
• Where does visual perception learning take place? Schwartz et al., 2002 participants were trained in visual perception task in one eye --> increase of performance was only observable for one eye --> increased acitivity in visual cortex for upper left visual field, only for trained eye
• component of neuroplasticity synaptic plasticity
• Hebb rule presence of correlated acitivity in pre- and post-synaptic neurons promote potentiation of synaptic transmission -de-correlated acitivity promotes depression of synaptic transmission!
• Spike-time dependent plasticity synaptic efficacy can be increased or decreased according to the relative firing rate of pre- and postsynaptic neurons (long-term potentiation vs long-term depression; LTP vs LTD)
• mechanisms of neuroplasticity on synaptic level -anatomical change (change in the shape, size of the post-synapse; number of synapses) -change in connectivity -change in locus
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• homeostatic plasticity (vs hebbian pl.) the associated neurons increase their firing rate -neural acitvity is moved to original state -considered to counteract Hebbian plasticity to prevent system breakdowns (due to positive feedback loops)
• Hebbian plasticity pre- and postsynaptic acitivy emerges at the same time -> connection is strengthened -expresses cooperation and competition
• Overlearning - Towards consolidation Shibata et al., 2017 retrogade interference vs anterogade interference -retro.: second task did not interfere with the first task -antero.: interference of the first task with the second task --> But aftewr 3.5 h learning is stabilized, no interference is observed --> measured excitatory (glutamate) and inhibitory (GABA) measures --> after learning, neural representations are destabilized, overlearning guarantees stabilization and thus prevents forgetting!
• Neurogenesis Kempermann, 2008, 2012 -neural proliferation is found in the dental gyrus of hippocampus -physical activity seems to enhance neurogenesis -environm. enrichment leads to recruitment of new born neurons -neurogenesis in dental gyrus seems to be important for learning and memory (temporal storage and association of temporal close pieces of information)
• Influencing factors of neurogenesis Fuchs & Flügge, 2014 Positive modulators: -environmtental stimuli -exercise -learning -estrogen -antidepressants Negative modulators: -acute & chronic stress -nmda receptor activation -aging -glucocorticoids
• Neurogenesis- Exercising, Mouse- Human Pereira et al, 2007 Mouse-model: Exercising increases the CBV (Cerebral Blood Volume) in the dentate gyrus (part known to increase the rate of neurogenesis after exercising) -increase of CBV= most likely angiogenesis --> increase of neurogenesis and change in CBV is highly correlated in the dentate gyrus --> neurogenesis most likely accompanied by angiogenesis Human-study: 12 weeks exercising 4 times/week --> increase of CBV in the dentate gyrus!
• Aerobic fitness - hippocampus spatial memory Erickson et al, 2009 -MRI images to analyze the volume of hippocampus -increase in aerobic fitness --> increase in hippocampal volume  -hippocampal volume partially mediates accuracy in memory task and response speed
• Cardiovascular fitness and memory Holzschneider et al, 2012 +Hötting et al, 2012 --> increase in cardiovascular fitness led to an increase in brain activity during spatial memory task in a range of brain regions, eg hippocampus, ... subregions of frontal, temporal, occipital,congulate cortices... --> long-term: individuals who maintained their fitness, maintained their increase of memorizing in the spatial task compared to i. who did not maintain their fitness
• Ressource hypothesis! Kempermann, 2008 -lack of exposure and training during younger age (sensitive phase of neurogenesis) leads to reduced cellular and functional plasticity with increased age -exposure and training in younger age builds a neurogenic reserve for cellular and functional plasticity in the aging hippocampus!
• Behavioural POSITIVE consequences of neuroplasticity -faster learning -faster access to knowledge -increased processing efficiency -more "knowledge" -longer storage
• behavioral NEGATIVE consequences of neuroplasticity -phantom sensations (phantom pain, tinnitus) -seizures -dystonia ("musicians cramp", "writers cramp") -limitations in learning (critical period, sensitive phase)
• +++++++++ Summary +++++++++++ -neuroplasticity allows for lifelong learning -neuroplasticity early in life sets up a scaffold for adult learning -np involves strucutral and functional changes -multiple factors influence np, including neuromodulators (like glucocorticoids) and neurotropic factors -experience dependent=Hebbian plasticity and homeostatic plasticity guarantee plasticity and stability at the same time -more recently it was shown that the CNS (thus np) interacts with the immune system and other body systems!

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