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Unformatted text preview: Plasticity Cognitive Neuroscience McClelland, McNaughton & O'Reilly (1995) Two learning systems: neocortical and hippocampal n Hippocampus: q q q learns quickly rapid, onetrial learning local representations during consolidation serves as "teacher" to the neocortex, until neocortical connection changes are robust n Neocortex: q q q learns slowly, by making small adjustments to connections among neurons allows integration into complex knowledge structures distributed representations Quiroga et al. (2005) n n Intracranial singleunit and multiunit recording Medial Temporal lobe q n n 8 patients 993 sites n Shown pictures of people, animals, objects, famous buildings. q 132 sites (14%) responded to a least one picture. 51 sites (38.6% of responding sites 5% of all sites) showed invariant recognition of 1 or 2 objects q q Items were chosen based on each subject's knowledge. ~100 items per subject. q Responded to different views of same object No response to other objects Most Startling Response n Single cell in right anterior hippocampus Responded only to pictures of Halle Berry, and to the printed words "Halle Berry". n Evidence for Sparse Encoding in MTL n Can't say for sure that it's a local encoding, because there may be other (untested) items to which a given cell would respond. Statistical analyses indicate: Assume ~9 billion cells in MTL, ~20,000 percepts q A single percept activates ~2 million cells (0.02%) q Each cell responds to ~100 percepts q Sparse encoding, not local encoding
q n Hippocampal Neurogenesis n New cells generated in adult hippocampus (mammals including humans) q q q q q Adult neurogenesis thought only to occur in the hippocampus. ~9000 a day in rodents Maturation takes about 30 days. New cells (428 days old) necessary for acquisition of spatial LTM in rats. Posterior hippocampi are larger in London taxi drivers than in control subjects. n n n London taxi drivers have extensive spatial knowledge They must pass stringent navigation tests in order to be licensed Typically takes 2 years to acquire this knowledge Hippocampal Neurogenesis Neurogenesis is increased by exercise. n Neurogenesis is decreased in: n Sleep deprivation q Depression q n n Antidepressants, ECT increase neurogenesis In rats, if hippocampal neurogenesis is blocked, antidepressants are not effective. Localization of function: Evidence n n n n n Cases such as Broca's: restricted damage selective cognitive deficits Cortical stimulation Single cell recording Functional neuroimaging Exquisite intricacy of connectivity (primary sensory areas) Suggests that specific, complex circuitry supports cognitive processing Similar localization across individuals suggests a detailed neural blueprint Plasticitythe paradox On the one hand: Evidence of precise localization of function and failure to recover function subsequent to damage and early deprivation n On the other hand: Remarkable learning capacity, requiring subtle, complex and extensive neural change/plasticity n Plasticity: n What is it? q How and when does it happen? q What are the limits?
q blueprint & learning nature & nurture William James (1890) On the one hand: "....the elementary qualities of cold, heat, pleasure, pain, red, blue, sound, silence, etc., are original, innate or a priori properties of our subjective nature.... On the other hand: "though they ..... require the touch of experience to waken them into actual consciousness, and should slumber to all eternity without it" Plasticity and its Limitations 1. 2. 3. 1. Visual system: Limitations of plasticity Evidence from critical periods Visual system: Possibility of plasticity Evidence from blindness Somatosensory system: Plasticity Peripheral manipulations (changing the input) n n n 2. Deprivation/Amputation Syndactyly Enrichment/practice Cortical lesions Central manipulations (changing cortex) n 4. Mechanisms of plasticity Critical Periods n Period of time during which, if the animal does not receive the appropriate exposure to structured stimuli or experiences, a system will not develop normally Visual system q Language system
q Plasticity "failures" Critical Periods Effects of Deprivation (1) Ocular Dominance columns Normal animal: Distribution of V1 neurons as a function of the degree to which they respond to Contralateral (e.g., right eye) and Ipsilateral (e.g., left eye) stimulation (4= binocular neuronsrespond equally well to contra and ipsi stimulation A: Right eye of normal monkey was injected with a radiolabeled amino acid Autoradiograph in V1 taken 10 days later. Radioactivity forms white strips. B: Animal deprived of vision in one eye during the critical period, and the eye which had been open was injected reduction in ocular dominance column (Hubel & Wiesel, 1977) Plasticity "failures" Critical Periods Effects of Deprivation (2) Human strabismus: imbalance in eye muscles upsetting the coordination between the two eyes > ambliopia (one eye becomes dominant) leading to: q q loss of cortical representations and acuity in the less dominant eye Loss of binocular cells and reduction in stereo vision n Loss of acuity is virtually permanent beyond a certain age (approx 57) and stereo at an even younger age n n Critical period: 26 years of age Treatment: correct muscle imbalance alternating patching Plasticity "failures" Critical Periods Effects of Deprivation (3) Orientation selectivity: Blakemore & Cooper (1970): n Deprivation of exposure to specific edge orientation during the critical period leads to loss of orientation perception Plasticity and its Limitations 1. 2. 3. 1. Visual system: Limitations of plasticity Evidence from critical periods Visual system: Possibilities of plasticity Evidence from blindness Somatosensory system: Plasticity Peripheral manipulations (changing the input) n n n 2. Deprivation/Amputation Syndactyly Enrichment/practice Cortical lesions Central manipulations n 4. Mechanisms of plasticity Plasticity in the visual system Sadato et al (1996) n PET study n Subjects: n n Blind (congenital or early onset) Sighted subjects Nondiscrimination task: sweep index finger over a rough surface homogeneously covered with Braille dots NonBraille discrimination: line angle, line width, characters Braille lexical decision (blind Ss only) n 3 tactile tasks presented to index finger n n n Sadato et al. (1996) For voxels in Primary Visual Cortex: Compare PET signal for: task vs. rest Nondiscrim. Sighted Blind nonBraille discrim. Sighted Blind Braille LD Blind + sig + sig + sig nonsig nonsig Blind subjects increased activation in V1 for tactile discrimination. Indicates V1 is processing somatosensory information. Sighted subjects decreased activation in V1, likely a result of attention to haptic modality. Dilks et al.(2007) n BL suffered stroke at age 45. Damaged optic radiations for upper LVF information (i.e., projections from LGN to lower bank of right calcarine sulcus). V1 intact. Perception of shapes presented to lower LVF. Shape is perceived as extending into upper LVF. (6 months poststroke.) Hypothesis: Distortion results from reorganization of V1: lower LVF information now extends into upper LVF region. Dilks (2007) fMRI retinotopic mapping proves reorganization of right V1 in BL. Plasticity and its Limitations 1. 2. 3. 1. Visual system: Limitations of plasticity Evidence from critical periods Visual system: Possibilities of plasticity Evidence from blindness Somatosensory system: Plasticity Peripheral manipulations (changing the input) n n n 2. Deprivation/Amputation Syndactyly Enrichment/practice Cortical lesions Central manipulations n 4. Mechanisms of plasticity Somatotopic maps Plasticity in the Somatosensory System: Mapping Somatosensory cortex Plasticity in Somatosensory cortex: Amputation Merzenich et al. (1984) n n n Amputation of digits in owl monkeys 244342 penetrations within and bordering 3b hand area Stimulation skin (finetipped glass probe) while recording cortical receptive fields (anesthetized monkeys) What happens to the neurons that used to get input from digit 3? n Area of cortical surface that responds to stimulation to a specific digit (D) Plasticity in Somatosensory cortex: Amputation Results: (1) n Remapping: Neurons dedicated to amputated digit 3 respond to stimulation by digits 2 & 4 Remapping maintains topography n (2) Smaller receptive fields in the reorganized area n Possible consequences for acuity? n What does it `feel" like? n When neurons that previously responded to stimulation to digit 3 become active as a result of stimulation to digits 2 or 4? Plasticity in Somatosensory Cortex: Syndactyly Allard et al. (1991) Skin of digits 3 and 4 in adult monkeys was surgically connected to create artificial syndactyly > Increases the amount of simultaneous input from normally separated fingers Maps were obtained 37 months later n n n Results: Normal discontinuity between representations was obliterated > twodigit receptive fields that are only rarely seen in the normal hand Plasticity in the Somatosensory System: Practice Merzenich et al. n Finger tips (distal 2, 3, 4) are stimulated by being set on a revolving corrugated metal drum for 1 hours per day for 3 months Results: cortex expands receptive fields are unusually small Plasticity in Somatosensory Cortex: Removal of Syndactyly Moligner et al (1993) Using MEG mapped hand area of somatosensory cortex in two human adults with congenital syndactyly n Remapped area 15 weeks following surgery
n Normal subject MEG normal Results: presurgical maps were largely nonsomatotopic significant postsurgery reorganization with clear somatotopy the degree of reorganization correlated with the severity of the syndactyly Plasticity and its Limitations 1. 2. 3. 1. Visual system: LimitationsEvidence from critical periods Visual system: PlasticityEvidence from Blindness Somatosensory system: Plasticity Peripheral manipulations (changing the input) n n n 2. Deprivation/Amputation Syndactyly Enrichment/practice Cortical lesions Central manipulations n 4. Mechanisms of plasticity Somatosensory system: Plasticity after central lesion
Jenkins & Merzenich(1987) Aimmediately after lesion B58 days after lesion, ulnar aspect Neurons previously responsive to 4 or 5 now responsive to 3 Reorganization of 4 and 5 maps Representational "compression" Less cortical space available To represent more info Somatosensory system: Plasticity after cortical lesionHow might it "feel" Rapp et al. (2002) 2 Ss with left hemisphere parietal lesions affecting somatosenstory areas n Very accurate tactile detection (always report they were touched) n Tactile localization?
n Stimulation locations Perceptual Space: RSB Palmar surface Dorsal surface Perceptual Space: AKH Mechanisms of plasticity (1) "Growth" Cortical neurons deprived of sensory input secrete neurotrophic factors, causing nearby neurons to sprout new synapses, dendrites, axon terminals Some evidence of neurogenesis Circuits released from inhibition Syntaptic reweighting/remodeling, recruitment of "silent" synapses q q (2) Unmasking of "silent" inputs q q Unmasking of silent inputs?The case of amputation n Assume that sensory cells from face normally project both to cortical face and hand neurons skin F H F H brain n Assume that the signal from face to hand is normally inhibited by intact connections from handhand skin F H F H brain n Loss of handhand input "reveals: handfact connection Mechanisms of plasticity n How to distinguish between these two hypotheses? q Growth and unmasking? Calford & Tweedale (1990) Flying foxes: Calford & Tweedale (1990) Flying foxes (large bats) 1Localized neurons that respond to stimulation of thumb 2Anesthetized thumb 3Recorded from "thumb" neurons 4Dark areas indicate receptive field location of these neurons **notice how rapidly the receptive fields expand and contract --What implications does this have for the two hypotheses under consideration? Unmasking of silent inputs?The case of amputation/anaesthesia n Assume that sensory cells from face normally project both to cortical face and hand neurons skin F H F H brain n Assume that the signal from face to hand is normally inhibited by intact connections from handhand F H F H skin brain n What happens if hand input is removed? reveals: handfact connection Plasticitythe paradox On the one hand: Evidence of precise localization of function and failure to recover function subsequent to damage and early deprivation n On the other hand: Remarkable learning capacity, requiring subtle, complex and extensive neural change/plasticity n Plasticity: n What is it? q How and when does it happen? q What are the limits?
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