Cross Modal Plasticity, Multisensory Integration, and Synaptic Plasticity

fMRIs

indirect measure of using activity, how O2 use (oxygenated to deoxygenated blood) to show activity

Blood oxygen level dependent response

more oxygenated blood, more activity in that area

Transcranial magnetic stimulation

a magnetic field induces an electrical response (AP) either inhibitory or excitatory, in a specific region

Reading braille fMRI

primary visual cortex (v1) active while reading, increased visual association area activity, decreased S1 activity

Timing pattern for blind patient fMRI

regardless of timing of blindness, V1 active while reading braille

Interference of V1 when reading braille

decreases touch perception of blind patients (not sighted)

Reading braille v. non-reading touch

visual word forming areas active while reading braille

Teaching sighted people braille

show learning effect with increased activity

Reading braille & reading speed

increased activity of ventral visual system in faster readers

Echolocation

making clicking/tapping sounds, returning echos help perceive physical aspect of surroundings

Brain processing of echolocation

sounds processed in visual parts, not brain

Dorsal/upper visual pathway

spatial info, “where”

Ventral/lower visual pathway

object recognition, “what”

Visual system pathway locations

run in parallel to occipital lobe

Echolocator visual systems

dorsal active when locating, ventral active when identifying

Repurposing visual system

for non-sensory functions like language

Verbal memory tasks

blind outperformed sighted individuals, visual cortex active during verbal memory

deaf brains

widespread changes, auditory cortex rewired to process vision

Peripheral sight in deaf people

increased area for optic disk, better dorsal/”where” stream

functional connectivity changes in deaf people

changes in S1 to thalamus pathway

Summary of deaf and blind studies

localization of functions are not fixed, regions can switch roles (especially visual)

McGurk Effect

Discrepancy of sensory info, hear something/see another

Synesthesia

sensory info of one type appears as another, not a conscious choice but can be learned

Grapheme-color synesthetes

each letter of the alphabet or number is always seen as a different color

Auditory-visual synesthetes

sound sensations from seeing different colors

Synapses

site of neurochemical transmission/transduction

Synaptic plasticity

ways in which synapses can be modified

Neuronal Signal pathway

dendrites → axon hillock → axon → axon terminal → conversion of electrical to chemical

Effector organs

skeletal muscle fibers, glands(hormones), or other brain neurons

Axodendritic

axon terminals synapses at another’s dendrites

Axosomatic

axon synapses at another’s soma (cell body)

Axoaxonic

axon terminals synapses at another’s axon

Axon terminal naming

synaptic boutons

Excitatory synapse

glutamate released, increased probability of AP firing, depolarizing

Dendritic spines

variety of shapes, not uniform

Inhibitory synapse

GABA released, decreased probability of AP firing, hyperpolarizing

Physiology of sending an AP

Ca2+ volt gated channels open, causing vesicles to fuse and exocytose into cleft, 1) bind to receptors on post-synaptic membrane OR 2) couple with proteins to produce biochemical changes in post-synaptic neuron

Long Term potentiation people

Alexander Bain and Donald Hebb

Long term potention

memories strengthen synaptic connections

Long term potentiation experiment

stimulated rabbit hippocampus, repetitive stimulations showed larger spikes in EPSPs (more depolarizations), response lasted longer than

Long term potentiation timing

lasts days, weeks, maybe longer

Normal State of AMPA/NMDA receptors

glutamate binds with AMPA and kainate receptors

Long term potentiation requirement

glutamate must bind to NMDA receptor

Long term potentiation physiology

glutamate binds to AMPA and kainate, high frequency increases glutamate, Mg+ released (was blocking NMDA), Ca2+ influx triggers secondary messengers to insert more AMPA receptors into membrane

Reversibility of long term potentiation

can remove receptors and decrease vesicles, called long-term depression

Long term depression requirement

NMDA dependent, but different Ca+ secondary messenger cascade

Long term depression physiology

low frequency stimulus releases glutamate, fewer NMDA and less Ca+ than LTP, different Ca+ secondary cascade, causes AMPA receptors to be removed (less available)