Motor Cortex

imissyou419's version from 2017-01-28 22:43


Question Answer
3 main techniques used to demonstrate function of a particular brain regionstimulation, lesion, recording
What do they use for stimulation?electrical, magnetic, or naturally occuring (epileptic discharge)
What do they use for lesion?electrical, chemical, naturally occuring (stroke, degeneration) to destroy neurons
what do they use for recording?single neurons, evoked potentials, EEG (ElectroEncephaloGraphy), PET (Positron Emission Tomography), fMRI (functional Magnetic Resonance Imaging)
Define motor cortexareas of cortex which LOW INTENSITY electrical stimulation produces skeletal muscles contractions which are contralateral for arm and leg
Location of motor cortexpre-central gyrus
Somatopic organization for motor cortexsomatotopic map on precentral gyrus from medial to lateral: leg, trunk, shoulder, elbow, hand, face, tongue (referred to as distorted motor homunculus) "2 people lying with their feets touching"
Electrically stimulating motor cortex vs. electrically stimulating somatosensory cortex of the region representing the handmotor cortex -> movement of contralateral hand; somatosensory cortex -> tingly of contralateral hand
Which 2 regions of the body have the largest representation?hands and face
What are the 4 evidence for somatotopic organization?1. A somatotropic map was first interred by Hughlings Jackson from observations of epileptic motor seizures (Jacksonian March) (epileptic starts with flexing of fingers, then hand, arms, shoulder and spread up to face, down trunk because of lesion that causes epilespy in finger area);
2. confirmed by electrical stimulation (Penfield);
3. lesion (strokes) in this area lead to paralysis (in extreme cases) and weakness (in lesser cases), spasticity, e.g. a large legion in medial side of right precentral gyrus will cause paralysis of left leg;
4. recording of neural activity (neuron discharge before movement occurs)
What are the 3 evidence that motor cortex representation is for MOVEMENTS, not muscles1. a particular muscle can be activated by stimulating widely dispersed motor cortical sites;
2. Single motor cortical neurons make monosynaptic connections with motoneurons innervating several different muscles;
3. motor cortex microstimulation produce purposeful-like movements (feeding, reaching, defense) (if you stimulated hand, monkey makes purposeful movement such as feeding)
What are the 2 evidence that somatotopic organization is plastic?1. learning (increased in size of finger representation upon learning a complex task); 2. experimental injury (small artery supplying hand region of motor cortex was blocked so neurons died; trained monkeys now had hand representation in adjacent elbow/shoulder region, non-trained monkeys had no hand representation)
What is one explanation for rehabilitation of damaged hand representation?silent synapses for hand in the adjacent region, these silent synapses involved in long term potentiation NMDA receptor lets Ca2+ in which increase sensitivity of Na+ channels, insert existing Na+ channels in membrane, make more Na+ channels - for AMPA (AP), silent synapses can become activate under conditions of training and learning
3 output pathways from motor cortex1. corticospinal (pyramidal tract), 2. corticorubral (to red nucleus), 3. corticoreticular (to reticular formation in pons and medulla)
Corticospinal tract phylogenetic developmentonly occurs in mammals and shows progressive development up mammalian tree especially in primates
Corticospinal tract termination10% of axons make MONOSYNAPTIC connections with alpha motorneurons - go to fingers (90% have interneuron)
Corticospinal tract LESIONmonkeys first appear normal i.e. they can walk, run climb (this is because they have circuits for locomotion in spinal cord, descending pathways from brainstem (corticoreticular, corticorubral), other descending pathways from motor cortex) but there is loss of refined movements (loss of speed and agility in movements/loss of control of force, loss of independent finger movements which is associated with loss of corticospinal monosynaptic connection)
Corticospinal evolutionpyramidal tract/corticospinal tract + DC/ML evolved together up mammalian scale, for accurate identification and manipulation of objects and tool
Effects of a lesion of motor cortex in manweakness or paralysis and spasticity (increased muscle tone - increased resistance to passive movement caused by an increase in stretch reflex, which in turn is partly caused by loss of inhibition from motor cortex)
Lesion in motor cortex has bigger effect than corticospinal tract lesiona stroke will take out everything compared to just cutting the pyramidal tract
What are the 3 findings about the discharge of pyramidal tract neurons1. some discharge before movement onset, 2. discharge preferentially for 1 direction of movement (i.e. biceps does not discharge for extension), 3. discharge proportional to force or rate-of-change of force (increase discharge frequency to produce more force)
Discharge of many pyramidal tract neurons ismuscle-like
What are the factors that cause the time delay between onset of motor cortex discharge and movementconduction time from cortex to spinal cord, time for summation of EPSPs to threshold in alpha motorneurons, conduction time from spinal cord to NMJ, synaptic delay at NMJ (1ms) (50 ms), electrical mechanical coupling time 50ms (time from muscle AP to movement onset i.e. myosin & actin + time for muscle contraction to overcome mass/inertia of limb)

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