Biological Psychology Week 5

Front 1

Name the three types of Reflexes

Back 1

Stretch Reflex

Golgi tendon reflex

Flexion reflex.

Front 2

Stretch reflex what is it?

Knee reflex test.

Back 2

Controlled by muscles spindle cell.

Annulospiral nerve ending embedded.

The axons increase by firing rate when the muscles is stretched.

Stretch reflex are used to counter balance, helps maintain posture.

Front 3

Golgi tendon Reflex, what is it?

Back 3

Nerve endings are located in the tendon.

Occurs during muscle contraction.

When stimulated causes inhibitory, interneuron connection by muscles and bones.

It inhibit to the muscles to over use them. during heavy lifting. Muscles relaxes.

Front 4

Flexion reflex?

Back 4

Dangerous stimulation causes that reflex.

Not brain reactive.

Makes sense for signal to remove arm then pain signal is received.

Sensory nerve axons that singal pain send excitory signals to flex muscles (control) and inhibitory to extension.

Front 5

Motor Programs

Back 5

Pre - programmed automatic sequences of movement.

Some are hardwired into the circuitry of spinal cord and brain. Into basal ganglia and cerebellum.

Walking...the brain turns it on and off pace.

Front 6

What does the medula do?

Back 6

Controls involuntary movement - breathing, sneezing, chewing.

Unlearned and learned (instinctive) behaviours.

Alzheimer's example can still use automatic responses. Medulla can still be functional, where as the substantia nigra and basal ganglia is effected. Parkinson's afflicts the SN and BG with lack of serotgenic.

Front 7

How does the brain control movement?

Back 7

The three areas Basal Ganglia, Motor Cortex and Medulla.

Front 8

Ptimary motor cortex (movements)

Back 8

The priotal lobe and the frontal lobe.

Somatosensory cortex of parietal lobe, help modulate the senses.

Front 9

What is the motor map?

Back 9

Neuron's map out the body's muscles on the opposite side.

Anterior means front.

Not on the physical size but the size on the motor neuruon.

Large numbrr of mu

Front 10

What is large and small aspects of the motor map.

Front 11

Giant Pyramdial Cells

Back 11

They initiate motor programs and complex movoemnts.

Front 12

Pyramidal System

Back 12

Very High Convergence of pyramidal cell axons onto motor neurons in the spinal cord.

It is like neural democracy, rather than a dictatorship. for energy conservation.

Front 13

Columnar organisation

Back 13

Adjacent coumns control opposing muscles groups

Later inhibitory interactions? between adjacent columns of cells.

Front 14

Pre motor and supplmentary motor cortices.

Back 14

In front of the primary motor cortex.

Organises, the direction of movement, step by step.

Front 15

What does the Basal Ganglia

Back 15

Three groups of culei - caudate nculeus 2. putamen 3. Globus Pallidus. The striatum

Disinibiting the thalamus from the stiratal neuron/ global pallidus. This allows the thalamus.

Self initiated movement

Front 16

Cerebellum

Back 16

Contains more neurons - great number because it is more compact.

Functions of timing of the movements with great precision.

contributes to the perception of time.

Front 17

Cerebellum gross structure

Back 17

Consider

Front 18

Cerebellur Cortex

Back 18

Receives input from different parts of the ervous system.

Organisaton fo the cerebellar cortex is extremely regular.

Primary fuctions: to inhibit the deep nuclei of the cerebellum and release from disinhibition from motor fibres.

Front 19

Purkinje Ceells

Back 19

Exclusively inhibitory - the deep nuclei which is the source of exhibitory of the cerebellum .

Long fibres activate them more. The longer the fibre, the longer the inhibition of the deep nuclei.

Short fibres

when active inhibit and movement signals.

Front 20

Cerebellum damage.

Back 20

Have difficulty with rapid movement - finger to nose test, eye saccades.

Cerebellar damage.

Patients have difficulty wiiht movments that require precise timing, speaking, writing.

Front 21

Extrapyramidal System

Back 21

Major tracts carry movment signals from the cerebellum and ganglia to the spinal cord.

Front 22

What are the movement disorders?

Back 22

MS - autoimmune disease where the immune system attack the oligodendrocytes that provide Myelin in the CNS.

Symptons - blindness. symptons can come back.

Drugs suppress the immune system can help reduce severity and slow progression.

Front 23

Myasthenia Gravis (Grave muscles weaknesses)

Back 23

Autoimmune disease attack the nicotine receptors in the muscles.

Occurs in elderly.

Treatment can be suppress the immuse sysemt and slow the progression.

Polio

Viral infection and attackand kills the motorneuron in the spinal.

Was a major scourge until the polio vaccine was developed.

Front 24

Polio

Back 24

Copy and paste from previous slides

Front 25

Parkinson's disease

Back 25

Most common after 65 ears of age.

Characterised by tremors, rigidity and in initiation of movements and substantia nigra.

difficulty in self initiated movement

Not know what has caused it. Can be genetic contribution especially for early onset of PD

Front 26

PD continued

Back 26

Backyard heroine - MPTP destryoed the substantia nigra.

Rapidly destroyed the serotonin.

Even though there are certain theories but it is largely uknown.

Front 27

What are the different in serotonin levels in parkinson's and non- parkinsons.

Back 27

In parkinson's disease, the normal neuron's dopamine, receptors are limited in transmission and receiving.

The self initiated proccess is ihibited. Guided stimuls can help them eg. marching in a group

The substantia nigra is degraded.

Front 28

L - Dopa (treatment for PD)

Back 28

it is converted in extra dopamine, to stimulate the substantia nigra - Basal gnaaglia.

Producing an agitation like writhing and agitation - when to much dopamine is in the brain.

Front 29

Using stem cells & Pallidotomy treatment for PD

Back 29

Successful in elinating abnormal movements from choronic use of L dopa. May slow progression of the disease.

Stem Cells: replace the lost cells in the substantia nigra.

Front 30

Huntington's disease

Back 30

Deteriation - of Basal ganglia, cerebellum and cerebral cortex.

Life in age of 40.

Symptons - uncontrollable

Genetic Component: if parent have HD 50% liklihood can be in children. Defective gene.

There is no effective treatment. It is fatal

Front 31

Amyotropic Lateral Scleroris ALS/ Motor neuron disease

Back 31

Disease wher moto neurons degenrate leading to weakness, excess glutamate release excitoxicity has been implicated.

Front 32

Cerebral Palsy

Back 32

Any non-aggressive neurological movement disorder from prenatal - perinatal brain damage.

Front 33

Muscular Dystrophy

Back 33

Muscles waste way, varying from early childhood disease to disability.

Defective production of dystrophin, which distablizes muscle structure.