CHAPTER 8: MOVEMENT

A. All animal movement depends on the contractions of muscles. Vertebrate muscles fall

into three categories:

1. Smooth muscles: Control movements of internal organs.

2. Skeletal or striated muscles: Control movement of body in relationship to the environment.

3. Cardiac muscles: Heart muscles.

B. Neuromuscular junction: A synapse between a motor neuron axon and muscle fiber.

1. In skeletal muscles, acetylcholine (Ach) is released at all axons terminals at the

neuromuscular junction.

C. Antagonistic muscles: Are necessary for moving limbs in opposite directions. 1. Flexor muscles allow limbs to be flexed or raised. 2. Extensor muscles extend or straighten limbs.

D. Myasthenia gravis: An autoimmune disease (a disease in which the immune system forms antibodies that attack the individual's own body). In myasthenia gravis the immune system attacks the acetylcholine receptors.

1. Symptoms include progressive weakness and rapid fatigue of skeletal muscles.

2. Treatment includes immune system suppressants and drugs that inhibit

acetylcholinesterase (enzyme which breaks down Ach at the synapse).

E. Fish are able to swim fast regardless of the water temperature because they use more

muscles in cold water and fewer muscles in warmer water.

F. Fish have three kinds of muscles: 1. Red muscles: Produce slow movements almost always without fatigue.

2. White muscles: Produce fast movements but fatigue quickly.

3. Pink muscles: Produce responses intermediate between the red muscles and white muscles.

G. Humans: different fibers can be mixed within same bundle:. Fast-twitch fibers produce fast contractions but fatigue rapidly; slow-twitch fibers produce less vigorous contractions without fatiguing.

H. Proprioceptor: A receptor that is sensitive to the position or movement of a part of the body. Muscle proprioceptors detect the stretch and tension of a muscle.

1. Stretch reflex: After a muscle is stretched, the spinal cord sends a signal to

contract the muscle.

2. Muscle spindle: A kind of proprioceptor; when stretched, its sensory nerve sends a message to a motor neuron in the spinal cord, which sends a message back to the muscles surrounding the spindle, causing a contraction.

3. Golgi tendon organ: Located in the tendons at opposite ends of muscles, these

proprioceptors inhibit muscle contraction when it is too intense.

I. Reflexes: Consistent automatic responses to stimuli which are generally involuntary.

1. Ballistic movements: Once initiated, this movement cannot be altered or corrected

(e.g., reflex).

2. Central pattern generators: Neural mechanisms that generate rhythmic patterns of motor output (e.g., wings flapping in birds, fin movements in fish, etc.).

3. Motor programs: Fixed sequence of movements; could be produced by a central pattern generator or another neural mechanism.

A. The role of the cerebral cortex.

1. Primary motor cortex: Sends messages to the medulla and spinal cord, which sends its axons to the muscles.

2. Posterior parietal cortex: Keeps track of the position of the body relative to the world. People with damage to the posterior parietal cortex have trouble converting their visual perceptions into actions.

3. Primary somatosensory cortex: Sends sensory information to the primary motor cortex.

4. Prefrontal cortex: Responds to sensory signals that lead to movements.

5. Premotor cortex: Mainly involved in preparations for a movement rather than the movement itself.

6. Supplementary motor cortex: Most active while preparing for a rapid series of movements (e.g., pushing, pulling and turning a knob or stick).

B. Connections from the brain to the spinal cord.

1. Dorsolateral tract: Axons from the primary motor cortex and from the red nucleus of the midbrain synapse in the spinal cord. In the medulla lie the pyramids where the dorsolateral tract crosses to the opposite side of the spinal cord. This tract controls movements of the distal limbs (e.g., hands, fingers and toes).

2. Ventromedial tract: Axons from both primary and supplementary motor cortices, as well as from the midbrain tectum, reticular formation and the vestibular nucleus; this tract is largely responsible for neck, shoulder and trunk movements.

C. Cerebellum (Latin for "little brain"): Involved in motor control and learned motor behavior; cerebellar damage or alcohol intoxication may lead to deficits in rapid ballistic movements.

1. Saccades: Ballistic eye movements from one fixation point to another. These movements depend on impulses from the cerebellum and the frontal cortex to the cranial nerves (patients with cerebellar damage may have difficulty following and fixating on moving objects).

2. Finger-to-nose test: This ability relies on the cerebellar cortex to relay information to synapses in the interior of the cerebellum.

3. Cerebellum appears linked to habit formation, timing, certain aspects of attention, and other psychological functions as well as motor functions.

4. The cerebellum receives input from the spinal cord, from each of our five senses via cranial nerve nuclei, and from the cerebral cortex. The information eventually reaches the cerebellar cortex, the surface of the cerebellum.

5. Action potentials of parallel fibers (axons parallel to one another) excite one Purkinje cell (very flat cells in sequential planes ) after another.

6. Purkinje cells inhibit cells in the nuclei of the cerebellum (clusters of cell bodies

in the interior of the cerebellum) and the vestibular nuclei in the brain stem.

D. The Basal Ganglia: Comprised of a group of subcortical structures in the forebrain (including the caudate nucleus, putamen, globus pallidus).

1. The basal ganglia has multiple connections with the cerebral cortex and the thalamus. The caudate nucleus and the putamen are receptive areas and the globus pallidus is the output area.

2. Basal ganglia damage impairs movement. The basal ganglia is also important for habit learning and the selection of movements.

A. Parkinson's Disease (PD): Symptoms include rigidity, resting tremor, slow movements and difficulty initiating physical activity.

1. The immediate cause of PD is the gradual progressive death of neurons in the substantia nigra and the amydala. Most of the focus of PD research has been on the death of dopamine containing neurons in the substania nigra.

2. MPTP: A chemical that our bodies convert to MPP+2, a toxin that destroys dopamine neurons.

3. Parkinson's disease probably results from a mixture of causes. A gene is responsible for many cases of early onset PD; exposure to toxins can increase risk however, most causes of PD are unknown at the present time.

4. L-Dopa: A precursor to dopamine. Commonly used as a treatment for Parkinson's disease.

5. - Alternative therapies for PD include:

antioxidant drugs

· direct dopamine agonists

· glutamate antagonists

· neurotrophins

· apoptosis blockers

· high-frequency electrical stimulation of the globus pallidus

· nicotine

· fetal brain grafts

B. Huntington's Disease (HD), Huntington disease or Huntington chorea: Symptoms include twitches, tremors and writhing movements.

1. Brain degeneration is especially severe in the caudate nucleus, putamen, and globus pallidus.

2. Psychological disorders include depression, memory deficits, anxiety, hallucinations, delusions, poor judgment, alcoholism, drug abuse, and sexual disorders.

3. HD onset can occur at any age but most often appears between the ages of 30 and 50.

4. HD is caused by an autosomal dominant gene on chromosome 4. The gene can be identified by a presymptomatic test (before the onset of symptoms) with almost

100 % accuracy.

5. The gene for HD codes for the protein, huntingtin, that is found inside brain

neurons.