Chapter 8 Flashcards
CONTROL THE DIGESTIVE SYSTEM AND OTHER ORGANS
DON’T HAVE A WHOLE LOT OF CONTROL OF THESE!
smooth muscles
CONTROL MOVEMENT OF THE BODY IN RELATION TO THE ENVIRONMENT
skeletal or striated muscles
HEART MUSCLES THAT HAVE PROPERTIES OF SKELETAL AND SMOOTH MUSCLES
cardiac muscles
A SYNAPSE BETWEEN A MOTOR NEURON AXON AND A MUSCLE FIBER
neuromuscular junction
RELEASE OF CHEMICALS CAUSES THE MUSCLE TO CONTRACT: - excites the muscle; makes it contract
acetylcholine
antagonistic muscles
flexor muscles
extensor muscles
FLEXES OR RAISES AN APPENDAGE
flexor
ONE THAT EXTENDS AN APPENDAGE OR STRAIGHTENS IT
extensor
FIbERS PRODUCE FAST CONTRACTIONS, BUT FATIGUE RAPIDLY
fast-twitch fibers
FIBERS PRODUCE LESS VIGOROUS CONTRACTION W/O FATIGUE
slow-twitch fibers
uses oxygen; SLOW TWITCH FIBERS; REQUIRE OXYGEN DURING MOVEMENT AND THEREFORE DO NOT FATIGUE
aerobic
does not use oxygen at the time; FAST TWITCH; USE REACTIONS THAT DON’T NEED OXYGEN= FATIGUE
anaerobic
receptor that detects position or movement of a part of the body
proprioceptor
OCCURS WHEN MUSCLE PROPRIOCEPTORS DETECT THE STRETCH AND TENSION OF A MUSCLE AND SEND MeSSageS TO THE SPINAL CORD TO CONTRACT IT
stretch reflex
knee jerk reflex
stretch reflex
receptor parallel to the muscle that responds to a stretch
muscle spindle
respond to increases in muscle tension; ANOTHER TYPE OF PROPRIOCEPTOR; LOCATED IN THE TENDONS AT THE OPPOSITE ENDS OF THE MUSCLE; ACTS AS A “BRAKE” AGAINST EXCESSIVELY VIGOROUS CONTRACTION BY SENDING AN IMPULSE TO THE SPINAL CORD WHERE MOTOR NEURONS ARE INHIBITED.
Golgi tendon organs
consistent automatic responses to stimuli
reflexes
they are insensitive to reinforcements, punishments, and motivations
involuntary
STRETCH REFLEX, DILATION OF THE PUPIL; MOVEMENTS THAT ONCE INITIATED, CANNOT BE ALTERED OR CORRECTED; THIS IS WHAT REFLEXES ARE
ballistic movements
neural mechanisms in spinal cord that generate rhythmic patterns of motor output
central pattern generators
a fixed sequence of movements THAT IS EITHER LEARNED OR BUILT INTO THE NERVOUS SYSTEM
motor program
do humans have any built-in motor programs?
yes, yawning
Infant reflexes
grasp reflex, babinski, reflex, rooting reflex
Pioneering work of Gustav Fritsch and Eduard Hitzig (1870); direct stimulation of the ______ elicits movements; does not send messages directly to the muscles
primary motor cortex
active when ppl “intend” a movement & “orders” an outcome
primary motor cortex
keeps track of the position of the body relative to the world
the posterior parietal cortex
DAMAGE TO THIS AREA CAUSES DIFFICULTY IN COORDINATING VISUAL STIMULI W/MOVEMENT; CAN’T WALK AROUND/TO OBJECTS; CAN’T REACH OUT TO GRAB IT
posterior parietal cortex
stores sensory information relevant to a movement and also plans movements according to their probable outcomes
prefrontal cortex
most active immediately before a movement. Receives info about a target to which the body is directing its movement, as well as information about the body’s current position and posture; INTEGRATES INFO ABOUT POSITION AND POSTURE OF THE BODY; ORGANIZES THE DIRECTION OF THE MOVEMENT IN SPACE
premotor cortex
along with the prefrontal cortex, is important for planning and organizing a rapid sequence of movements in a particular order; ORGANIZES RAPID SEQUENCE OF MOVEMENTS IN A SPECIFIC ORDER; INHIBITORY IF NECESSARY
supplementary motor cortex
I decide to do something, and then I do it.” This is obvious to us. Is it correct?
THERE’S SOME SORT OF DELAY; BRAIN BECAME AWARE OF IT BACK WHEN IT DECIDED TO DO IT, BEFORE YOU ACTUALLY DO IT
voluntary decision is at first…
unconscious
paths from cerebral cortex to the spinal cord
corticospinal tracts
A MIDBRAIN AREA W/OUTPUT MAINLY TO THE ARM MUSCLES
red nucleus
includes axons from many parts of cerebral cortex
medial corticospinal tract
A BRAIN AREA THAT RECEIVES INFO FROM THE VESTIBULAR SYSTEM!
vestibular nucleus
little brain
the cerebellum
one effect of cerebellar damage
CAUSES TROUBLE W/RAPID MOVEMENTS REQUIRING AIM/TIMING
EX: CLAPPING HANDS, SPEAKING, WRITING, ETC.
proposed that a key role of the cerebellum is to establish new motor programs that enable one to execute a sequence of actions as a whole
ito
flat cells in sequential planes
purkinje cells
axons parallel to one another and perpendicular to the planes of the Purkinje cells
parallel fibers
group lrg subcortical structures in the forebrain
caudate nucleus, putamen, globus pallidus
voluntary eye movement from one target to another
saccade
Parkinson’s disease
rigidity, muscle tremors, slow movements, difficulty initiating physical and mental activity, slow cognitive tasks
chemical that converts to MPP
MPTP
accumulates in, and then destroys, neurons that release dopamine
MPP+
the protein that codes the disease’s gene
huntingtin
what controls the speed of our movements?
- WALKING IN ITSELF REQUIRES SO MUCH EFFORT; MOVE AT A RATE OF HOW MUCH EFFORT WE HAVE TO PUT INTO IT. DEPENDS ON HOW MUCH EFFORT WE CHOOSE TO GIVE; OR ENERGY.
symptoms with parkinson’s
DEPRESSION, MEMORY, AND REASONING DEFICITS, LOSS OF OLFACTION (SMELL; ONE OF 1ST THINGS THAT TENDS TO GO), AND OTHER COGNITIVE DEFICITS
loss of dopamine activity leads to less stimulation of motor cortex and slower onset of movements
cerebral cortex
What about genetic influences?
- STRONG) STUDIES SUGGEST EARLY- ONSET PARKINSON’S HAS A GENETIC LINK
- GENETIC FACTORS ARE ONLY A SMALL FACTOR OF LATE ONSET PARKINSON’S DISEASE (AFTER 50)
smoking and coffee
• ARE RELATED TO A DECREASED CHANCE OF DEVELOPING PARKINSON’S DISEASE
why do coffee and smoking decrease chances?
• DAMAGED MITOCHONDRIA OF CELLS SEEMS TO BE COMMON TO MOST FACTORS THAT INCREASE THE RISK OF PARKINSON’S DISEASE
what effect of marijuana?
risk increases somewhat
PRIMARY TREATMENT FOR PARKINSON’S AND IS A PRECURSOR TO DOPAMINE THAT EASILY CROSSES THE BLOOD-BRAIN BARRIER
L-dopa Treatment
Problems with L-dopa
- Ineffective for some patients, especially those in late stages
- L-dopa does not prevent continued loss of neurons
- L-dopa produces unpleasant side effects; B/C IT ENTERS OTHER BRAIN CELLS
- Disorder is associated with gradual, extensive brain damage, especially in caudate nucleus, putamen, and globus pallidus. Also in cerebral cortex
Huntington’s disease
