Chapter 5 Flashcards
what is a receptor potential?
local change in membrane potential that resembles the EPSP
what is sensory transduction?
conversion of environmental stimuli into action potentials that are transmitted to the brain
why are sensory information separate and distinct?
AP for each sense are carried on separate nerve tracts
- labeled lines: brain recognizes senses as distinct because their AP travel along separate nerve tracts
what are skin sensations?
pressure, vibration, tickle, pins & needles, smoothness/ wetness all form touch
what is a skin receptor that is an example of sensory transduction?
Pacinian corpuscle -> sense texture
- stimuli stretching its membrane -> opens Na+ channels -> creates graded generator potential -> if potential exceeds threshold, fires AP
what are the different receptors in the skin?
Pacinian corpuscle: texture sensitivity
Meissner’s corpuscles: touch (changes)
Merkel’s discs: touch (edges)
Ruffini corpuscles: skin stretch
Free nerve endings: pain, heat, and cold
how is intensity of a stimulus measured?
- number and frequency of AP
- number of activated sensory receptors
what are the three key organizational principles that help sensory neurons tell the brain the location of a stimulus?
- labeled lines
- somatosensory map (body surface divided into discrete bands)
- receptive fields (area within which the presence of a stimulus will alter a sensory neuron firing rate)
what is sensory adaptation?
progressive decrease in receptor response to sustained stimulation
- avoid overload and remain vigilant for critical events
how does sensory adaptation occur?
phasic receptors display adaptation (most of touch receptors) while tonic receptors show little or no adaptation (pain receptors)
what are limited senses?
the sensory organs and pathways convey only limited (or distorted) information to brain
- brain receives highly filtered representation of external world
- stimuli critical for survival are strongly emphasized at expense of less important stimuli
how can sensory information be suppressed?
- removing the stimulus
- central modulation of sensory information (brain actively suppresses some sensory inputs and amplifies others)
- reciprocal neural connections descend from brain to synapse on lower sensory levels where they can inhibit activity in ascending sensory axons
how does the thalamus control sensory information?
information about each sensory modality sent to separate division of thalamus
- cortex directs thalamus to emphasize some sensory information and suppress other information
what is the difference between primary sensory cortex and non primary sensory cortex?
primary sensory cortex (one exists for each modality)
non primary sensory cortex (receives direct projections from primary sensory cortex area for that modality)
what are association areas of the brain?
association areas in the brain process inputs from different modalities allowing information from different modalities to interact
- polymodal neurons process input from different sensory neurons
what are the benefits of pain?
- withdraw from its source
- engage in recuperative actions
- warn others and elicit care from others
how do nociceptors activate?
peripheral receptors on free nerve endings that respond to painful stimuli
- when tissues injured, affected cells release chemicals (serotonin, histamine, and various enzymes and peptides- substance P) that activate nociceptors
how does pain get transmitted to the brain?
- damaged or injured cells release substance that excite free nerve endings that function as pain receptors or nociceptors
- produce action potential that send signals to spinal cord
- pain fibers release glutamate and substance P to signal brain about pain
what is substance P?
peptide transmitter involved in pain transmission
- promotes inflammation around injured tissue
how do you activate local pain response?
pain information is also transmitted to local blood vessels and mast cells
- engage in mechanism that helps heal damaged tissue and prevent further damage
1. blood vessels activated by substance P direct more blood to damaged cells
2. mast cels also activated by substance P release chemicals that produce inflammation response
what is the peripheral mechanism of pain?
- damaged or injured cells release chemicals that excite free nerve ending that function as pain receptors or nociceptors
- painful information then transmitted to spinal cord as well as blood vessels and mast cells
- blood vessels activated by substance P direct more blood to damaged cells
- mast cells activated by substance P release chemicals produce inflammatory response
what are the two types of fibers that transmit pain to CNS from spinal cord?
- A delta fibers: large myelinated axons that register pain quickly (allows for quick responses that prevent further damage)
- C fibers: small unmyelinated axons that conduct more slowly, producing lasting pain
how do the different fibers detect painful temperature changes?
A delta fibers detect very high temperatures via TRPM3 receptors that need a quick response -> does not respond to capsaicin
C fibers detect via TRPV1 receptors -> bind to capsaicin
what is the anterolateral system?
transmits the sensations of pain and temperature to brain via A delta and C fibers
- projection distinct from somatosensory system -> glutamate and substance P released to boost pain signals and remodel neurons
how is pain interpreted in CNS?
pain information is modulated by periaqueductal gray area -> pain information then sent to many different thalamic and cortical regions -> most conscious feelings of pain associated with cingulate cortex
how does the somatosensory cortex relate to pain perception?
pain information transmitted from thalamus to somatosensory cortex -> brain activity in somatosensory cortex correlates to how much discomfort each person report
- information about painful stimulus transmitted to cingulate cortex and other
what does the cingulate cortex do?
activity in the cingulate cortex also correlates to how much discomfort each person reports
- different subregions in cingulate cortex seems to mediate emotional pain vs. sensory aspects of pain
- become active when we empathize with a loved one experiencing pain
what is neuropathic pain?
pain that persists long after the injury that started it has healed
- ex: phantom limb pain
what are the three ways to reduce pain?
pharmacological, psychogenic, and stimulation
- all produce analgesia (absence of or reduction of pain)
what is the problem with chronic pain?
prefrontal cortex shrinks faster than normal
what is the hierarchy of movement control?
- primary and non primary motor cortex create motor plans
- basal ganglia and cerebellum provide adjustments to motor plans
- brainstem and spinal cord send motor commands to body
what are antagonist vs synergists?
antagonists: when one muscle group contracts, it stretches the other group (biceps and triceps)
synergists: muscles that act together to move a limb (triceps)
how does the CNS monitor rapid coordinated movements?
- state of muscle (are they contracted or lengthened)
- the positions of the limbs (where limbs are located in space without looking)
- accomplishes this via specialized receptors called proprioceptors (proprioception is collection of information about body movements and positions)
what are the two kinds of proprioceptors?
- muscle spindle (muscle receptor that lies parallel to muscle and signals to CNS when muscle is lengthened or stretched
- Golgi tendon organs (type of receptor found within tendons that send impulses to CNS when muscle contracts or tightens)
what are the steps for a stretch reflex?
- weight dropped into hand stretches biceps muscles
- stretch excites muscle spindles -> send AP to spinal cord (sensory neuron)
- stretch signal from biceps activates motor nerves to stimulate biceps motor neurons -> contraction
- stretch signal from bicep stimulates interneurons that inhibit motor nerves to antagonistic triceps motor neurons -> triceps to relax
- reflex generates compensatory movement that bring back to intended position
what are the two pathways that the brain controls body muscles?
- pyramidal motor system (corticospinal) -> include neurons within cerebral cortex and their axons that form pyramidal tract
- extrapyramidal motor system -> include basal ganglia, cerebellum, and some closely related brainstem structures
what is the pyramidal motor system?
primary and non primary motor cortex create motor plans that are sent to body via spinal cord to execute movement
- neurons within primary form pyramidal motor system -> axons pass through pyramid of medulla
what is an unique fact about M1?
M1 cells change firing rate according to direction of movement
what are the two parts of the non-primary motor cortex?
two main regions:
1. supplementary motor area (SMA)
2. premotor cortex
- located in frontal lobe and are implicated in planning and initiation of voluntary motor movements
what is the SMA important for?
initiation of preplanned movement sequences
- generates readiness potential which occurs before conscious awareness that a movement will be made
- receives input from basal ganglia and modulates activity of primary motor cortex
what does the premotor cortex do?
involved in selection of appropriate motor plans for voluntary movements
what are mirror neurons?
subarea of premotor cortex that fire when performing an action and watching another person make that same action
- important in understanding of other individuals’ actions
where are the parietal mirror neurons?
inferior parietal lobule, anterior intraparietal sulcus (aIPS), and ventral premotor cortex make up primary mirror neuron circuit
- inferior parietal lobule (reaching behavior controlled by vision -> Doral stream of visual association cortex contributes spatial information to parietal reaching region)
- anterior intraparietal sulcus (involved in controlling hand and finger movements involved in grasping objects)
what does the basal ganglia do?
- inhibits unwanted movements
- facilitates initiation of desired movements
- output is tonically inhibitory -> always preventing movement
- movement inhibition and facilitation achieved by direct, indirect, and hyperdirect pathways
what are the movement disorders of basal ganglia?
- parkinson’s disease (caused by progressive loss of dopaminergic cells in substantia nigra that project to basal ganglia that results in slowed movements, tremors, rigid posture, and reduced facial)
- Huntington’s disease (progressive damage to basal ganglia that results in excessive movement)
what does the cerebellum do?
receives input from sensory sources
- key for rapid motor adaption
- helps fine-tune skilled movements
- especially the kinds or rapid, repeated movements that become automatic
what are symptoms of damage to cerebellum?
- abnormal gait and posture especially ataxia (loss of coordination) of the legs
- decomposition of movements describes gestures that are broken into segments instead of executed smoothly
