Exam 3 Flashcards
How do we detect stimuli?
receptors convert detection of stimulus into electrical signals, and brain integrates the info
What categories of stimuli can we detect?
mechanical, visual, thermal, chemical, electrical
What are some themes of sensory processing?
Sensory neurons are specialized to translate specific stimuli into electrical signals, and spatial information about the source of stimulus is preserved in the organization of the CNS
How is the nervous system set up for difference detection?
Amplification of new signals and edge detection
Bottom-up modification
As information travels up to the brain, it is processed and integrated, allowing for more complex perception
Top-down modification
Brain inhibits and prevents some signals from occurring- inhibition of pain is one such example
true or false: receptors only respond to a specific type of stimulus at a specific intensity
true
How is intensity of a stimulus encoded?
Frequency of action potentials
How do we distinguish different stimuli?
Labeled lines organization- in which sensory neurons only respond to a specific input and the brain then interprets the signal based on the wiring/source
What are receptor potentials?
Local changes in membrane potential
what are the steps of sensory detection?
sensory stimulus detected, receptor potentials, cell reaches threshold, sensory neurons fire action potentials
Which is sensory, the dorsal or ventral root ganglia?
Dorsal
What is a pacinian corpuscle and how is it innervated?
Pacinian corpuscles are what respond to vibration because their ion channels are stretch sensitive, so when stretched, the sodium enters and depolarizes the cell. They are innervated by dorsal root ganglia
Range fractionation
the term that refers to the idea that different receptors have different thresholds of firing over a range of stimulus intensities, so some receptors require a higher intensity stimulus to fire which also allows for us to determine the intensity of the stimulus- high intensity inputs cause combined responses of all three neurons
Sensory adaptation
The process by which frequency of action potentials decreases with prolonged exposure to stimuli- this is what allows for emphasis of new stimuli
Phasic receptors
Display adaptation
Tonic receptors
Little to no adaptation
How do we control attention to information?
sensory adaptation, accessory structures like eyelids, top-down processing where higher brain centers suppress some inputs and amplify others
Receptive field
The part of the body surface in which a stimulus will trigger firing of that neuron- location and size of receptive field can give information about where a stimulus came from
Surround inhibition
stimulus on outside radius of receptive field provides inhibition/prevents cell firing
True or false: body is mapped onto somatosensory cortex
true
pathway of sensory info
dorsal root ganglia to spinal cord to thalamus to primary somatosensory cortex (S1)
How does sensory information arrive to the brain?
each sensory system has its own pathway, and passes through stations during processing; most sensory pathways pass through the thalamus
Where do sensory pathways terminate
cerebral cortex
in the touch receptors, where does an axon from the periphery make its first synapse?
in the medulla, where it then crosses midline and goes to thalamus
does the left thalamus receive info from the right or left side of the body
right side
what are primary sensory cortical areas
the first cortical areas to receive sensory info
what are secondary sensory cortical areas
perform higher processing on sensory info- secondary somatosensory cortex connects sensory info to brain areas associated with learning
what is pain and why is it important?
pain is an unpleasant experience associated with tissue damage, it helps us avoid potentially threatening situations
congenital insensitivity to pain
caused by mutation in vgnacs of nociceptive neurons- sensory neurons don’t fire action potentials so don’t communicate painful stimuli to brain
steps of sensory processing
- Info enters cns through brainstem or spinal cord and travels to the thalamus
- thalamus shares info with cerebral cortex, which directs thalamus to suppress some sensations
- primary sensory cortex swaps info with nonprimary sensory cortex
Paroxysmal Extreme Pain Disorder
rare inherited disorder, characterized by bouts of pain, mutation is in same gene as in cip but vgnacs are overactive
phantom limb pain/neuropathic pain
neurons that used to receive sensory input develop abberant activity in absence of normal input, often pain is from tight or clenched feeling- mirror therapy can help as it gives illusion that hand is still there so patient can unclench their hand
3 aspects of pain
sensory (throbbing, mild, shooting), cognitive (no pain, mild, excruciating), motivational (affective/emotional quality)
nociceptors: pain receptors
nociception- pain sensing, nociceptors are peripheral receptors that respond to painful stimuli, free nerve endings in dermis have specialized receptor proteins, and free nerve endings respond to temperature changes, chemicals, and pain
peripheral mediation of pain
- damaged cells release substances that excite free nerve endings that function as nociceptors
- action potentials generated in the periphery can reflexively excite blood vessels and mast cells to produce inflammation
- stimulated mast cells release histamine and another molecule
- info enters through dorsal root and synapses on neyrons in dorsal horn
- pain fibers release glutamate and substance p, then spinal cord sends info up to thalamus across midline
how is capsacin detected
trpv1 receptors, which are on c fibers, which are thin and unmyelinated and therefore allow for longer lasting pain
how is painful heat or cold detected
specialized receptors on sensory neurons that can also respond to chemicals
compare and contrast trp2 and trp1
trp2 detects higher temperatures, does not respond to capsaicin, and is found on a delta fibers which are myelinated and allow for quick detection of pain
how is cold detected?
cool-menthol receptor 1- responds to menthol and to cool temperatures and is located on c fibers
route of pain to brain
anterolateral or spinothalamic system transmits pain and temperature sensation; free nerve endings synapse on spinal neurons in the dorsal horn, and pain info crosses midline before moving on to thalamus
describe the 2 responses to pain across 2 brain regions
projections to motor cortex create movement, projections to limbic system assign affective aspect. anterior cingulate cortex which is responsible for things like empathy is highly stimulated by painful stimuli
how is analgesia (pain relief) produced?
analgesics like acetominophen and ibuprofen block synthesis of prostaglandins which act upon snesory nerves
how do local anasthetics work
local anasthetics like lidocaine block action potentials of sensory neurons
what does an epidural involve
injection of analgesic or anasthetic directly into spinal cord
analgesia vs anesthesia
analgesia=pain relief, anesthesia- loss of consciousness or feeling
top down processing of pain
brain can send signals to spinal cord that inhibit nociception, especially w/ release of peptide neurotransmitters like the endogenous opiates
PAG role in nociception
signals from PAG cause serotonin release in raphe nuclei, which activates opioid interneurons which inhibits ascending pathways
Describe the overall organization of the visual system
optic nerves cross over at optic chiasm and pass through the visual areas of the thalamus, where they then go to the visual cortex
describe the concept of binocular vision
info from right visual field goes down left optic tract and info from left visual field goes down right optic trac
does less overlap of visual field mean more or less crossing over
more crossing over since more info is specialized to just one field
accommodation
process of focusing the lens- lens then focuses light on retina, accommodation can also be pupil dilation to let in light
how is light entering the eye controlled
controlled by the pupil dilating or contracting
what is the optic disc
where optic nerve leaves the eye
layers of the retina
from bottom to top
- pigmented epithelium
- rods and cones
- bipolar cell layer
- ganglion cell layer- their axons form the optic nerve
- optic nerve
cell types in retina
interneurons- horizontal (associated with photoreceptors) and amacrine cells (associated with bipolar cells) form lateral contacts and facilitate lateral inhibition
compare rods vs cones
rods- activate in dim light, cones- associated w/ color - have lots of membrane space called photoreceptor disks that provide a large surface area for rhodopsin and the ion channel
fovea
center of where light focuses on retina- least cell density, only cones, highest visual acuity
blind spot
optic disc where optic nerve leaves
what is the largest portion of our visual cortex devoted to
processing info from the fovea
why are our eyes so sensitive to light?
amplification of signals downstream of photopigments- photopigments like rhodopsin capture photons
what are the two parts of rhodopsin?
retinal and opsin, which is a gpcr; when light activates rhodopsin, retinal dissociates and opsin is activated; retinal changes conformation when coming in contact with light
steps of signal amplification
- light changes retinal’s shape
- rhodopsin deformed to activate 500 molecules of g protein transducin
- gtp replaces a GDP bound to transducin, activating PDE, which reduces cgmp concentration
- this causes closure of vgnac’s and hyperpolarization of receptor, so one photon can block a million Na ions
how does the visual system deal with a wide range of light?
adjusting pupil size, range fractionation, adaptation
how does the visual system emphasize edges and change?
center-surround organization emphasizes edges and change- number and sensitivity of photoreceptor input onto ganglion cells is the receptive field of that ganglion cell and input to ganglion cell is moderated by bipolar cells and horizontal interneurons; receptor fields have center-surround organization, so the maximum action potentials are released when there is contrast in receptive field- edge detection is also facilitated as there is a different amount of action potentials for different stimuli
Effect of light on center and surround of receptive field
depending on how photoreceptors are hooked up light may inhibit or excite ganglion cells- in on center, light in center excites, and in off-center, light in center provides inhibition of ganglion cells
what is lateral inhibition?
excited neurons prevent excitation of other lateral neurons so the cells know exactly where the stimulus is instead of everything becoming excited
Light receptors receiving input from the lighter side of the edges produce a stronger visual response than receptors receiving input from the darker side. This action serves to enhance contrast at the borders making the edges more pronounced.
how many of each color cone do we have?
more l than m, fewest s (corresponding to wavelengths of light)
describe color receptive fields
opposing colors can have different affects on receptive field so red off center, green on surround- allow for increased color discrimination and contrast through lateral inhibition
what causes color blindness?
loss of functional cones dichromacy: one type gone - red: protanopia - green: deuteranopia - blue: tritanopia monochromacy: - missing 2 achromatopsia - missing all 3
what is retinotropic mapping
idea that spatial organization of info from each eye is preserved
Laterate geniculate nucleus
info from left and right visual field get sent to right and left lgn respectively, info from same part of visual field gets sent to adjacent parts of lgn in the thalamus; axons project back and forth between lgn and striate cortex
hemispatial neglect
damage to visual cortex or parietal lobe, patient ignores half of stimuli in one visual field
where does mixing of two visual pathways first occur
striate cortex
what parameters does the visual cortex use
orientation, movement, frequency
what does a simple cortical cell respond to
bars of specific orientation; complex cortical cells also respond to movement
organization of receptive fields
circular receptive fields can combine to form rod shaped receptive fields
what is v1
primary visual cortex
what is v2
detects shapes and contours, more complex relationships
v4
neurons responsive to particular increasingly complex shapes
what two processing streams originate in the primary visual cortex?
what (ventral, identifying objects) and where (dorsal, assessing location) damage to ventral causes agnosia where u cant name objects, ataxia causes difficulty in using vision to reach for objects
prosopagnosia
facial fusiform gyrus is in ventral stream, causes face blindness
pareidolia
perceiving patterns/faces where there is none
how do we perceive sound?
amplitude=loudness, frequency is pitch
which part of ear converts sound into neural activity?
inner ear
describe the cochlea
fluid-filled, a spiral structure with base and apex, 3 cavities, middle of which converts sound into action potentials (organ of corti)- sound vibrations cause basilar membrane of cochlea to oscillate, different parts respond to different frequencies so low frequency displaces lower floppier apex
3 main structures of organ of corti
sensory/hair cells with stereocillia, basilar membrane, and framework of supporting cells
how are cilia activated
vibration makes cilia sway, causing ion channels to open and ca2+ influx causes nt release at base of cell
where is sound processed?
info transmitted from cochlea to brain by vestibulocochlear nerve (cranial nerve viii)
what receives bilateral input (imporant for locating sound)
superior olivary nuclei- intensity and latency differences that by the duplex theory facilitate location of sound
inferior colliculi
in the midbrain, which then send output to medial gen nuclei in thalamus
where is primary auditory cortex located
temporal lobe
where is tonotopic organization reflected
cochlea, primary auditory cortex, inferior colliculus
conduction deafness
a middle ear problem that blocks sound vibrations from reaching the inner ear
sensorineural deafness
problems w/ structures like cochlea that convert sound to neural activity
central deafness
damage to auditory brain structures
what streams are in the auditory cortex
dorsal stream- in parietal lobe, associated with spatial location
ventral stream- in temporal lobe, associated with components of sound including processing of language
is language lateralized
yes it is processed in left temporal lobe mainly
language and the split brain patient
since info in left visual field goes to right visual cortex there is no crossover into left side so they can’t identify the object
right ear advantage
right eared person recognizes right ear stimuli first
right hemisphere auditory responsibilities
lots of music processing and emotional tone of voice
inability to understand speech
agnosia
inability to produce speech
aphasia- symptoms include paraphasia (substituting words for other words), neologisms, and nonfluent speech
types of aphasia
nonfluent/broca’s aphasia- difficulty producing speech but comprehension good, fluent or wernicke’s aphasia- can make speech sounds but difficulty in comprehension, global aphasia- deficits in both speech production and comprehension
discovery of brocas area
partient had nonfluent aphasia, led paul broca to find area specialized for speech
wernicke’s area
posterior regions of left superior temporal gyrus and part of adjacent parietal cortex, involved in perception and production of speech
What is the neuromuscular junction
where motor neuron terminal and nerve fiber meet
is the nmj effective
yes, almost every AP initiates a contraction
motor unit
motor neuron’s axon and all of its target fibers
spinal motor neurons
send axons out the ventral roots to the periphery, and each collateral innervates a different muscle fiber within the muscle
what is the neurotransmitter at the nmj
acetylcholine, which causes depolarization
myasthenia gravis
attacks ach receptors at nmj, characterized by muscle weakness that worsens with use, drugs that inhibit ach breakdown can help
proprioception
knowing where we are- collection of info about body movements and positions- sensory neurons in muscles give feedback about muscle tension with stretch sensitive nerve endings
2 kinds of proprioceptive nerve receptors
muscle spindles and golgi tendon organs
what are reflexes and how do they happen
spinal connections between dorsal and ventral roots
describe steps of knee jerk response
hammer tap stretches tendon which stretches sensory receptors in leg extensor muscle, sensory neuron excites interneuron and motor neuron in spinal cord, interneuron inhibits motor neuron to flexor muscles, motor neuron conducts ap to synapse on extensor muscle fibers, causing contraction, , flexor muscles relax, causing leg to extend
what does the primary motor cortex do
initiates commands for action, nonprimary motor cortex provide an additional source of motor commands, cerebellum, and basal ganglia modulate activities of these control systems, sometimes via thalamus in a loop back to cortex
hierarchy of motor control systems
brainstem integrates motor commands, spinal cord controls skeletal muscles, skeletal system allows for movement
where are skeletal muscles innervated from
mainly from spinal cord, but muscles of head and neck also innervated by cranial motor nuclei in brainstem
2 major pathways of commands to muscles
pyramidal (originate from neurons in primary motor cortex, axons pass through brainstem to spinal cord)
extrapyramidal: modulatory role in motor learning+motor coordination
nonprimary cortical areas
in front of m1, include premotor and supplementary motor area
SMA function
receives info from basal ganglia, involved in rehearsal of actions
premotor cortex
broca’s area partly involved, has to do w/ control in speech- important for motor sequences externally guided so this is where mirror neurons are
mirror neurons
active when an individual makes a movement, important in understanding+imitating others
ALS
lower motor neurons and m1 cortex degenerate, leading to muscle atrophy
extrapyramidal system
include basal ganglia and cerebellum, basal ganglia have a collection of circuits initiating and inhibiting motion
parts of basal ganglia
caudate nucleus, putamen, globus pallidus, (substantia niagra and subthalamic nuclei are associated structures)
Functions of basal ganglia
amplitude, direction, initiation of movement, esp/ w movement influenced by memory, also modulate other circuits like motor pathways of motor cortex, bidirectionally modulate voluntary movement
huntingtons
degenerative disorder involving cell loss in striatum and cortex, degeneration of neurons in striatum leads to involuntary movement since bj modlates movement, 36 CAG lead to HD, more repeats is earlier onset
function of cerebellum
cerebellar cortex has purkinje muscles which send inhibitory muscles, loss of cerebellum results in ataxia esp w/jerky movements, tremors, etc
wernicke’s area
perception and production of speech, damage results in fluent aphasia- complex verbal output with unintelligible speech, difficulty understanding language, word deafness or blindness can indicate site of lesion
global aphasia
total loss of ability to understand or produce language, results from large left hemisphere regions
arcuate fasciculus
connects brocas and wernickes areas- lesions produce conduction aphasia- connectionist model may be too simplistic
deep dyslexia
word interpreted as different word, acquired after brain injury
surface dyslexia
rely on rules to pronounce words
developmental dyslexia
struggle w/ reading, may be genetic, associated w/ ectopic cell clusters and micropolygria
songbirds common model of language acquisition
refining song based on hearing others, critical period for learning, but not really language similar to primates and alex the parrot because innate, not learned,
