Physiology Flashcards
(121 cards)
1
Q
The pacinian corpuscle is comprised of alternating layers of membrane with fluid between them, surrounding the nerve ending.
Why is this important if something touches you?
A
-The pacinian corpuscle will not compress
2
Q
When we touch something, all the layers of the membrane are deformed, but the fluid inside is not compressible.
What does that mean about the force transmitted?
A
-The force is transmitted all the way to the centrally-located nerve fiber
3
Q
The deformation of the pacinian corpuscle membranes leads to:
A
The opening of mechanosensitive Na+ channels on the membrane and Na+ influx … generation of AP back to the CNS
4
Q
If the touch stimulus is maintained, the APs gradually die away as ________ occurs.
A
Adaptation (Na+ channels not open anymore)
e.g., First feel clothes going on, but don’t feel them on in the middle of the day
5
Q
Much (but not all) of the adaptation that occurs is the result of:
A
Changes in the periphery (directly altering the afferent)
-similar to olfactory system getting used to smell
6
Q
In some cases of receptor adaptation, the removal of the stimulus triggers APs as the ending “reforms.” This is known as an:
A
Afterdischarge
7
Q
Why is an afterdischarge physiologically important?
A
- Gives the brain a signal that the object has actually been removed (the stimulus is gone)
(e. g., Don’t need to feel clothes while they’re on all day, but you feel when you take them off)
8
Q
__________ is assoc with the persistence of the sensation after the stimulus eliciting the discharge has been removed.
A
Afterdischarge
e.g., Phantom sunglasses
9
Q
Sensory unit:
A
The sensory nerve and all of its branches.
10
Q
T/F: A pacinian corpuscle has many branches.
A
False - A pacinian corpuscle is for fine touch
11
Q
Receptive field:
A
The area from which stimulation produces activation of the neuron.
12
Q
T/F: Intensity of stimulus is directly proportional to number of APs.
A
True
13
Q
With further increases in stimulus intensity, we may see:
A
Patterned discharges (doublets or triplets, etc.)
14
Q
Patterned discharges cue the brain in recognizing that:
A
A large stimulus is there for whatever receptor
15
Q
T/F: The number of receptors firing increases with increased intensity.
A
True
16
Q
Just Noticeable Difference:
A
The smallest difference that can be detected.
-A change of about 10% is usually required for conscious recognition of the change
17
Q
New formula from Weber-Fechner Law:
A
Perceived intensity = K(measured intensity)^A
18
Q
K and A in the new formula vary depending on the type of sensory receptor.
-In muscle senses, both are close to 1 - what does this translate to?
A
Our perceived intensity matches the actual (measured) intensity very closely.
19
Q
Why would muscle senses have to have the almost 1:1 (perceived:measured) intensity ratio?
A
To control our motion!
20
Q
Why is there more variability for cutaneous senses with regard to K and A?
A
What we perceive may diverge substantially from the actual.
21
Q
The physiological importance to senses is that we know the:
A
Generality
e.g., The temp has gone up (not precise)
22
Q
There are multiple pathways to the brain: (4)
A
- Dorsal Columns - proprioceptive and discriminative (fine touch)
- Spinothalamic Tract - thermal, nociceptive, and ‘coarse’ touch
- Spinoreticulothalamic system - nociceptive
- Spinocerebellar Tract
23
Q
T/F: In the most sensitive parts of our bodies, a stimulus activates only ONE receptor.
A
False - due to the overlap of receptive fields, multiple receptors will be activated.
24
Q
What is pre-synaptic inhibition?
A
Special case of inhibition
- axo-axonal synapse
- the post-synaptic cell is a pre-synaptic terminal
25
What is the end result of pre-synaptic transmission?
Reduced NT release from the inhibited pre-synaptic terminal.
26
On the "Pre-Synaptic Inhibition" slide, what does Neuron C release when activated? What does this cause?
Neuron C releases GABA (binds GABA receptors)
- Causes Cl- to enter Neuron A (pre-synaptic terminal of Neuron A hyperpolarizes and less Ca++ enters)...
- Less glycine (NT) release from Neuron A...
- Less APs in Neuron B.
27
Where does pre-synaptic inhibition occur?
| Why is this important?
- Occurs between neighboring receptors at the first synapse in their pathway.
- This increases the brain's ability to localize the signal.
28
Regardless of which pathway is used, every synapse along the way represents a chance to:
Modify or respond to the stimulus.
29
The gateway for sensory signals is the:
Thalamus
30
How is the sensory cortex arranged?
Somatotopically
31
Like the visual cortex, the somatosensory cortex has ___ layers, and they're arranged in _______.
- Six
| - Columns
32
In contrast to the visual cortex, each column in the somatosensory cortex deals with:
One sensory modality in one part of the body.
33
Sensory information arrives at its respective column in Layer __ via the ________.
- Layer 4 (similar to visual cortex - receives the inputs)
| - Thalamus
34
What is the role of Layer 5 in the somatosensory cortex?
To relay information to other parts of the brain for final interpretation.
35
Neighboring columns receive information from the (same/different) part of the body, but a (similar/different) sensory modality.
- Same part of the body
| - Different sensory modality
36
- Post-central gyrus
- Brodmann's 1, 2, and 3
- First stop for most cutaneous senses
- Somatotopic representation (toes medial)
Somatic Sensory Area 1 (S1)
37
- Wall of lateral (Sylvian) fissure
- Receives input from S1
- Somatotopic representation (not as detailed as S1)
Somatic Sensory Area 2 (S2)
38
T/F: Processing of sensory information in S1 is fully complete.
False - Processing of sensory information in S1 is NOT complete ... you know the characteristics of the object in hand, but you don't know what the object is.
-S1 = initial processing (similar to V1)
39
S2 is required for: (3)
'Cognitive touch' - higher level processing
- Stereognosis - ability to recognize an object in your hand that you cannot see (e.g., car keys in pocket)
- Comparisons between two different tactile sensations
- Determining whether something becomes a memory related to touch
40
Because of the wiring, damage to (S1/S2) will impair the functioning of (S1/S2); however, damage to (S1/S2) will not impair the function of (S1/S2).
Because of the wiring, damage to S1 will impair the functioning of S2; however, damage to S2 will not impair the function of S1.
41
The parieto-temporal-occipital (PTO) association cortex is required for:
High-level interpretation of sensory inputs - so it receives information from all the different sensory cortical areas, including S1 and S2.
42
With inputs, the PTO functions in: (2) + many others
-Analysis of the spatial coordinates of self/surrounding objects
-Naming of objects
+ Many others
43
If an area of the body is amputated (or otherwise denervated), what will happen to those afferent inputs?
The afferent input from remaining parts of the body will reinnervate the cortex.
44
If an area of cortex is lost, what happens to the afferent inputs?
Those afferents will innervate neighboring (remaining) columns.
45
What is the trade-off of re-routing the sensory information away from the damaged area of cortex?
(+): You still have some way of interpreting the signal.
| (-): The signal is not as precise as it used to be.
46
The 'doctrine of specific nerve energies' states:
Stimulation of a sensory pathway at any point leads to the perception of a sensation that is dictated by the receptor that started the pathway.
47
What does the 'doctrine of specific nerve energies' actually mean?
(e.g., pacinian corpuscle)
If I stimulate the cortical column that receives input from a specific pacinian corpuscle, I'll perceive the sensation of light touch.
48
The 'Law of Projections' states:
No matter where along the path we stimulate it, the perceived sensation is always referred back to the area of the body in which the receptor is located.
49
The 'Law of Projections' actually means that:
If the cortical column I stimulated receives input from a pacinian corpuscle in your left index finger, you perceive the touch as occurring on your left index finger.
50
Types of nociceptive fibers: (2)
1. A-delta fibers: small, sparsely myelinated (fast, sharp pain)
2. C fibers: unmyelinated fibers (dull, slow pain)
51
Mixed modality nociceptors also express a mechanosensitive Na+ channel (2)
- Mutations in this channel lead to an absence of pain sensation
- Another class of mutation produces a paroxysmal pain syndrome
SCN9A or Na(V)1.7 channels
52
Unlike other receptors, nociceptors express a number of:
Ligand-gated receptors (in addition to the stimulus-gated channels), which alter the sensitivity of the nociceptors to input.
53
```
The class of nociceptors has receptors for: (4)
What's interesting about these four chemicals?
```
-Substance P
-the Kinins (e.g., bradykinin)
-ATP
-H+
These four chemicals also exist in the spinal cord, where they influence nociceptive inputs at those synapses.
54
When these four chemicals (Substance P, the Kinins, ATP, or H+) bind to their receptors:
They change the sensitivity of the nociceptors (usually increasing) and activate the silent nociceptors.
I.e., They make it so you're more sensitive to pain. (e.g., hitting the corner of the table twice in a row - hurts even worse the second time)
55
A-delta fibers will travel into the spinal cord and release ___, acting primarily on ___-____ receptors.
- EAA
| - Non-NMDA receptors
56
C fibers release: (2)
- Substance P
| - EAA
57
Nociceptors that travel with the spinoreticulothalamic pathway (slow pain) synapse on an __________ in the spinal cord before crossing and ascending to the reticular formation.
-Why is this important? (2)
Interneuron
- Descending inputs from the brain meet in this location.
- This synapse is the site of much modulation of spinal cord function: local (gate theory) and descending (opioid pathways)
58
The visceral afferents travel with _________ nerves.
Autonomic
59
Unlike other senses, how is nociceptive input distributed?
| What is one consequence of this distribution?
- Widely in the cortex
- In someone experiencing chronic neuropathic pain, there isn't one place in the brain that you can eliminate to get rid of pain
60
S1 and S2 receive input from the nociceptors and play a role in:
Localizing the pain
61
The _______ cortex is important in the interpretation of nociceptive inputs.
- Processes information about the internal state of the body
- Contributes to the autonomic response to the pain
- *Integrates all signals related to the pain (asymbolia - pain dissociation)*
Insular cortex
62
T/F: Lesions in any one area abolish the ability to experience pain.
False - Lesions in any one area do NOT abolish the ability to experience pain, although the experience is changed.
63
Many nociceptive inputs go to the ________, which is important for activating/producing the emotional components in sensing pain.
Amygdala
64
Visceral nociceptors, traveling with the autonomic nerves, have additional synapses within the ___________ and the _______.
- Hypothalamus
| - Medulla
65
The 'Gate Theory of Pain' is based in part on the observation that:
Other somatic input can alleviate pain (rubbing the area)
66
The Gate Theory of Pain
| 3 steps:
1. Activate an A-beta fiber by the normal stimuli.
- The A-beta fiber has a branch that travels via the dorsal columns, BUT it also branches within the spinal cord.
2. The A-beta fiber releases EAA and activates an inhibitory interneuron in the spinal cord.
3. The inhibitory interneuron releases glycine to inhibit the activity of the second-order neuron in the pain pathway.
67
The Gate Theory of Pain
| End result:
Rubbing the area of skin activated by the A-beta fiber will reduce the sensation of pain.
68
Basic idea of the Descending Mechanism to modify painful inputs:
Use pre-synaptic inhibition to reduce activation of the second-order nociceptive neuron in the spinal cord.
69
Descending Influences
| 5 steps:
1. Neurons in the 'Periaqueductal Gray' are activated by numerous inputs, including opiate, EAA and the cannabinoids.
2. Axons from the PAG neurons travel to the midline Raphe nuclei and release enkephalins --> activate the raphe neurons.
3. Axons from the raphe neurons travel to the spinal cord and release serotonin --> activate inhibitory interneurons --> release opiates (suppress second-order neurons)
4. The opiates released by the interneuron activate mu receptors on the pre-synaptic terminal of the C fiber.
5. This produces pre-synaptic inhibition that reduces the release of substance P from the nociceptor and reduces pain transmission.
70
Chronic pain results from alterations at all levels of the nociceptive system: (3)
- Receptors
- Spinal cord
- Higher CNS
71
Chronic pain is a state in which nociceptive input ceases to be correlated with physiological pain (i.e., actual damage), but is:
- No longer protective in nature
- No longer linked to an appropriate stimulus
Associated with:
- Hyperalgesia - pain not correlated to degree of stimulation
- Allodynia - pain in response to non-noxious stimuli
72
TQ: Which ions or substances are particularly good at producing chronic pain and sensitizing the nociceptors? (3)
- H+
- Bradykinin
- Nerve Growth Factor (NGF)
73
How do H+, Bradykinin, and NGF interact with the nociceptors? (4)
What do these ultimately create?
- Directly activate nociceptors
- Sensitize the nociceptors
- Activation of immune system - modulators then contribute
- Increase substance P release from nociceptors
These create a positive feedback that reinforces the occurrence of pain.
(explains hyperalgesia)
74
Recruiting non-nociceptive fibers:
A-beta fibers can be converted into ________. This conversion can be triggered by exposure to __, ___, and __________. This alters protein expression in the A-beta fiber.
- Nociceptors
| - H+, NGF, and Bradykinin
75
Although the A-beta fibers are now expressing channels that make them nociceptive, they retain their:
LOW threshold (easy to depolarize!)
76
Alterations in peripheral afferents
| Produces a double-whammy:
- Nociceptors become hyperactive (lower threshold) and may become spontaneously active.
- Allodynia (normal sensation perceived as painful) results when the A-beta fibers become nociceptive.
77
The descending opioid inputs appear to be crucial in preventing ______ ____ from happening any time you experience pain - but with severe or persistent pain, the pre-synaptic inhibition is unable to keep the system down-regulated.
Chronic pain
78
Alterations in spinal cord function:
| NT released by nociceptor can start process:
EAA
- Non-NMDA receptor - acute pain
- NMDA receptor - pathologic pain
79
Activation of NMDA receptors leads to:
"Wind up" of second-order afferents - the same input from the nociceptor initiates a greater response in the interneuron or second-order neuron.
80
- Stretch (myotatic)
- Golgi tendon reflex
- Crossed extensor
Spinal reflexes
81
- Vestibular
- Righting reflex
- Suckle*
- Yawn*
- Eye/head movements*
* = appear in anencephalic babies
Brainstem/midbrain reflexes
82
- Placing reaction
| - Hopping reaction
```
Cortical reflexes
(bypass voluntary motor control systems)
```
83
________, in order to be effective, must be "precise," which makes them look like volitional movement.
-The important difference:
Reflexes
| -A reflex movement occurs faster than the fastest voluntary motion.
84
- Precise motions in response to afferent stimuli
- Mediated at all levels of the CNS
- Rapid initiation
- Many elicited even during unconsciousness
Reflex activity
85
- Originates in cortical areas associated with judgment, initiative, and motor control
- Longer onset latency due to processing
- Require conscious awareness
Volitional activity
86
- Contraction (shortening) of a stretched muscle
- Protect muscle from tearing due to stretch
- Initiated by *muscle spindle*
- Monosynaptic, segmental reflex
Myotatic (stretch) reflex
87
- Not contractile
- Portion sensitive to length
- Is actually TWO sensors - with different afferents
- nuclear bag fiber
- nuclear chain fiber)
What portion of the muscle spindle is described?
Sensory portion
88
TQ:
- Large Ia fiber (heavily myelinated, fast velocity, low threshold)
- Innervates both the nuclear bag and nuclear chain fiber
- Sensitive to both:
- Length of muscle
- How fast the length is changing
The primary afferent
89
Number of APs in the primary afferent (increases/decreases) with stretch?
Number of APs in the primary afferent INCREASES with stretch.
-Fast stretch --> more APS
90
TQ:
- Group IIa fiber (smaller diameter, less myelin, still pretty fast)
- Innervates ONLY the nuclear chain fiber
- Sensitive ONLY to the length of the muscle
The secondary afferent
91
The motor portion consists of the __________ contractile elements.
Intrafusal
92
- Same as skeletal muscle
- Innervated by a gamma motoneuron
- *Control the length of the sensory portion*
The motor portion
93
By contracting the intrafusal muscles, we stretch the sensory portion.
-Why is this important in terms of sensitivity of the sensory portion?
This renders the sensory portion more sensitive to a superimposed stretch.
-
94
Which class of motoneuron is crucial to controlling the sensitivity of the afferent portion of the muscle spindle?
Gamma motoneurons
95
- Large, heavily myelinated fiber
- Innervates (via NMJ) the skeletal muscle
- Responsible for activating muscle
- Activity directly leads to motion
Alpha motoneuron
96
- Slightly smaller, slower than alpha (still fast overall)
- Innervates the contractile component of the muscle spindle via NMJ
- Activity causes contraction
- Controls sensitivity of muscle spindle
- Activity does NOT directly lead to motion
Gamma motoneuron
97
The Ia afferent enters the spinal cord through (ventral/dorsal) horn, synapses on an alpha-motoneuron via EAA, and the alpha-motoneuron then exits through the (ventral/dorsal) horn.
- Dorsal
| - Ventral
98
The motoneuron is excited by the activation of the Ia afferent...
What happens next in terms of the discharge rate?
Contraction relieves the stretch, returning the Ia discharge rate back to normal.
99
For reciprocal inhibition:
The Ia afferent enters the spinal cord through (ventral/dorsal) horn, synapses on an ___________, where it then synapses on the alpha-motoneuron to the antagonist muscle.
- Dorsal
| - Interneuron
100
For reciprocal inhibition, what NT would the interneuron release onto the alpha-motoneuron?
Glycine (located in the spinal cord)
| -Helps to open Cl- channel (hyperpolarizes)
101
- Sudden (abrupt) relaxation of a contracted muscle
- Protect muscle from damage due to excessive force
- Initiated by golgi tendon organ
- Polysynaptic, segmental reflex
Golgi tendon reflex
102
- Innervate tendon
- Bare nerve ending with lots of branches
- APs increase with tension
- Ib fiber to spinal cord (fast, but not as fast as muscle spindle)
Golgi tendon organs
103
For golgi tendon reflex:
The Ib afferent enters the spinal cord and synapses on an interneuron, where it then releases the inhibitory NT, _______, to synapse on the alpha-motoneuron.
-Glycine
104
The motoneuron is inhibited by the activation of the spinal interneuron....
What happens in terms of the golgi tendon organ discharge rate?
Abrupt relaxation of the muscle occurs, returning the golgi tendon organ discharge back to normal.
105
- Initiated by muscle spindle
- Passive stretch of the muscle
- Monosynaptic reflex
- Contraction of stretched muscle back to normal length
Myotatic reflex
106
- Initiated by golgi tendon
- Active contraction of muscle
- Polysynaptic reflex
- Abrupt relaxation of contracted muscle to prevent damage
Golgi tendon (reverse myotatic)
107
Cortical influences tend to be (stimulatory/inhibitory) to spinal reflexes.
Cortical influences tend to be INHIBITORY to spinal reflexes.
(e.g., looking at patellar tendon being performed on you)
108
Spinal shock
| Recovery is believed to result from: (2)
- Axons sprouting below the level of the transection
| - Expression of receptor phenotypes that are self-activating (5HTC receptor)
109
Loss of all structures rostral to the pons results in:
Decerebrate posturing (Rigidity + Spasticity)
110
- Pt resists motion in all directions
- Maintained contraction of anti-gravity muscles in the absence of other stimuli
- Continual activation of alpha-motoneurons (not due to reflexes)
- Cause: Loss of cortical influence that inhibits a medullary input to the alpha-motoneuron
Rigidity
111
- Pt resists a passive stretch of their muscles
- Contraction doesn't start until the stretch occurs
- Hyperactive myotatic reflex due to increased gamma motoneuronal firing
- Continual activation of gamma-motoneurons
- Contracts intrafusal muscle
- Lengthens nuclear bag/chain fibers
- Cause: Damage to cortex that abolishes activation of the brainstem inhibitory region (brain arousal systems)
Spasticity
112
The brainstem facilitatory region makes muscle spindle more sensitive by activating gamma-motoneurons.
Why is this important?
This region is spontaneously active.
113
The brainstem inhibitory region makes muscle spindle less sensitive by inhibiting gamma-motoneurons.
This region requires activation from:
Cortical regions
| i.e., On its own, the brainstem inhibitory region is not that active
114
With the loss of the cortex, is the brainstem (—) region activated?
What happens to the brainstem (+) region?
- Loss of the cortex means that the brainstem (—) region is NOT activated
- The brainstem (+) region is left to dominate.
115
What is the end result of an uncontrolled brainstem facilitatory region?
Stretch reflexes fight any passive motion (aka Spasticity)
116
- Flexion of the upper limb joints
- Extension of the lower limbs with internal rotation
- Dependent on head position
Decorticate posturing (rigidity)
117
Unlike decerebrate posturing, decorticate posturing is dependent on ____ ________ and will change as the head is moved passively.
-Head position
118
Strokes in the vicinity of the internal capsule result in:
Decorticate posturing
-Results from postural reflexes arising from the neck that are being released due to the loss of the cortical input on that side
119
- Transection of the spinal cord
- All reflexes abolished, even if circuit is intact
- Cause: Hyperpolarization of spinal neurons due to loss of excitatory input from cortex?
Spinal shock
120
- Internal rotation of legs in extended position; flexion of arms; dependent on head position
- May be bilateral or unilateral
- Loss of cortical input - most commonly caused by lesion of internal capsule
Decorticate posture
121
- Contraction of all anti-gravity muscles (arms in extension)
- Loss of input from all structures rostral to the pons
- Usually bilateral and indicative of severe brain injury
Decerebrate posture
