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27 Cards in this Set

  • Front
  • Back
What is presynaptic facilitation and what is the time frame associated with it?
Immediate effect of repetitive stimulation (even 2 APs)
Increased intracellular Ca leads to increased NT
Second APs benefit from ‘left over’ Ca
lasts ~ 200msec
What is presynaptic depression?
Depletes NT vesicle supply up to 80% reduction in subsequent SPs.
One part of muscle fatigue
What is Presynaptic Augmentation and what is the time frame associated with it?
(10-20 seconds)
Similar to mechanism to Facilitation
Aug. + Facilitation leads to 5x SPs amplitude
What is Post tetanic Potentiation, and how long does it last?
(presynaptic, lasts 10s of minutes)
High frequency APs saturate intracellular Ca buffer system and increase NT release

Delayed onset, long lasting vs. Facilitation and Augmentation
Prolonged vesicle docking
What is Long term potentiation (LTP), how long does it last, and is it a form of plasticity?
High freq stimulation leads to EPSPs increase for hours (msec to tens of min) or longer
Important factor: increased postsynaptic Ca.

Hippocampus: NMDA-type glutamate receptor.

is a form of plasticity

Glutaminergic neurons A or B active alone
EPSPs from non-NMDA receptors leading to EPSPs (no LTP)

Neurons A and B active together (in ‘association’)
Larger depolarization gates NMDA receptor/channel resulting in large Ca influx
Increased postsyn Ca levels activate cell machinery including gene expression (ex. up regulation of specific receptors)
Neuron now may be more ‘attuned/sensitive’ to specific signals or specific signals in association.
What types of information can we sense?
modality: type of energy transmitted by stimulus, type of receptor

Location and Size (space, size): set of receptors active

Intensity: receptor potential (RP) amplitude leads to AP frequency

Timing: receptors on/off leads to AP frequency
What are 4 modalities we can sense?
Mechanical: touch, proprioception, jt. position, hearing, balance; deformation. Mechanism: ‘stretch activated’ ion channels.

Chemical: pain, itch, taste, smell.

Thermal: internal and external temperature

Electromagnetic: light.
Intensity: how much is needed?
Sensory threshold: lowest energy of receptor or subject response.

Sensation intensity from : 1) frequency of APs + 2) number active neurons (****perception intensity is COMLETELY different)

Stim – receptors activated -- RP amplitude –AP frequency.

More intense stimuli leads to more receptor cells which leads to more APs.
More intense stimuli leads to higher RP amplitude which leads to higher AP freq
Describe slowly adapting receptors.
slow inactivation of Na, Ca channels and/or activity of Ca dependent K channels (increase repolarization)
Describe rapidly adapting receptors.
respond to onset/offset, due to inactivation at axon (?) and/or receptor deformation.
Signal change in stimulus intensity.
Describe and illustrate the general organization or ‘plan’ common to various sensory systems.
- a receptor is activated and an AP is generated.
-mechanosensory information travels along the 1st order neuron through the dorsal root ganglion (where its cell body is) into the dorsal horn of the spinal cord
-it then travels up the dorsal column-medial lemniscus (DC-ML) pathway to the brain stem (specifically the caudal medulla)
-Axons traveling in the DC are arranged with those from the lower extremity most medially, and those from the upper extremities most laterally. Axons from the lower body synapse with the 2nd order neurons in the gracile nucleus and axons from the upper body synapse with their 2nd order neurons in the cuneate nucleus of the medulla
- 2nd order axons cross the midline of the medulla (decussate) and travel in the ML to the ventral posterior lateral(VPL) nucleus of the thalamus
- As the 2nd order axons ascend to the thalamus they switch places, resulting in the upper body information now being medially and the lower body info now being laterally
-Here in the thalamus the 2nd order neurons synapse on the 3rd order neurons that are projected to the somatic sensory cortex, located in the anterior parietal lobe, just posterior to the central sulcus.
What are the characteristics of mechanical nociceptors?
Well defined response only with tissue damage.
High threshold receptors, fast conducting axons.
Sensitization (repeated stimulation decreases threshold).
What are the characteristics of polymodal nociceptors
50% of unmyelinated axons respond to mechanical, heat and noxious stimulation
Lower threshold, slower conducting axons.
Response to tissue damage
Release substance P
Are thermal nociceptors slow-conducting or fast-conducting?
What are characteristics of silent nociceptors?
-Not typically nociceptors
-Threshold for noxious stimuli reduced via inflammation
-May underlie secondary hyperalgesia and central sensitization
What are characteristics of A delta afferent fibers?
Sharp, prick, acute, fast pain (fast, 6-30m/sec)
High spatial resolution->well localized
Easily tolerated, underlies flexion withdrawal
What are characteristics of C fibers?
Burning, aching, slow pain
(.5-2m/sec), 1 sec slower from fingertips
Low resolution---> often only to gross body part
large ‘affective’ component
Poorly tolerated
Substance P
Where do nociceptive afferents typically terminate?
Lamina I and II
Lamina I neurons
- Many are ‘nociceptive-specific’ and project to higher centers
- Some are ‘wide-dynamic-range’
Lamina V neurons
- are ‘wide’, receive A beta, delta and C.
- Many receive visceral nociceptive input
Primary Hyperalgesia
Increased pain at site of injury
Lowered threshold for mechanical, thermal stimuli
Peripheral mechanism: local release of a cocktail
Prostaglandins locally lead to pain with non noxious stimuli
Secondary Hyperalgesia
- Increased pain and sensitivity beyond site of injury
- Lowered threshold for subsequent mechanical stimuli
Central neural origin (ex. ‘silent nociceptors’ and spinal cord excitability)
- Painful response to innocuous mechanical stimuli
- Hypersensitivity of spinothalamic neurons and decrease in inhibition by descending systems.
Central Pain Control
1) Descending or Central biasing
Inhibition of Lamina I, II, V neurons from midbrain-medulla

2) Descending Opiate-induced analgesia
Release of endogenous opiates in spinal cord

Pain can be influenced by supraspinal centers.
Nociceptive input blocked before projected up cord.
Modulation, blockage at multiple sites
Lasts for minuteshours
Stress causes increase release
Powerful enough to block flexion withdrawal
(Watch ‘Cops’, talk with a combat veteran)
Peripheral Pain Control
Gate Theory
Projection neurons receive 3 inputs: C, non-noci A beta, inhibitory IN

Balance of nociceptive and non nociceptive inputs to cord

Normally: spontaneously active –IN inhibits projection neuron
Pain gate open: C fibers inhibit –IN, excite projection
Pain gate closed: A betas excite –IN (gate closed), inhibit projection
Descending Opiate-Enduced Analgesia
-Opium poppy---> strong analgesic effects
-Morphine, codeine (exogenous)
-Endogenous receptors located throughout CNS
-High density: p-a gray, medulla, dorsal cord
-Endogenous opioid peptides
ex. Enkephalins, Endorphin (released during stress)

-Postsynaptic inhibition of projection neuron (K+)
-Presynaptic inhibition of primary sensory NT/peptide release
Descending Opiate-Enduced Analgesia
-Opium poppy---> strong analgesic effects
-Morphine, codeine (exogenous)
-Endogenous receptors located throughout CNS
-High density: p-a gray, medulla, dorsal cord
-Endogenous opioid peptides
ex. Enkephalins, Endorphin (released during stress)

-Postsynaptic inhibition of projection neuron (K+)
-Presynaptic inhibition of primary sensory NT/peptide release