Receptive fields and lateral inhibition

Question 1

Complexity of recepetive fields. Where do the neurons synapes?

Answer 1

Receptive fields of sensory neurons become more complex as information moves up the pathway
-Touch fibers synapes on neurons in the dorsal column
-The dorsal column neurons have more complex, center-surround receptive fields

Question 2

Where do touch receptors synapse and what happens?

Answer 2

-The touch receptors synapses directly on the dorsal column neuron. This creates an excitatory center in the receptive field of the dorsal column neuron
-When no stimulus is present, the dorsal column neuron fires at a baseline rate
-When a stimulus touches the center of the receptive field, the firing rate increases

Question 3

What is lateral inhibition

Answer 3

-Surrounding touch receptors can also connect to the dorsal column neuron indirectly via interneurons
-The interneuron has an INHIBITORY effect on the dorsal column neuron
-Lateral inhibition allows the sensory systems to enhance the perception of edges of stimuli
-Center-surround receptor field gives more precise localization sensation

Question 4

What is critical for lateral inhibition to occur?

Answer 4

-The dorsal column nuclei have receptive fields that are divided into center and surround regions
-The center-surround structure of the receptive field is critical for lateral inhibition

Question 5

Dorsal Column- Medial Lemniscal Pathway

Answer 5

-In general, the sensory information travels along different pathways depending on the modality of information
-For SOMATIC TOUCH, the signal travels along the dorsal column-medial lemniscal pathway from the peripheral to the brain

Question 6

Dorsal column- medial lemniscal pathway –> How the pathway works

Answer 6

1) In medulla, output from the dorsal column nuclei crosses midline and forms recognizable bundles: medial lemniscus
2) Medial lemniscus fibers ascend to the thalamus and synapes in the ventral posterior nuclei of the thalamus
3) Thalamic axons ascend to primary somatosensory cortex

Question 7

Primary somatosensory cortex

Answer 7

-somatosensory cortex is divided into areas 3a, 3b, 1, and 2, each with its own input and function. Each area carries out independent functions
-TOUCH information feeds to region 3b
-As processing of information continues, 3a and 3b then send and receive information from areas 1 and 2
-Area 1: TEXTURE
-Area 2: SIZE and SHAPE

Question 8

Organization of somatosensory cortex

Answer 8

-Neurons in cortex are arranged in layers and columns
-cells in each column respond to a particular type of input (vibration, pressure, temperature, etc) from a particular location on the body
-total of 6 different layers
-touch is layer 4

Question 9

Organization of somatosensory cortex

Answer 9

-Neurons in cortex are arranged in layers and columns
-cells in each column respond to a particular type of input (vibration, pressure, temperature, etc) from a particular location on the body
-total of 6 different layers
-touch is layer 4

Question 10

What does higher level processing of touch information consist of?

Answer 10

-Secondary somatosensory cortex (SII)
-> Object recognition
-> Discerning texture, shape, and
size
-The SII (secondary somatosensory cortex) sends projections to the posterior parietal cortex, the premotor cortex, the amygdala, and the hippocampus

Question 11

Higher level processing of touch information in the posterior parietal cortex

Answer 11

-recognizing touch characteristics like orientation and movement
-combining the touch and motor components of actions like grasping
-The posterior parietal cortex outputs to the frontal motor cortex

Question 12

Oral somatosensation

Answer 12

-Tooth pulp: Pain receptors
-Periodontal ligaments: free nerve endings (pain fibers)
-> Free nerve endings (pain
fibers)
-> Ruffini mechanoreceptors

Question 13

Periodontal Ruffini endings

Answer 13

-provide sensory information about tooth position and forces to facilitate reflex jaw activity during chewing movements
-detect directions of tooth movement

Question 14

Pain and temperature

Answer 14

-both travel in the same ways
-nociceptors

Question 15

Thermoreceptor types

Answer 15

-Cold-pain: TRPA1
-cool receptor: TRPM8
-Warm receptor: TRPV3 and TRPV4
-Heat-pain: TRPV1 and TRPV2

Question 16

How temperature receptors are polymodal

Answer 16

-Other than temperature, many of these receptors can also respond to chemical agonists
-TRPV1 is activated by capsaicin, the hot ingredient in chilli peppers
-TRPM8 is activated by menthol in mint oil
-Therefore menthol is “cool” while peppers are “hot”
-TRPA1 is activated by irritating compounds (e.g. mustard oil)

Question 17

Nociceptive substances

Answer 17

-Tissue damage results in a release of a variety of substances from lysed cells as well as from new substances synthesized at the site of injury

-“The inflammatory soup”
->Protons
-> ATP
-> Adenosine
-> Bradykinin
-> Prostaglandins, etc

Question 18

Nociceptive substances

Answer 18

-Action potentials spread to non-stimulated nociceptor branches
-Excited terminals release substance P and Calcitonin Gene-Related Peptides (CGRP)
-Substance P activates immune cells (mast cells), immune effector cells (macrophages), neutrophils, etc.
-Mast cells and neutrophils release PGE2, bradykinin, histamine, etc.
-Macrophages release growth factors, cytokins, etc.
-CGRP and Substance P cause vasodilation
-platelets, neutrophils,…
-Tissue injury is a multiplicative degradation process.

Question 19

Pain producing Nociceptive substances

Answer 19

-GLOBULIN and PROTEIN KINASE are believed to be the most active pain-producing substances. They are released when nociceptors respond to an injury or stimulus that damages the body

-ARACHIDONIC ACID, which can be metabolized into PROSTAGLANDIN (and cytokines). Prostaglandins block the potassium efflux released from nociceptors following damage, which results in additional depolarization, making nociceptors more sensitive. Aspirin is an effective pain killer because it blocks the conversion of arachidonic acid to prostaglandin.

Question 20

Hyperalgesia and Allodynia

Answer 20

-Effects of nociceptive substances
-Hyperalgesia: Normally painful stimuli elicit pain of greater intensity
-Allodynia: Normally innocuous stimuli are perceived as painful (light touch, warmth,…)

Question 21

What causes hyperalgesia?

Answer 21

-Hyperalgesia results from lowered threshold for pain in the area surrounding an inflamed or injured site and/or…
-the inflammation activates silent nociceptors
-damage elicits ongoing nerve signals (prolong stimulation)
-These together may lead to long-term changes and sensitized nociceptors

Question 22

What causes Allodynia?

Answer 22

-Allodynia develops if nociceptors have been sensitized as a result of reducing the threshold of the silent nociceptor (e.g. TRPV1).
-Damaged peripheral neurons reroute and make connection to sensory receptors (i.e., touch-sensitive fibers reroute and make synaptic connection into areas of the spinal cord that receive input from nociceptors).

Question 23

Receptor sensitization

Answer 23

-The activity of temperature receptors such as TRPV2 and TRPV3 is intrinsically use-dependent
-prolonged stimulation can shift temperature threshold to below body temperatures
-long term sensitization

Question 24

Central sensitization

Answer 24

Increased responsiveness of nociceptive neurons in the central nervous to their normal or subthreshold afferent input
-recruitment of additional, subthreshold synaptic inputs to nociception resulting in a greater field of receptivity
-increased output of nociception
-inhibition of descending pathways
-over-activation of ascending, pain facilitatory pathways

Question 25

Central sensitization

Answer 25

-Activity-dependent central sensitization
-pain hypersensitivity in rats following repeated noxious stimuli
-over-activation of NMDA receptors

Question 26

Types of pain

Answer 26

-Nociceptive pain: Response of our bodies sensory nervous systems towards actual or potentially harmful stimuli. Physiological
-Inflammatory Pain: Response of tissues in reaction to harmful stimuli in order to eradicate necrotic cells. Associated with hyperalgesia, allodynia. Signs: hot inflamed, redness, swelling
-Neuropathic pain
-Arthritis
-Phantom limb pain

Question 27

Neuropathic pain

Answer 27

-nerve injury due to trauma and inflammation or metabolic diseases (e.g. diabetes, toxins, tumors, primary neurological diseases, herpes zoster infection)
-pathological
-associated with allodynia
-> peripheral sensitization
-> Central sensitization
-> rerouting of nerve fibers
-> sprouting of new axon terminals and dendritic spines
-> glia release pain-promoting substances

Question 28

Arthritis

Answer 28

Joint inflammation

Question 29

Phantom limb pain

Answer 29

-neuropathic pain
-result from limb or digit amputation
-sensation of pain in the absent limb
-mirror box therapy

Question 30

Pulpitis

Answer 30

-Inflammation of dental pulp
-symptoms: pain which may be sharp or throbbing, sensitivity to sweet, hot, or cold foods and beverages, inflammation
-Causes: Bacteria irritate the dental pulp through an area of tooth decay, including dental caries. Trauma or injury to a tooth

Question 31

Transmission of pain signals:

Answer 31

A-delta fibers and C fibers

A-delta fibers: thinly myelinated, faster conducting, “fast” pain (sharp, pricking, localized), thermal or mechanical, small receptive fields, good for pain localization and triggering immediate protective reflexes

C fibers: unmyelinated, slower conducting, “slow” pain (diffuse, burning), thermal, mechanical, chemical, large receptive fields, poor localization and dull pain sensation