6.3 THERMORECEPTION

THERMORECEPTION

• usually free endings with small receptive fields.

THERMORECEPTION two types

• Activated by cold

• Activated by heat

Activated by cold

• Temperatures below body temperature, no longer stimulated if the skin is under 5ºC

Activated by heat

• Beyond 45ºC nociceptors take control, to avoid damage to the skin & underlying tissues.

Location of THERMORECEPTION

• Widely distributed through the skin, but also in the hypothalamus & the spinal cord to detect body temperature.

Thermoreceptors

• heat receptors

• cold receptors

heat receptors

• They begin to activate when the skin surface rises above 30°C & are most stimulated at 45°C.

• Beyond this temperature, pain receptors take control, to avoid damage to the skin and underlying tissues.

cold receptors

• They start having activity when the skin surface drops below 35°C & are most stimulated when the skin surface is at 25°C.

• They are no longer stimulated once the skin surface drops below 5°C, explaining why the tissues stop perceiving the cold after a long time in icy temperatures.

perception of pain  (pathways)

• specific

pain receptors

• Nociceptors

• although stimuli is different →specific receptors for pain

Nociceptors

• They are the sensory afferents responsible for transmitting pain, generally free nerve endings.

How is increasing temperature (pain intensity) encoded by nociceptors?

• Higher temperature →

  • More action potentials

  • Higher firing frequency

👉 This is called frequency coding

• After threshold (~45°C):

  • Pain intensity = rate of firing of nociceptors

The axons of the neurons that transmit pain neuronal information are

• slower compared to sensory fibers that transmit touch & proprioception.

Perception of pain can be separated into

• early perception of sharp pain (first pain)

• later duller & burning sensation (second pain)

1st pain

• Aδ fibers

• Early perception of acute pain

• Small, myelinated fibers

• Phasic or rapidly adapting. Several types

• Mechanosensitive: Respond to mechanical stimuli

• Mechanothermal: respond to thermal & mechanical stimuli

 2nd pain

• C-fibers

• more diffuse & burning sensation

• Small & unmyelinated fibers

• Tonic or slow adapting

• Polymodal nociceptors: Mechanical, thermal, & chemical

PAIN GATE THEORY

• rubbing a damaged area can reduce pain

• Transmission of nerve impulses from afferent fibers to 2nd order neurons in the spinal cord is modulated by a gating mechanism in the dorsal horns.

• Activation of mechanoreceptors modulates the transmission of nociceptive information to higher centers.

• Interactions in the local circuits of the dorsal horn, reduce the sensation of pain

PAIN MODULATION: DESCENDING PATHWAY and LOCAL CIRCUITS

• descending neurons that can modulate (inhibit) active neurons in the dorsal horn of the spinal cord

• These neurons activate local circuits and cause the release of inhibitory molecules that MODULATE the pain signal, decreasing it.

Pain modulators in the descending pathway

- Enkephalins

- Endorphins

- Dynorphin

• Cannabinoids

• Norepinephrine

• Serotonin

Endogenous opioids

• Enkephalins

• Endorphins

• Dynorphin

pain modulation is a mechanism behind

• opioid analgesia — morphine mimics endogenous opioids.

• Also explains why adrenaline, exercise, and placebo inhibit pain.

-Alterations in pain processing when the peripheral or central afferent fibers are damaged

• generate chronic pain spontaneously or with mild stimuli.

Peripheral sensitization:

• activation of peripherial nociceptor (1st order neuron) is lowered

• the nociceptor itself that modifies its trigger threshold by inflammatory molecules present in the tissue

• Reason for increased pain → First order neuron interaction with immune system-derived molecules

Central sensitization

• It takes place due to an increase in the excitability of 2nd order neurons the dorsal horn of the spinal cord.

Hyperalgesia

• exaggerated pain response to a normally painful stimulus. It is due to sensitization.

Allodynia

• induction of pain by an innocuous stimulus or in the absence of a stimulus. It is often due to central sensitization.

Neuropathic pain

• both peripheral & central sensitization usually disappear when an injury heals.

• When this does not happen, we speak of neuropathic pain (source in the somatosensory nervous system).

Paresthesia/dysesthesia:

•  abnormal sensation (tingling, burning, itching) in response to touch.

• It can be central or peripheral (After radiation therapy)

Phantom limb syndrome

• sensory perceptions (spikes, pain...) in a limb that has been amputated.

• Caused by the reorganization of the somatosensory cortex.

• Activity in adjacent areas activates neurons previously representing the lost limb

• Interpreted by the brain as sensations in the missing limb

• CNS origin & usually disappears after the reorganization of the circuits (plasticity).

REFERRED PAIN

• Pain perceived in the skin or muscle, even though the actual source is visceral

Visceral sensory neurons

• from organs

Somatic sensory neurons

• from skin

angina pectoris

• heart

• kidneys

Heart (angina pectoris)

• Actual source: Heart (visceral pain)

• Signals enter spinal cord

• These same spinal segments also receive input from → Left arm, chest, & jaw (females)

Kidney (angina pectoris)

• Actual source: Kidneys

• Signals enter spinal cord at lower thoracic/lumbar levels

• These correspond to:

  • Lower back (lumbar region)

The fibers of the visceral nociceptors share

• same dorsal root ganglion & segment of the spinal cord with the fibers that come from skin nociceptors

→ brain misinterprets pain as coming from the skin.

The response to pain is multifactorial

• parallel pathways of pain → Sensory-discriminative aspects & Affective-motivational aspects

Sensory-discriminative aspects

• Processing of the sensory information → Location, Intensity, Duration & Type of pain

Affective-motivational aspects

• Unpleasant feeling, autonomic activation fear, anxiety, (fight or flight) autonomic activation

Sensory-discriminative

aspects

• Pathway: Spinothalamic tract → Thalamus (VPL) → Somatosensory cortex (SI, SII)

• Function:

  • Location of pain

  • Intensity of pain

  • Type of stimulus

→ “Where is the pain and how strong is it?”

Affective-motivational

aspects

• Pathway: Spinothalamic tract → medial thalamus → limbic system

  • Includes:

    • Anterior cingulate cortex

    • Insula

    • Amygdala

    • Hypothalamus

• Function:

  • Emotional response to pain

  • Suffering/unpleasantness

  • Motivation to react

→ “How does the pain feel emotionally?”

Mechanoreceptors

• provide information on the position of the limbs and other parts of the body in space

muscle spindles

• detects changes in muscle length

Golgi tendon organ:

• Detects changes in muscle tension

PROPIOCEPTION RECEPTOR TYPE 

• muscle spindle

(Tendons, joints & muscles)

TOUCH RECEPTOR TYPE 

• encapsulated:

  • Merkel corpuscles

  • Meissner corpuscles

  • Pacinian corpuscles

  • Ruffini's corpuscles

PAIN, TEMPERATURE RECEPTOR TYPE 

• Nerve endings free

PAIN TEMPERATURE PRURITUS RECEPTOR TYPE 

• Nerve endings free (unmyelinated)