General Sensation and Special Senses

general sensation

sensation we feel due to presence of receptors all over the body (e.g., temperature, pressure, touch)

specialized sensation

sensation due to specialized receptors in the head (e.g., vision, hearing, taste, smell)

sensation

refers specifically to the activation of sensory receptors and transmission of that info to the CNS (via electrical signals), no conscious awareness of this activity

perception

occurs when our cerebral cortex receives this info and assigns meaning to it, requires selective attention of the cortex, dangerous stimuli are prioritized

exteroceptors

respond to stimuli in external environment (somatic sensory receptors)

interoceptors

respond to changes in body’s internal environment (visceral sensory receptors)

location and modality

sensory receptors are classified by these two categories

chemoreceptors

respond to chemicals (blood gases, pH)

mechanoreceptors

respond to touch, stretch, body position; osmoreceptors and proprioceptors

osmoreceptors

type of mechanoreceptor; respond to changes in solute concentrations via sensing changes in volume and shape of cells

proprioceptors

type of mechanoreceptor; detect body position by degree of stretch and contraction of skeletal muscle

thermoreceptors

sense changes in temperature

nociceptors

respond to tissue damage and physical trauma

referred pain

when pain originating form visceral organs is felt elsewhere in the body, may be due to convergence of visceral and somatosensory fibers at same level of spinal cord → brain perceives pain in the chest area as originating in the brachial region

glutamate

primary neurotransmitter in the pain pathway, inhibiting it can shut down the pain pathway

pain pathway

ascending pathways, 1st and 2nd order neurons synapse in spinal cord, 2nd and 3rd order neurons synapse in thalamus, 3rd order neuron terminates in somatosensory cortex (postcentral gyrus) → perception of pain

endogenous modulation

natural pain modulation occurs via descending inhibitory neurons from the brain, GABA and endogenous opiods

endogenous opiods

beta-endorphins, enkephalins, dynorphins, block spinal cord transmission of pain to brain by inhibiting release of substance P from 1st order neurons

substance P

molecule that stimulates pain transmission

exogenous modulation

analgesics and anesthetics

analgesics

alter synaptic transmission in spinal cord; NSAIDs, opioids, glutamate antagonists, GABA agonists

nonsteroidal anti-inflammatory drugs

analgesic, advil and aspirin, block cyclooxygenases, which inhibits synthesis of prostaglandins (increase sensation of pain by sensitizing nociceptors)

opioids

analgesic, work through same method as endogenous opioids, inhibit substance P which will inhibit synaptic transmission

glutamate antagonists

analgesic, bind to glutamate receptors and prevents glutamate from binding, slow down transmission of pain

GABA agonsists

analgesic, molecules that are similar to GABA to inhibit postsynaptic neurons

anesthetics

exogenous modulation, act by blocking conduction in neurons, e.g., lidocaine, block voltage-gated sodium channels → prevent action potentials