Chapter 8: Somatosensory Neurotransmission: Touch, Pain, & Temperature

Somatosensory Neurotransmission: Touch, Pain, & Temperature begins by classifying sensory receptors based on their adequate stimuli and adaptation rates, including mechanoreceptors like Meissner corpuscles, Merkel cells, Ruffini endings, and Pacinian corpuscles which encode tactile sensations such as vibration, pressure, and stretch via myelinated A-alpha and A-beta fibers. The text explores sensory coding principles, explaining how the central nervous system deciphers stimulus modality, location, intensity, and duration through mechanisms like receptive field density and lateral inhibition. A significant portion of the chapter is dedicated to nociception, distinguishing between the rapid, sharp first pain mediated by myelinated A-delta fibers and the delayed, diffuse second pain transmitted by unmyelinated C fibers. It details the molecular basis of transduction, highlighting the role of transient receptor potential (TRP) channels (such as TRPV1 and TRPM8) and acid-sensing ion channels in detecting thermal and chemical noxious stimuli. The summary contrasts the two primary ascending pathways: the dorsal column-medial lemniscus system, which decussates in the medulla and carries proprioceptive and tactile information, and the ventrolateral spinothalamic tract, which decussates in the spinal cord and transmits pain and temperature signals. Both pathways project to the ventral posterior lateral (VPL) nucleus of the thalamus before reaching the primary somatosensory cortex, where the body is mapped somatotopically on the sensory homunculus. Clinical concepts such as hyperalgesia, allodynia, and sensitization are explained through the release of inflammatory mediators like bradykinin, prostaglandins, and substance P. The chapter also covers the convergence-projection theory of referred pain, visceral pain characteristics, and the distinct symptoms of spinal cord hemisection known as Brown-Sequard syndrome. Finally, physiological mechanisms of pain modulation are discussed, including the gate-control theory, the role of endogenous opioids (enkephalins, dynorphins), and descending inhibitory pathways originating in the periaqueductal gray and nucleus raphe magnus that suppress nociceptive transmission in the dorsal horn.