1-4 of 4 Results

  • Keywords: sensory transduction x
Clear all

Article

Jeffrey R. Holt and Gwenaëlle S.G. Géléoc

The organs of the vertebrate inner ear respond to a variety of mechanical stimuli: semicircular canals are sensitive to angular velocity, the saccule and utricle respond to linear acceleration (including gravity), and the cochlea is sensitive to airborne vibration, or sound. The ontogenically related lateral line organs, spaced along the sides of aquatic vertebrates, sense water movement. All these organs have a common receptor cell type, which is called the hair cell, for the bundle of enlarged microvilli protruding from its apical surface. In different organs, specialized accessory structures serve to collect, filter, and then deliver these physical stimuli to the hair bundles. The proximal stimulus for all hair cells is deflection of the mechanosensitive hair bundle. Hair cells convert mechanical information contained within the temporal pattern of hair bundle deflections into electrical signals, which they transmit to the brain for interpretation.

Article

Taylor Follansbee, Mirela Iodi Carstens, and E. Carstens

Pain is defined as “An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage,” while itch can be defined as “an unpleasant sensation that evokes the desire to scratch.” These sensations are normally elicited by noxious or pruritic stimuli that excite peripheral sensory neurons connected to spinal circuits and ascending pathways involved in sensory discrimination, emotional aversiveness, and respective motor responses. Specialized molecular receptors expressed by cutaneous nerve endings transduce stimuli into action potentials conducted by C- and Aδ-fiber nociceptors and pruriceptors into the outer lamina of the dorsal horn of the spinal cord. Here, neurons selectively activated by nociceptors, or by convergent input from nociceptors, pruriceptors, and often mechanoreceptors, transmit signals to ascending spinothalamic and spinoparabrachial pathways. The spinal circuitry for itch requires interneurons expressing gastrin-releasing peptide and its receptor, while spinal pain circuitry involves other excitatory neuropeptides; both itch and pain are transmitted by ascending pathways that express the receptor for substance P. Spinal itch- and pain-transmitting circuitry is segmentally modulated by inhibitory interneurons expressing dynorphin, GABA, and glycine, which mediate the antinociceptive and antipruritic effects of noxious counterstimulation. Spinal circuits are also under descending modulation from the brainstem rostral ventromedial medulla. Opioids like morphine inhibit spinal pain-transmitting circuits segmentally and via descending inhibitory pathways, while having the opposite effect on itch. The supraspinal targets of ascending pain and itch pathways exhibit extensive overlap and include the somatosensory thalamus, parabrachial nucleus, amygdala, periaqueductal gray, and somatosensory, anterior cingulate, insular, and supplementary motor cortical areas. Following tissue injury, enhanced pain is evoked near the injury (primary hyperalgesia) due to release of inflammatory mediators that sensitize nociceptors. Within a larger surrounding area of secondary hyperalgesia, innocuous mechanical stimuli elicit pain (allodynia) due to central sensitization of pain pathways. Pruriceptors can also become sensitized in pathophysiological conditions, such as dermatitis. Under chronic itch conditions, low-threshold tactile stimulation can elicit itch (alloknesis), presumably due to central sensitization of itch pathways, although this has not been extensively studied. There is considerable overlap in pain- and itch-signaling pathways and it remains unclear how these sensations are discriminated. Specificity theory states that itch and pain are separate sensations with their own distinct pathways (“labeled lines”). Selectivity theory is similar but incorporates the observation that pruriceptive neurons are also excited by algogenic stimuli that inhibit spinal itch transmission. In contrast, intensity theory states that itch is signaled by low firing rates, and pain by high firing rates, in a common sensory pathway. Finally, the spatial contrast theory proposes that itch is elicited by focal activation of a few nociceptors while activation of more nociceptors over a larger area elicits pain. There is evidence supporting each theory, and it remains to be determined how the nervous system distinguishes between pain and itch.

Article

Daniel W. Wesson, Sang Eun Ryu, and Hillary L. Cansler

The perception of odors exerts powerful influences on moods, decisions, and actions. Indeed, odor perception is a major driving force underlying some of the most important human behaviors. How is it that the simple inhalation of airborne molecules can exert such strong effects on complex aspects of human functions? Certainly, just like in the case of vision and audition, the perception of odors is dictated by the ability to transduce environmental information into an electrical “code” for the brain to use. However, the use of that information, including whether or not the information is used at all, is governed strongly by many emotional and cognitive factors, including learning and experiences, as well as states of arousal and attention. Understanding the manners whereby these factors regulate both the perception of odors and how an individual responds to those percepts are paramount for appreciating the orchestration of behavior.

Article

Alan C. Spector and Susan P. Travers

Everything a person swallows must pass a final chemical analysis by the sensory systems of the mouth; of these, the gustatory system is cardinal. Gustation can be heuristically divided into three basic domains of function: sensory-discriminative (quality and intensity), motivational/affective (promote or deter ingestion), and physiological (e.g., salivation and insulin release). The signals from the taste buds, transmitted to the brain through the sensory branches of cranial nerves VII (facial), IX (glossopharyngeal), and X (vagal), subserve these primary functions. Taste buds are collections of 50–100 cells that are distributed in various fields in the tongue, soft palate, and throat. There are three types of cells that have been identified in taste buds based on their morphological and cytochemical expression profiles. Type II cells express specialized G-protein-coupled receptors (GPCR or GPR) on their apical membranes, which protrude through a break in the oral epithelial lining called the taste pore, that are responsible for the sensing of sweeteners (via the taste type 1 receptor (T1R) 2 + T1R3), amino acids (via the T1R1+T1R3), and bitter ligands (via the taste type 2 receptors (T2Rs)). Type III cells are critical for the sensing of acids via the otopetrin-1 (Otop-1) ion channel. The sensing of sodium, in at least rodents, occurs through the epithelial sodium channel (ENaC), but the exact composition of this channel and the type of taste cell type in which the functional version resides remains unclear. It is controversial whether Type I cells, which have been characterized as glial-like, are involved in sodium transduction or play any taste signaling role. For the most part, receptors for different stimulus classes (e.g., sugars vs. bitter ligands) are not co-expressed, providing significant early functionally related segregation of signals. There remains a persistent search for yet to be identified receptors that may contribute to some functions associated with stimuli representing the so-called basic taste qualities—sweet, salty, sour, bitter, and umami—as well as unconventional stimuli such as fatty acids (in addition to cluster of differentiation-36 (CD-36), GPR40, and GPR120) and maltodextrins. The primary neurotransmitter in taste receptor cells is ATP, which is released through a voltage-gated heteromeric channel consisting of the calcium homeostasis modulator 1 and 3 (CALHM1/3) and binds with P2X2/X3 receptors on apposed afferent fibers. Serotonin released from Type III cells has been implicated as an additional neurotransmitter, binding with HT3a receptors, and possibly playing a role in acid taste (which is sour to humans). Taste bud cells undergo complete turnover about every two weeks. Although there remains much to be understood about the operations of the taste bud, perhaps the one very clear principle that emerges is that the organization of signals transmitted to the brain is not random and arbitrary to be decoded by complex algorithms in the circuits of the central gustatory system. Rather, the transmission of taste information from the periphery is highly ordered.