Amphid

Abstract: The complete structure of the anterior sensory nervous system of the small nematode C. elegans has been determined by reconstruction from serial section electronmicrographs. There are 58 neurons in the tip of the head. Fifty-two of these are arranged in sensilla. These include six inner labial sensilla, six outer labial sensilla, four cephalic sensilla and two amphids. Each sensillum consists of ciliated sensory neurons ending in a channel enclosed by two non-neuronal cells, the sheath and socket cells. The amphidial channel opens to the outside as does that of the inner labial sensilla so that these probably contain chemoreceptive neurons. The endings of the other sensilla are embedded in the cuticle and may be mechanoreceptive. The cell bodies of all the neurons lie near the nerve ring and their axons project into the ring or into ventral ganglia. One of the ciliated sensory neurons in each of the six inner labial sensilla makes direct chemical synapses onto a muscle making these sensory-motor neurons. The anatomy of four isogenic animals was compared in detail and found to be largely invariant. The anatomy of juveniles is nearly identical to that of the adult, but males have four additional neuron processes.

Abstract: C. elegans has a highly developed chemosensory system that enables it to detect a wide variety of volatile (olfactory) and water-soluble (gustatory) cues associated with food, danger, or other animals. Much of its nervous system and more than 5% of its genes are devoted to the recognition of environmental chemicals. Chemosensory cues can elicit chemotaxis, rapid avoidance, changes in overall motility, and entry into and exit from the alternative dauer developmental stage. These behaviors are regulated primarily by the amphid chemosensory organs, which contain eleven pairs of chemosensory neurons. Each amphid sensory neuron expresses a specific set of candidate receptor genes and detects a characteristic set of attractants, repellents, or pheromones. About 500-1000 different G protein-coupled receptors (GPCRs) are expressed in chemosensory neurons, and these may be supplemented by alternative sensory pathways as well. Downstream of the GPCRs, two signal transduction systems are prominent in chemosensation, one that uses cGMP as a second messenger to open cGMP-gated channels, and one that relies upon TRPV channels. These sensory pathways are modulated and fine-tuned by kinases and phosphatases. Chemosensory preferences can be modified by sensory adaptation, developmental history, and associative learning, allowing C. elegans to integrate context and experience into its behavior.

Abstract: As a sensory response to starvation or overcrowding, Caenorhabditis elegans second-stage larvae may molt into a developmentally arrested state called the dauer larva When environmental conditions become favorable for growth, dauer larvae mold and resume development Some mutants unable to form dauer larvae are simultaneously affected in a number of sensory functions, including chemotaxis and mating The behavior and sensory neuroanatomy of three such mutants, representing three distinct genetic loci, have been determined and compared with wild-type strain Morphological abnormalities in afferent nerve endings were detected in each mutant Both amphid and outer labial sensilla are affected in the mutant CB1377 (daf-6)X, while another mutant, CB1387 (daf-10)IV, is abnormal in amphidial cells and in the tips of the cephalic neurons The most pleitropic mutant, CB1379 (che-3)I, exhibits gross abnormalities in the tips of virtually all anterior and posterior sensory neurons The primary structural defect in CB1377 appears to be in the nonneuronal amphidial sheath cells The disruption of neural organization in CB1377 is much greater in the adult than in the L2 stage Of all the anterior sense organs examined, only the amphids are morphologically affected in all three mutants Thus, one or more of the amphidial neurons may mediate the sensory signals for entry into the dauer larva stage in normal animals Using temperature-sensitive mutants we determined that the same defects which block entry into the dauer stage also prevent recovery of dauer larvae