Development of the Special Senses

Taste and Smell at Birth and in Old Age

The senses of taste and smell develop in the intrauterine environment and can deteriorate with age.

Learning Objectives

Describe the status of taste and smell at birth and in old age

Key Takeaways

Key Points

  • Newborns are born with odor and taste preferences acquired in the womb from the smell and taste of amniotic fluid, influenced by the mother’s diet.
  • A significant change takes place in the regulation of olfaction just after birth so that odors related to the offspring are no longer aversive, allowing the female to positively respond to her babies.
  • Anosmia is a lack of functioning olfaction: an inability to perceive odors.
  • Ageusia is the loss of taste function, particularly the inability to detect sweetness, sourness, bitterness, saltiness, and umami (savory taste).

Key Terms

  • olfactory bulb: The structure of the vertebrate forebrain involved in olfaction, the perception of odors.
  • anosmia: The inability to perceive odors.
  • taste bud: Sensory receptors located around the small structures on the upper surface of the tongue, soft palate, upper esophagus, and epiglottis.

Examples

Failure to detect odors (anosmia) is one reason that older individuals may not enjoy eating, since an inability to smell is related to an inability to taste (ageusia). Caretakers of such individuals must ensure they continue to eat healthy foods.

The senses of taste and smell first develop in neonates and can be diminished by the effects of aging.

Smell

At birth, infants can show expressions of disgust or pleasure when presented with pleasant (honey, milk) or unpleasant (rotten egg) odors and tastes. Newborns have inherent smell and taste preferences acquired in the womb from the smell and taste of amniotic fluid, which is influenced by the mother’s diet.

Intrauterine Olfactory Learning

Intrauterine olfactory learning is demonstrated by behavioral evidence that newborns respond positively to the smell of their own amniotic fluid. Infants recognize and react favorably to scents emitted from their own mother’s breasts, despite the fact that they also may be attracted to breast odors from unfamiliar nursing females in a different context. The unique scent of the mother (to the infant) is referred to as her olfactory signature. Infants are also able to recognize and respond with familiarity and preference to their mother’s underarm scent.

In newborn mammals, the nipple area of the mother is the sole nutritional source, so the maternal olfactory scent becomes associated with food intake. Newborns who do not gain access to the mother’s breasts would die shortly after birth, so this olfactory cue helps maintain and establish effective breast feeding. The mother’s olfactory signature is experienced with reinforcing stimuli such as food, warmth, and tactile stimulation, enhancing further learning of that cue.

As demonstrated by animals in the wild (apes, for example), offspring are held by the mother immediately after birth without cleaning and continually exposed to the familiar odor of the amniotic fluid (making the transition from the intrauterine to extrauterine environment less overwhelming).

Studies demonstrate that the changes to the olfactory bulb and main olfactory system following birth are extremely important and influential for maternal behavior. Pregnancy and childbirth result in a high state of plasticity of the olfactory system that may facilitate olfactory learning within the mother. A significant change takes place in the regulation of olfaction just after birth so that odors related with the offspring are no longer aversive, allowing the female to positively respond to her babies.

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Olfactory System: Human olfactory system. 1: Olfactory bulb 2: Mitral cells 3: Bone 4: Nasal epithelium 5: Glomerulus (olfaction) 6: Olfactory receptor cells

Anosmia and Aging

Older people experience a decline in the sense of smell. Anosmia, a lack of functioning olfaction (inability to perceive odors), may be temporary, but traumatic anosmia can be permanent. Anosmia is due to an inflammation of the nasal mucosa, blockage of nasal passages, or a destruction of one temporal lobe. A common cause of anosmia is old age.

Taste

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Taste Receptors in Humans: Structure of the taste bud, including afferent nerve, connective tissue, basal cell, taste receptor cell, lingual epithelium, oral cavity, and taste pore.

Taste buds contain the receptors for taste and are located around the small structures ( papillae ) on the upper surface of the tongue, soft palate, upper esophagus, and epiglottis. These papillae are involved in detecting the five known elements of taste perception: salty, sour, bitter, sweet, and umami. Via small openings in the tongue epithelium (taste pores), parts of the food dissolved in saliva come into contact with taste receptors (taste buds). The taste receptor cells send information detected by clusters of various receptors and ion channels to the gustatory areas of the brain via the seventh, ninth, and tenth cranial nerves. On average, the human tongue has 2,000–8,000 taste buds.

The average life of a taste bud is 10 days. Ageusia is the loss of taste function, particularly the inability to detect sweetness, sourness, bitterness, saltiness, and umami. It is sometimes confused with anosmia, a loss of the sense of smell. Because the tongue can only indicate texture and differentiate between sweet, sour, bitter, salty, and umami, most of what is perceived as the sense of taste is actually derived from smell. True ageusia is relatively rare compared to hypogeusia (a partial loss of taste) and dysgeusia (a distortion or alteration of taste). Local damage and inflammation that interferes with the taste buds or local nervous system such as that stemming from radiation therapy, glossitis, tobacco use, and denture use also cause ageusia. Other known causes include loss of taste sensitivity from aging causing a difficulty detecting salty or bitter taste, anxiety disorder, cancer, renal failure and liver failure.

Development of Vision

The eye forms from the neural tube, epidermis, and periocular mesenchyme, with sequential inductions of tissue during development.

Learning Objectives

Describe the development of vision

Key Takeaways

Key Points

  • Organogenesis of the eye is an example of a developmental cascade of inductions.
  • Development of the optic vesicles starts in the three-week embryo from a progressively deepening groove in the neural plate called the optic sulcus.
  • The optic vesicles come into contact with the epithelium and induce the epidermis to thicken to form the lens placode.
  • The periocular mesenchyme migrates in during the formation of the optic cup and is critical for the induction of the retinal pigment epithelium and the optic nerve.

Key Terms

  • optic cup: During embryonic development of the eye, the outer wall of the bulb of the optic vesicles becomes thickened and invaginated, converting it to a cup consisting of two strata of cells. These strata are continuous with each other at the cup margin, which ultimately overlaps the front of the lens and reaches as far forward as the future aperture of the pupil.
  • optic sulcus: A progressively-deepening groove in the neural plate from which the optic vesicles develop.
  • lens placode: A thickened portion of ectoderm which serves as the precursor to the lens.

The eye develops from the neural tube, the epidermis, and the periocular mesenchyme, which receives contributions from both the neural crest and mesoderm lineages. The organogenesis of the eye is an example of a developmental cascade of inductions, with three different tissues contributing to its differentiations.

Neural Tube

This diagram of the optical vesicle indicates the forebrain, bulbus cordis, atrium, ventricle, and vitelline vein.

Chick embryo head with optic vesicle: The eyes make their appearance before the closure of the anterior end of the neural tube. After the closure of the tube they are known as the optic vesicles.

First, an outpocketing of the neural tube occurs, creating optic vesicles. Development of the optic vesicles starts in the three-week embryo from a progressively deepening groove in the neural plate called the optic sulcus. As this expands, the rostral neuropore (the exit of the brain cavity out of the embryo) closes and the optic sulcus and the neural plate becomes the optic vesicle.

Epidermis

The optic vesicles come into contact with the epithelium and induce the epidermis. The epithelium thickens to form the lens placode. The lens differentiates and invaginates until it detaches from the epithelium. The lens then acts as an inducer back to the optic vesicle to transform it into the optic cup and back to the epidermis to transform it into the cornea. The optic cup then delaminates into two layers: the neural retina and the retinal pigment epithelium.

Periocular Mesenchyme

This image of the optic stalk and cup indicates the telencephalon, edge of optic cup, choroidal fissure, arteria centralis retina, optic stalk, and thalamencephalon.

The Optic Stalk and Optic Cup: During embryonic development of the eye, the outer wall of the bulb of the optic vesicles becomes thickened and invaginated, and the bulb is thus converted into a cup, the optic cup.

The periocular mesenchyme migrates inward during the formation of the optic cup and is critical for the induction of the retinal pigment epithelium and the optic nerve. The mesenchyme contributes to the cornea, iris, ciliary body, sclera, and blood vessels of the eye.

Chordamesoderm

Chordamesoderm induces the anterior portion of the neural tube to form the precursors of the synapomorphic tripartite brain of vertebrates, a bulge called the diencephalon. Further induction by the chordamesoderm forms a protrusion: the optic vesicle. This vesicle is subsequently invaginated by further inductions from the chordamesoderm, and induces the ectoderm that thickens (lens placode) and further invaginates to a point that detaches from the ectoderm and forms a neurogenic placode. The lens placode is triggered by the chordamesoderm to invaginate and form the optic cup, composed of an outer layer of neural retina and inner layer of pigmented retina that unite and form the optic stalk. The pigmented retina is formed by rods and cones and composed of small cilia typical of the ependymal epithelium of the neural tube. Some cells in the lens vesicle will form the cornea and the lens vesicle will develop completely to form the definitive lens. Iris is formed from the optic cup cells.

Development of Hearing and Balance

Critical periods have been identified for the development of the hearing and vestibular system.

Learning Objectives

Describe the development of the inner ear for hearing and balance

Key Takeaways

Key Points

  • The human inner ear develops during week four of embryonic development from the auditory placode, a thickening of the ectoderm that gives rise to the bipolar neurons of the cochlear and vestibular ganglions.
  • The auditory vesicle gives rise to the utricular and saccular components of the membranous labyrinth.
  • Beginning in the fifth week of development, the auditory vesicle also gives rise to the cochlear duct, which contains the spiral organ of Corti and the endolymph that accumulates in the membranous labyrinth.
  • In our vestibular system, neurons are undeveloped at neuronal birth and mature during the critical period of the first two to three postnatal weeks.
  • Many studies have supported a correlation between the type of auditory stimuli present in the early postnatal environment and the topographical and structural development of the auditory system.

Key Terms

  • inner ear: The portion of the ear located within the temporal bone that includes the semicircular canals, vestibule, and cochlea. It is responsible for hearing and balance.
  • organ of Corti: Found only in mammals, this inner ear organ contains auditory sensory cells, or “hair cells.”
  • vestibular system: The sensory system that provides the leading contribution about movement and sense of balance in most mammals.

The human inner ear develops during week four of embryonic development from the auditory placode, a thickening of the ectoderm that gives rise to the bipolar neurons of the cochlear and vestibular ganglions. As the auditory placode invaginates towards the embryonic mesoderm, it forms the auditory vesicle or otocysts.

This diagram of the mammalian ear indicates the cupula, helicotrema, lamina spiralis ossea, tymphanic cavity, vestibular fenestra, fissura vestibuli, recessus sphericus, fossa cochlearis, lateral semicircular canal, vestibule, posterior semicircular canal, aquaductus vestibuli, reces suscepticus, interior acoustic meatus, scala tympani, scala vestibuli, and cochlea.

Formation of the Mammalian Ear: The cochlea and vestibule viewed from above.

The auditory vesicle gives rise to the utricular and saccular components of the membranous labyrinth. They contain the sensory hair cells and otoliths of the macula of utricle and of the saccule, respectively, which respond to linear acceleration and the force of gravity. The utricular division of the auditory vesicle also responds to angular acceleration, as do the endolymphatic sac and duct that connect the saccule and utricle.

Beginning in the fifth week of development, the auditory vesicle also gives rise to the cochlear duct, which contains the spiral organ of Corti and the endolymph that accumulates in the membranous labyrinth. The vestibular wall will separate the cochlear duct from the perilymphatic scala vestibuli, a cavity inside the cochlea. The basilar membrane separates the cochlear duct from the scala tympani, a cavity within the cochlear labyrinth. The lateral wall of the cochlear duct is formed by the spiral ligament and the stria vascularis, which produces the endolymph. The hair cells develop from the lateral and medial ridges of the cochlear duct, which together with the tectorial membrane make up the organ of Corti.

Critical periods have been identified for the development of hearing and the vestibular system. In our vestibular system, neurons are undeveloped at neuronal birth and mature during the critical period of the first two to three postnatal weeks. Disruption of maturation during this period can cause changes in normal balance and movement through space. Animals with abnormal vestibular development tend to have irregular motor skills. Studies have consistently shown that animals with genetic vestibular deficiencies during this critical period have altered vestibular phenotypes, most likely as a result of lack insufficient input from the semicircular canals and dopaminergic abnormalities.

Moreover, exposure to abnormal vestibular stimuli during the critical period is associated with irregular motor development. Many studies have supported a correlation between the type of auditory stimuli present in the early postnatal environment and the topographical and structural development of the auditory system. First reports on critical periods came from studies of deaf children and animals that received a cochlear implant to restore hearing. Approximately at the same time, other studies demonstrated that the adaptation to the cochlear implant is subject to an early developmental critical (sensitive) period. These corresponding data demonstrated both on children and in animals that this sensitive period has consequences for medical therapy of hearing loss.