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Cormack, Chs. 4, 10; Guyton and Hall, Chs. 45-59; Michael and Rovick, Unit 4; van Wysberghe and Cooley, Cases 2, 4,, 7; Young and Young, Chs. 2-16, 21

W. Crone (303 FTZ, 629-7439, cronewil@hvcc.edu, http://www.hvcc.edu/academ/facultycrone/index.html)

possible web sites: http://www.pitt.edu/~mattf/NeuroRing.html

(Neuro Ring home page--multiple neuro sites)

http://www.erowid.org/entheo_issues/chemistry/chemistry.shtml (may be a bit bizarre, but an interesting exploration of many mind-altering substances, their chemistry, biology, and social uses)

Nervous system: central nervous system (CNS) of brain and spinal cord vs. peripheral nervous system (PNS) of cranial and spinal nerves

Two types of cells:

a) Neurons and their three major parts of cell body, dendrites, axon

b) Supporting cells are also ectodermally derived. The myelin sheath is formed by Schwann cells wrapping about 1 mm around an axon, leaving exposed axon in the gaps known as the nodes of Ranvier. In contrast, in the CNS, oligodendrocytes extend, tentacle-like, to form myelin sheaths around several axons, leading to the macroscopic picture of white matter (vs. the gray matter of cell bodies).

Neurons are excitable, As fondly (?) remembered, the charge separation generated by differences in ion concentration creates the membrane potential of about -90 mV (at least in large nerves). At the resting potential, the Na+ conductance is low, the K+ conductance is high. Overall, above a certain threshold strength, a depolarizing current will trigger an action potential. The amplitude of an action potential is all or none (spike potential), since gates stay open for a set length of time regarding of the level of stimulus. Stimulus strength of action potentials is therefore frequency modulated (will contrast this all-or-none behavior with EPSP behavior at synapses).

Binding of the neurotransmitter to its receptor protein to open up ion channels (hence the term, chemically regulated gates). With these opened ion channels, two possibilities:


excitatory postsynaptic potential (EPSP)


inhibitory postsynaptic potential (IPSP)

Without the voltage channels of the axons, the membrane potential changes induced by the neurotransmitters at the synapse are not all or none. They can show summation:

spatial summation:

presynaptic nerve fibers converging on a postsynaptic neuron

temporal summation:

successive waves of neurotransmitter release

IPSP and EPSP can sum up, cancel each other out, etc., so many possible levels of control.



Acetylcholine (ACh) has varying responses, depending on the type of receptors, named for toxins that can stimulate them: nicotinic ACh receptors and muscarinic ACh receptors.

nicotinic ACh receptor: when ACh binds, opens up ion channel. Na+ comes in to depolarize, and hence, an EPSP. This is a graded depolarization, so that an EPSP is graded and capable of summation without a refractory period, in contrast to the all-or-none action potential. At the neuromuscular junctions, the postsynaptic membrane is the motor end plate. EPSPs lead to opening of voltage-regulated gates, which lead to action potentials in muscle fibers.

muscarinic ACh receptor: G-protein involved as intermediary between receptor and ion channel, so that different G-protein subunits involved will influence the effect of ACh binding. For example, one type of muscarinic ACh receptor effect is where the vagus nerve synapses with cardiac pacemaker cells and opens up K+ channels, leading to hyperpolarization and hence, an IPSP.1

The ACh-receptor interaction is brief, but can quickly return as long as there's free ACh around. Usually ACh inactivated by acetylcholinesterase (AChE), present on the postsynaptic membrane.

nerve gas: inhibition of AChE in skeletal muscles, leading to spastic paralysis.


In the CNS, many monamines can act as neurotransmitters. The monoamine neurotransmitters work through second messengers, e.g., cAMP.

the catecholamines:

norepinephrine, dopamine (epinephrine is a monoamine, but not a neurotransmitter)

derived from tryptophan:


These monoamines have a similar process of neurotransmission as does ACh, with inhibition of the message occurring by three means:

1) reuptake of monamines into presynaptic neuron endings


blocks general reuptake of monoamine neurotransmitters, hence the stimulatory CNS effects

2) enzymatic degradation of monoamines in presynaptic (and postsynaptic) neuron endings with monoamine oxidase (MAO)

MAO inhibitors

prevent this degradation and so increase transmission at the synapses with antidepressive effects (but watch out for eating bioactive tyramine in e.g, cheese, red wine when on MAOI)

3) enzymatic degradation of catecholamines in the postsynaptic neuron by catechol-O-methyltransferase (COMT)


Dopamine is used as a neurotransmitter in dopaminergic neurons. These neurons are concentrated in the substantia nigra of the midbrain, sending fibers to the basal nuclei.


precursor of dopamine that can cross the blood-brain barrier, used in the treatment of Parkinson's disease

The therapeutic mechanism of antipsychotic drugs is hazy, with the major action apparently being blockade of dopamine receptors. Dopamine blockade in the mesolimbic system is beneficial for schizophrenia, but blockade at other regions is not, e.g., blockade of the dopamine receptors in the pituitary lead to interference with PIH function, so high prolactin levels. More seriously, dopamine receptor blockage in the basal nuclei can lead to extrapyramidal effects of parkinsonism, akathisia (restlessness), and tardive dyskinesia (stereotyped involuntary movements).2


Serotonin is found in serotonergic neurons innervating many parts of the CNS, with their cell bodies found in the brain stem. These have major influences on mood and sleep, e.g., on the reticular activating system (RAS) that runs through the midbrain, pons, and medulla oblongata.


fluoxetine specifically blocks the reuptake of serotonin into presynaptic axons, thus promoting serotonin action. The selective serotonin reuptake inhibitors (SSRIs) are now the most broadly prescribed antidepressants.


Norepinephrine is also a neurotransmitter: noradrenergic neurons are located in the medulla and pons, and play major roles in setting mood and affect, e.g., depression, panic attacks.2


stimulate pathways that use norepinephrine as a neurotransmitter, primarily by causing release of norepinephrine from storage sites.


The glutamic acid derivative GABA (gamma-aminobutyric acid) is also important. GABA is the most prevalent neurotransmitter in the brain. It is inhibitory and involved in motor control, e.g., large Purkinje cells of cerebellum.1


increase effectiveness of GABA in brain and spinal cord, thus the muscle relaxatory effects of Valium (diazepam).


Other neurotransmitter substance include a variety of polypeptides: substance P is involved in the brain pathway of pain sensation. Beta-endorphins as polypeptides in brain and pituitary, blocking transmission of pain. Beta-endorphin levels are increased during exercise.


by interacting with opioid receptors, morphine and the like cause analgesia, respiratory depression, GI muscle spasm, and miosis

Pain: as a sensation, picked up by free-nerve endings, with sharp pain transmitted by myelinated fibers and duller pain by slower, unmyelinated fibers.


For continuous sensory feedback to allow control:

1) tension on tendons from Golgi tendon organs

2) muscle length from muscle spindle apparatus

A hand muscle with a fine level of control will have many muscle spindle apparati, which contain several thin intrafusal fibers, in contrast to the extrafusal (typical contractile) fibers outside.

proprioception: ability to sense position of limbs and their movements with eyes closed; propioceptors in joints and muscles

Two types of LMNs in spinal cord:

1) alpha motoneurons innervate the extrafusal muscle fibers.

2) gamma motoneurons innervate the intrafusal fibers, so that appropriate levels of gamma motoneuron activity is appropriate for muscle tone.

UMNs will coactivate the two types of motoneurons for coordinated muscle contraction..


Sensory receptors transduce sensations into nerve impulses. One may/may not see sensory adaptation (yes for odor, no for pain).

In the sensory endings, receptor or generator potentials are so named because they serve to generate action potentials in response to the sensory environment. After a threshold depolarization is produced, increases in the amplitude of the generator potential result in increases in the frequency with which action potentials are produced. This is a frequency code, since we are dealing with an action potential (all or none situation) again.

Generally speaking, sensory information from receptors throughout most of the body is relayed to the brain via ascending tracts of fibers that conduct impulses up the spinal cord.

In summary, somatesthetic senses, or sensations from cutaneous receptors and proprioceptors, will eventually map to the postcentral gyrus of the parietal lobe via the thalamus. Generally speaking, these neurons sense via receptive fields, which are large if there are few receptors, small if many, e.g., as shown by light touch testing two-point discrimination.


The sense of equilibrium comes from the inner ear, with the vestibular apparatus consisting of the utricle and saccule (otolith-containing structures), and the semicircular canals. Also in the inner ear is found the cochlea, which is involved in hearing. The utricle and saccule provide information about linear acceleration. Rotational (angular) acceleration is provided by the semicircular canals.

The equilibrium receptors are hair cells with stereocilia and one larger true cilium or kinocilium. When the stereocilia are bent in the direction of the kinocilium, the cell membrane is depressed and depolarized, so off goes a synaptic transmitter stimulating the dendrites of sensory neurons part of CN VIII. Conversely, bend away from the kinocilium, the membrane hyperpolarizes and less transmitter.

The utricle and saccule contain maculae. These have sensory hairs embedded in an otolith membrane in the endolymph (similar in composition to intracellular fluid) of the membranous labyrinth. Statoconia (otoliths) are CaCO3 crystals that increase the inertia of the membrane. With their orientations, the utricle is more sensitive to horizontal acceleration and the saccule more sensitive to vertical acceleration. The changes with sudden movement change the patterns of action potentials.

The semicircular canals, in X-Y-Z planes, have an ampulla where sensory hair cells found. The processes of these sensory cells are embedded in the cupula of the crista ampullaris, in the endolymph of the membranous canals. CN VIII to cerebellum to vestibular nuclei of medulla oblongata, which send signals to oculomotor center of brain and spinal cord, so eyes and body track accordingly.

Sound waves are measured by the frequency of waves, Hertz (Hz), and the amplitude of the waves, decibels (dB). Sound waves are funneled by the pinna (auricle) to the external auditory meatus. The meatus channels and intensifies the sound waves to the tympanic membrane (eardrum).

middle ear: between tympanic membrane and cochlea. Middle ear ossicles of malleus (hammer), incus (anvil), stapes (stirrup). The stapes is attached to the oval window in the cochlea, which will vibrate. The scala media (cochlear duct) is part of the membranous labyrinth. The cochlear duct spirals to form 3 levels, apical, middle, and basal. The cochlear duct contains endolymph, while the scala vestibuli above it and the scala tympani below it contain CSF-like perilymph.

How does this all work? Vibrations at the oval window are transmitted by stapes movement. Pressure waves built up in the scala vestibuli, which transmit them to the scala tympani. Movement of perilymph in the scala tympani then travel to the cochlear base and cause displacement of the round window into the middle ear cavity. As the sound frequency increases, the perilymph pressure waves can build up and be transmitted through the vestibular membrane and then to the basilar membrane.

Movement of the basilar membrane is important for pitch discrimination. Higher pitch causes vibrations of the region of the basilar membrane closer to the stapes (and lower pitch therefore further away from the oval window). Sensory hair cells are on the basilar membrane, with the stereocilia projecting into the endolymph of the cochlear duct. Outer cell stereocilia are embedded in a tectorial membrane, which overhangs the hair cells in the cochlear duct. Organ of Corti: the basilar membrane, hair cells, tectorial membrane. As the cochlear duct is displaced by perilymph pressure waves, the created shearing forces cause stereocilia to move and bend, opening up ion channels, leading to depolarization, etc. More bending occurs from louder sounds.


The eye takes visible light and turns that into nerve impulses. Light is refracted at the cornea and lens, so that the image formed on the retina is upside down, right to left, hence making the visual field reversed.


loss of accomodation ability with age


nearsightedness, with an eyeball too long. Correct by concave lens which cause light rays to diverge and hence, with a longer focal length.


farsightedness, with an eyeball too short. Convex lens increase light convergence and so shorten the focal length.


assymetry of cornea and/or lens. Uneven cylindrical lens needed to correct.

In the retina there are two types of photoreceptors.


black and white vision under conditions of low light intensities


sharp color vision with greater light intensities

Both contain pigment molecules that undergo dissociation in response to light. Neural layers of retina are a forward extension of the brain, and so the light must pass through several layers before reaching the photoreceptors. Outer layers of neurons that contribute axons to the optic nerve: ganglion cells. Bipolar cells connect them to the photoreceptors.

Rods contain the purple pigment rhodopsin. The bleaching reaction occurs when light hits, rhodopsin dissociates into retinene [all-trans retinal] (derived from vitamin A) and opsin. The dissociation causes changes in ionic permeability of the cell and so allows the creation of nerve impulses.2

In cones, the trichromatic theory of color vision suggests that our color perception dpends on stimulation of only 3 cone types. These contain retinene and 3 different proteins (not opsin) for blue, green, and red -sensing cones, so that color blindess is a loss of one of these cone types. The fovea centralis is within the macula lutea, and there is the greatest concentration of photoreceptors.2

TASTE AND SMELL are chemical sensations localized (in humans) to the tongue and nostrils. Taste buds are modified epithelial cells that sense four primary stimuli:

salty (through Na+ or similar cations)

sour (through H+ ions)

bitter and sweet (through receptors associated with G-proteins)

Olfaction involves actively dividing receptor neurons, with receptors linked with G-proteins.

Anosmia can follow head injuries that damage the olfactory nerves or infections that damage the cells, and will contribute to ageusia because of the contribution of smell to taste.


Smell triggers deep-seated emotions because of its association with the limbic system that controls basic emotional drives. The Papez circuit runs among different components of the system. The hippocampus is associated with establishing memories, the amygdala with fear, and the hypothalamus with the"Fs" of fever, feeding, fighting, and fornication (etc.) . Forgetfulness in Alzheimer's is associated with a loss of neurons in the hippocampal formation.4


  1. SI Fox, Human Physiology, 6th ed. (WCB McGraw-Hill, Boston, 1999), pp. 169, 177, 420.
  2. AC Guyton, JE Hall, Textbook of Medical Physiology, 9th ed. (WB Saunders, Philadelphia, 1996), pp. 640, 644, 767, 768.
  3. JL Stringer, Basic Concepts in Pharmacology: a Student's Survival Guide (McGraw-Hill, 1996), pp. 62, 151.
  4. PA Young, PH Young, Basic Clinical Neuroanatomy (Williams & Wilkins, Baltimore, 1997), p. 204.

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Please send comments and questions to: cronewil@hvcc.edu


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This web page updated on April 25, 2000