Arashiramar Mihaela rated it it was amazing Mar 12, This item may be a floor model or store return that has been used. Lists with This Book. Internal Organs and Volume 3: Now in its sixth edition, this classic work makes the task of mastering this vast body of information easier and less daunting with its many user-friendly features: A locomltor understanding of the structure and Praise for this book: Home Contact Us Help Free delivery worldwide. Refresh and try again. Account Options Sign in. A sound understanding of the structure and shstem of the human body in all of its intricacies is the foundation of a complete medical education.
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Usage subject to terms and conditions of license. Nevertheless, they are classified according to their functionally most important neurotransmitter as glutamatergic, cholinergic, catecholaminergic noradrenergic and dopaminergic , serotoninergic, and peptidergic neurons.
The catecholaminergic and serotoninergic neurons can be identified by fluorescence microscopy because their transmitters show a green-yellow fluorescence following exposure to formalin vapor A, B. It is thus possible to trace the axon and to recognize the perikaryon and the outline of its nonfluorescent nucleus.
The fluorescence is very faint in the axon, more distinct in the perikaryon, and most intense in the axon terminals. It is here that the highest concentration of transmitters occurs.
Cholinergic neurons can be demonstrated by a histochemical assay for acetylcholinesterase, the enzyme required for the degradation of acetylcholine. Since this enzyme is also produced by noncholinergic neurons, the proper assay is by immunocytochemistry using antibodies against choline acetyltransferase, the acetylcholine-synthesizing enzyme.
Other transmitters and neuropeptides can also be demonstrated by immunocytochemistry C. It has been shown by double-labeling that many neuropeptides are produced together with classical neurotransmitters within the same neuron. So far, the functional significance of cotransmission, i. The retrograde transport in the direction of the cell body and toward the minus end of the microtubules is mediated by dynein D2 , while the anterograde transport in the direction of the axon terminal and toward the plus end of the microtubules is mediated by kinesin D3.
The transporting vesicles are endowed with several motor proteins, the ATP-binding heads of which interact with the surface of the microtubule in an alternating and reversible fashion. This results in ATP being hydrolyzed, and the released energy is converted into molecular movement that causes the vesicles to roll along the microtubules in the target direction. The velocity of the rapid intra-axonal transport has been calculated at — mm per day. Proteins, viruses, and toxins reach the perikaryon by retrograde transport from the axon terminals.
In addition to the rapid intra-axonal transport, there is also a continuous flow of axoplasm which is much slower, namely, 1 — 5 mm per day. It can be demonstrated by ligating a single axon E ; proximal to the constricted site, the axoplasm is held back and the axon shows swelling.
The anterograde and retrograde transport mechanisms are used in neuroanatomy to study connecting tracts see p. Axonal Transport D, E The transmitter substances or their synthesizing enzymes are produced in the perikaryon and must be transported to the axon terminal.
The microtubules of the neuron, neurotubules D1 , play a key role in this transport mechanism. If they are destroyed by applying the mitotic poison colchicine, the intra-axonal transport stops. Most neurotransmitters do not bind to ligand-gated channels but to receptors coupled to G protein.
The main difference between the two types of receptors is in the speed of the synaptic response. In the case of ligand-gated ion channels, the activation causes a rapid synaptic potential lasting only for milliseconds. Activation of G protein-coupled receptors results in responses that last seconds or minutes. G proteins regulate enzymes that produce intracellular messenger substances. These have an effect on ion channels or, via regulatory proteins, on the expression of genes.
Basic Elements Ligand-gated Ion Channels Ligand-gated ion channels consist of different subunits A1 that are inserted into the cell membrane A2.
Binding of the neurotransmitter to the specific receptor causes the channel to become permeable to certain ions B. Excitatory amino acid receptors. Receptors for the excitatory transmitter glutamate are classified according to the synthetic ligands binding to them. Binding to the AMPA receptor causes an influx of sodium ions, thus leading to depolarization of the cell. Under conditions of resting potential, the NMDA receptor is blocked by magnesium; the magnesium blockade is lifted by depolarization through AMPA receptors.
This temporal shift in activities of the AMPA and NMDA receptors results in a graduated response of the postsynaptic neurons to the neurotransmitter glutamate. Inhibitory GABA and glycine receptors. GABA is the most common inhibitory transmitter in the brain, and glycine in the spinal cord. Both receptors are ligand-gated ion channels that cause the influx of chloride ions when activated.
The cell thus becomes hyperpolarized and inhibited. Ligand-gated ion channels include the excitatory, cation-permeable nicotinic acetylcholine receptor and the serotonin 5-HT receptor.
Synaptic Transmission C The synaptic transmission is essentially characterized by three processes: 1 Conversion of the action potential arriving at the axon terminal into a chemical signal. Depolarization results in the opening of calcium channels C5 and in the influx of calcium, which, mediated by certain proteins, causes fusion of synaptic vesicles C6 with the presynaptic membrane and release of the transmitter into the cleft C7. The activation of G protein-coupled receptors results in a long-lasting response that may finally lead to a change in gene expression in the postsynaptic neuron.
COLOR ATLAS OF HUMAN ANATOMY WERNER PLATZER PDF
Color Atlas of Human Anatomy