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Nerve diagram

When X is a topological space, we shall say that a family of sets Xj jg/ is a covering of X if [Pg.266]

We say that a covering has some specific property (such as open or locally finite) if every set in the covering has this property. Another covering Yj j j [Pg.266]

We shall see later that under further conditions on the covering spaces X and their intersections, there exists a close relationship between the topology of the space X and the topology of the nerve complex Af U). [Pg.267]

The importance of the nerve diagram will come to the fore in the rest of this section. [Pg.267]


Proof of nerve lemma. Let T> be the nerve diagram of tl, and let D be the trivial diagram over BdA/"(W), i.e., all associated spaces are points. Consider the unique diagram map X -.V V. Since all maps X cr) for a Af(U) are homotopy equivalences, we can conclude by the homotopy lemma that also the map hocolimX hocolimP — hocolimH is a homotopy equivalence. [Pg.269]

Proof of the gluing lemma. lfXnB = CnB = 0, then the statement is trivial, so assume that these are nonempty. Let T>i be the nerve diagram... [Pg.271]

Figure 49-8. Diagram of the relationships among the sarcolemma (plasma membrane), a T tubule, and two cisternae of the sarcoplasmic reticulum of skeletal muscle (not to scale). The T tubule extends inward from the sarcolemma. A wave of depolarization, initiated by a nerve impulse, is transmitted from the sarcolemma down the T tubule. It is then conveyed to the Ca release channel (ryanodine receptor), perhaps by interaction between it and the dihydropyridine receptor (slow Ca voltage channel), which are shown in close proximity. Release of Ca from the Ca release channel into the cytosol initiates contraction. Subsequently, Ca is pumped back into the cisternae of the sarcoplasmic reticulum by the Ca ATPase (Ca pump) and stored there, in part bound to calsequestrin. Figure 49-8. Diagram of the relationships among the sarcolemma (plasma membrane), a T tubule, and two cisternae of the sarcoplasmic reticulum of skeletal muscle (not to scale). The T tubule extends inward from the sarcolemma. A wave of depolarization, initiated by a nerve impulse, is transmitted from the sarcolemma down the T tubule. It is then conveyed to the Ca release channel (ryanodine receptor), perhaps by interaction between it and the dihydropyridine receptor (slow Ca voltage channel), which are shown in close proximity. Release of Ca from the Ca release channel into the cytosol initiates contraction. Subsequently, Ca is pumped back into the cisternae of the sarcoplasmic reticulum by the Ca ATPase (Ca pump) and stored there, in part bound to calsequestrin.
The sensation of colour that we experience arises from the interpretation by the brain of the signals that it receives via the optic nerve from the eye in response to stimulation by light. This section contains a brief description of the components of the eye and an outline of how each of these contributes to the mechanism by which we observe colours. Figure 2.2 shows a cross-section diagram of the eye, indicating some of the more important components. [Pg.15]

The diagram shows the synaptic cleft, which is found at the junction of the nerve terminal and the muscle membrane. [Pg.188]

The diagram below shows the pathway of pain transmission from the peripheral nerves to the cerebral cortex. There are three levels of neuronal involvement and the signals may be modulated at two points during their course to the cerebral cortex. Descending inhibitory pathways arise in the midbrain and pass to the dorsal horn as shown. Multiple different neurotransmitters are involved in the pathway and include gamma-aminobutyric acid (GABA), N-methyl-D-aspartate (NMDA), noradrenaline and opioids. [Pg.199]

Figure 14.1 Schematic diagram of the blood-retinal barrier (BRB). The retinal cell layers seen histologically consist of retinal pigment epithelium (RPE) photoreceptor outer segments (POS) outer limiting membrane (OLM) outer nuclear layer (ONL) outer plexiform layer (OPL) inner nuclear layer (INL) inner plexiform layer (IPL) ganglion cell layer (GCL) nerve fiber layer (NFL) inner limiting membrane (ILM). Figure 14.1 Schematic diagram of the blood-retinal barrier (BRB). The retinal cell layers seen histologically consist of retinal pigment epithelium (RPE) photoreceptor outer segments (POS) outer limiting membrane (OLM) outer nuclear layer (ONL) outer plexiform layer (OPL) inner nuclear layer (INL) inner plexiform layer (IPL) ganglion cell layer (GCL) nerve fiber layer (NFL) inner limiting membrane (ILM).
Figure 9.8 Simple diagram of mitochondrial H -ion movement and axonal K -ion movement to establish membrane potentials across membranes. Note that H movement from the mitochondrial matrix to the outer surface of the inner membrane requires a specific proton pump that requires energy, which is transferred from electron transfer, whereas the K ion movement occurs via an ion channel with energy provided from the concentration difference of K ions on either side of the membrane (approximately 100-fold). The movement of both the protons and K ions generates a membrane potential. The potential across the membrane of the nerve axon provides the basis for nervous activity (see Chapter 14). Figure 9.8 Simple diagram of mitochondrial H -ion movement and axonal K -ion movement to establish membrane potentials across membranes. Note that H movement from the mitochondrial matrix to the outer surface of the inner membrane requires a specific proton pump that requires energy, which is transferred from electron transfer, whereas the K ion movement occurs via an ion channel with energy provided from the concentration difference of K ions on either side of the membrane (approximately 100-fold). The movement of both the protons and K ions generates a membrane potential. The potential across the membrane of the nerve axon provides the basis for nervous activity (see Chapter 14).
Figure 9.30 Flow diagram of the energy chain from food to essential processes in human life. The ATP utilised by the NayK ATPase maintains the ion distribution in nerves that is essential for electrical activity and, in addition, maintains neurotransmitter synthesis, both of which provide communication in the brain and hence consciousness, learning and behaviour (Chapter 14). ATP utilisation by myosin ATPase is essential for movement and physical activity. ATP utilisation by the flagellum of sperm is essential for reproduction and ATP utilisation for synthesis of macromolecules is essential for growth. Figure 9.30 Flow diagram of the energy chain from food to essential processes in human life. The ATP utilised by the NayK ATPase maintains the ion distribution in nerves that is essential for electrical activity and, in addition, maintains neurotransmitter synthesis, both of which provide communication in the brain and hence consciousness, learning and behaviour (Chapter 14). ATP utilisation by myosin ATPase is essential for movement and physical activity. ATP utilisation by the flagellum of sperm is essential for reproduction and ATP utilisation for synthesis of macromolecules is essential for growth.
Figure 13.11 Motor units. The diagram shows two motor units. In reality, the fibres would be much more tightly packed. In large fast nerves (e.g. supplying limb muscles), a single motor unit will innervate many fibres (up to 1000) via a synapse on each fibre. Figure 13.11 Motor units. The diagram shows two motor units. In reality, the fibres would be much more tightly packed. In large fast nerves (e.g. supplying limb muscles), a single motor unit will innervate many fibres (up to 1000) via a synapse on each fibre.
Figure 14.1 A diagram, based on an electron micrograph, of a cross section of a nerve bundle. It shows three axons enclosed in myelin sheaths. The sheaths completely surround the axoplasm. Between the myelinated axons are clusters of nonmyelinated axons. Except for smaller diameter and absence of myelination they are structurally similar to myelinated axons. (Drawn from an electron micrograph of Telford Bridgman, 1995.)... Figure 14.1 A diagram, based on an electron micrograph, of a cross section of a nerve bundle. It shows three axons enclosed in myelin sheaths. The sheaths completely surround the axoplasm. Between the myelinated axons are clusters of nonmyelinated axons. Except for smaller diameter and absence of myelination they are structurally similar to myelinated axons. (Drawn from an electron micrograph of Telford Bridgman, 1995.)...
Figure 2.2 Diagram of a voltage-activated sodium channel protein. The channel is composed of a long chain of amino acids intercormected by peptide bonds. The amino acids perform specific functions within the ion channel. The cylinders represent amino acid assemblies located within the membrane of the nerve cell and responsible for the foundation of the ion pore. Figure 2.2 Diagram of a voltage-activated sodium channel protein. The channel is composed of a long chain of amino acids intercormected by peptide bonds. The amino acids perform specific functions within the ion channel. The cylinders represent amino acid assemblies located within the membrane of the nerve cell and responsible for the foundation of the ion pore.
In simple terms, messages travel along neurons (nerve cells) in the form of an electrical current that moves from one end of the neuron to its opposite end. The electric current is produced by a flow of sodium ions (Na ") and potassium ions (K ) across the nerve membrane, as shown in the diagram on page 11. When the electrical current reaches the end of the neuron, it causes the release of a chemical known as a neurotransmitter. Some examples of neurotransmitters are acetylcholine, serotonin, dopamine, GABA (gamma-aminobutyric acid), and norepinephrine. [Pg.10]

The key to nerve transmission—like most of the biochemical reactions that occur in living organisms—is the concept of a reeeptor molecule, a molecule to which some other molecule hinds. In the example just described, a receptor molecule is a specihc chemical compound with a distinctive shape into which the neurotransmitter molecule can fit. The diagram on page 12 shows how a specihc neurotransmitter has the correct shape to ht into a receptor molecule. [Pg.10]

Examine the head, upper and lower jaws and lips, snout, naris, diagrams and relevant descriptions correspond. Nasolabial sul-cus/cleft, nasal cavity and septum, oral cavity, palate, palatine ridges, incisors, cranium, pinna, eyelid, eye/lens, retina, cornea, vitreous and aqueous chambers, nasopharynx, olfactory lobe, cerebral hemispheres, lateral ventricles, cranial nerves, third ventricle, pituitary, pineal gland, thalamus, perimeningeal space, and internal ear. [Pg.236]

Schematic diagram comparing some anatomic and neurotransmitter features of autonomic and somatic motor nerves. Only the primary transmitter substances are shown. Parasympathetic ganglia are not shown because most are in or near the wall of the organ innervated. Cholinergic nerves are shown in blue noradrenergic in red and dopaminergic in green. Note that some sympathetic postganglionic fibers release acetylcholine or dopamine rather than norepinephrine. The adrenal medulla, a modified sympathetic ganglion, receives sympathetic preganglionic fibers and releases epinephrine and norepinephrine into the blood. ACh, acetylcholine D, dopamine Epi, epinephrine M, muscarinic receptors N, nicotinic receptors NE, norepinephrine. Schematic diagram comparing some anatomic and neurotransmitter features of autonomic and somatic motor nerves. Only the primary transmitter substances are shown. Parasympathetic ganglia are not shown because most are in or near the wall of the organ innervated. Cholinergic nerves are shown in blue noradrenergic in red and dopaminergic in green. Note that some sympathetic postganglionic fibers release acetylcholine or dopamine rather than norepinephrine. The adrenal medulla, a modified sympathetic ganglion, receives sympathetic preganglionic fibers and releases epinephrine and norepinephrine into the blood. ACh, acetylcholine D, dopamine Epi, epinephrine M, muscarinic receptors N, nicotinic receptors NE, norepinephrine.
Schematic diagram of a primary afferent neuron mediating pain, its synapse with a secondary afferent in the spinal cord, and the targets for local pain control. The primary afferent neuron cell body is not shown. At least three nociceptors are recognized acid, injury, and heat receptors. The nerve ending also bears opioid receptors, which can inhibit action potential generation. The axon bears sodium channels and potassium channels (not shown), which are essential for action potential propagation. Synaptic transmission involves release of substance P, a neuropeptide (NP) and glutamate and activation of their receptors on the secondary neuron. Alpha2 adrenoceptors and opioid receptors modulate the transmission process. Schematic diagram of a primary afferent neuron mediating pain, its synapse with a secondary afferent in the spinal cord, and the targets for local pain control. The primary afferent neuron cell body is not shown. At least three nociceptors are recognized acid, injury, and heat receptors. The nerve ending also bears opioid receptors, which can inhibit action potential generation. The axon bears sodium channels and potassium channels (not shown), which are essential for action potential propagation. Synaptic transmission involves release of substance P, a neuropeptide (NP) and glutamate and activation of their receptors on the secondary neuron. Alpha2 adrenoceptors and opioid receptors modulate the transmission process.
Schematic diagram of the typical sites of injection of local anesthetics in and around the spinal canal. When local anesthetics are injected extradurally, it is known as epidural (or caudal) blockade. Injections around peripheral nerves are known as perineural blocks (eg, paravertebral block). Finally, injection into the subarachnoid space (ie, cerebrospinal fluid), is known as spinal blockade. Schematic diagram of the typical sites of injection of local anesthetics in and around the spinal canal. When local anesthetics are injected extradurally, it is known as epidural (or caudal) blockade. Injections around peripheral nerves are known as perineural blocks (eg, paravertebral block). Finally, injection into the subarachnoid space (ie, cerebrospinal fluid), is known as spinal blockade.
Schematic diagram of a typical motor neuron (a nerve cell conducting impulses to muscle cells). Schematic diagram of a typical motor neuron (a nerve cell conducting impulses to muscle cells).
FIGURE 12-3 Schematic diagram showing mechanism of action of local anesthetics on the nerve membrane. Local anesthetics appear to bind directly to a site within the sodium channel, thereby locking the channel in a closed position, thus preventing sodium entry and action potential propagation. [Pg.155]

Schematic diagram showing some of the potential sites of action of antidepressant drugs. Chronic therapy with these drugs has been proved to reduce reuptake of norepinephrine or serotonin (or both), reduce the number of postsynaptic Preceptors, and reduce the generation of cAMP. The MAO inhibitors act on MAO in the nerve terminals and cause the same effects on Preceptors and cAMP generation. Schematic diagram showing some of the potential sites of action of antidepressant drugs. Chronic therapy with these drugs has been proved to reduce reuptake of norepinephrine or serotonin (or both), reduce the number of postsynaptic Preceptors, and reduce the generation of cAMP. The MAO inhibitors act on MAO in the nerve terminals and cause the same effects on Preceptors and cAMP generation.
Figure 3.2 This diagram of a neuron shows the complex structure that allows signals to travel back and forth between the brain and the nerves of the body. The human brain is made up of billions of these neurons. Scientists who believe ADHD may have a biological cause are researching possible links between connections between neurons and the behavioral problems that are associated with the condition. Figure 3.2 This diagram of a neuron shows the complex structure that allows signals to travel back and forth between the brain and the nerves of the body. The human brain is made up of billions of these neurons. Scientists who believe ADHD may have a biological cause are researching possible links between connections between neurons and the behavioral problems that are associated with the condition.

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