Synapse diagram

Figure 20.1 Schematic diagram illustrating how antidepressants increase the concentration of extraneuronal neurotransmitter (noradrenaline and/or 5-HT). In the absence of drug (b), monoamine oxidase on the outer membrane of mitochondria metabolises cytoplasmic neurotransmitter and limits its concentration. Also, transmitter released by exocytosis is sequestered from the extracellular space by the membrane-bound transporters which limit the concentration of extraneuronal transmitter. In the presence of a MAO inhibitor (a), the concentration of cytoplasmic transmitter increases, causing a secondary increase in the vesicular pool of transmitter (illustrated by the increase in the size of the vesicle core). As a consequence, exocytotic release of transmitter is increased. Blocking the inhibitory presynaptic autoreceptors would also increase transmitter release, as shown by the absence of this receptor in the figure. In the presence of a neuronal reuptake inhibitor (c), the membrane-bound transporter is inactivated and the clearance of transmitter from the synapse is diminished...

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.

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.

Figure 30-15 (A) Diagram of the two-dimensional tree formed by dendrites of a single Purkinje cell of the cerebellum. From Llinas.404 (B) Schematic diagram showing input and output pathways for Purkinje cells. (C) Recordings of output from four different neurons of the inferior olive. These action potentials are thought to arise from oscillations that arise within the neurons or within arrays of adjacent neurons coupled by electrical (gap junction) synapses. These oscillations synchronize the generation of action potentials so that some cells oscillate in synchrony while others (e.g., cell 4 above) do not. From McCormick.412...

Classically, the central nervous system has been envisioned as a series of hard-wired synaptic connections between neurons, not unlike millions of telephone wires within thousands upon thousands of cables (Fig. 1—4). This idea has been referred to as the anatomically addressed nervous system. The anatomically addressed brain is thus a complex wiring diagram, ferrying electrical impulses to wherever the wire is plugged in (i.e., at a synapse). There are an estimated 100 billion neurons, which make over 100 trillion synapses, in a single human brain. 

Pathways in the central nervous system. A shows two relay neurons and two types of inhibitory pathways, recurrent and feed-forward. The inhibitory neurons are shown in black. B shows the pathway responsible for presynaptic inhibition in which the axon of an inhibitory neuron synapses on the axon terminal of an excitatory fiber. C Diagram illustrating that dendrites may be both pre-and postsynaptic to each other, forming reciprocal synapses, two of which are shown between the same dendrite pair. In triads, an axon synapses on two dendrites, and one of these dendrites synapses on the second. In serial synapses, a dendrite may be postsynaptic to one dendrite and presynaptic to another, thus connecting a series of dendrites. Dendrites also interact through low-resistance electrotonic ("gap") junctions (two of which are shown). Except for one axon, all... 

Figure 3.3 Ritalin works by affecting the communication between neurons and the neurotransmitters serotonin, dopamine, and norepinephrine. Ritalin and other stimulants increase the number of neurotransmitters released into the synapses (the spaces between individual neurons) and help keep the neurotransmitters in the synapse longer than they would remain without the drugs. This diagram demonstrates the flow of neurotransmitters between neurons, across a synapse.

Figure 11.3 Diagram of autonomic and somatic motor neurons. Presynaptic neurons are depicted with solid cell bodies. Postsynaptic neurons are speckled. The neurotransmitter released by the presynaptic neuron and the type of receptor it activates are listed below each synapse.

Figure 7.2 Diagram of a nerve cell and a cholinergic synapse. (From Corbett, J.R., Wright, K., and Baillie, A.C., Eds., The Biochemical Mode of Action of Pesticides, 2nd ed., Academic Press, New York, 1984. With permission.)...

Figure 10.11. Examples of receptor mediated synaptic plasticity, (a) Long-term potentiation. (LTP). Synaptic Uansmission at hippocampal synapses (in tliis example tire CA3/CA1 synapse) is potentiated following application of a tetanus (period of rapid stimulation) to tlie pre-synaptic nerve. Tliis phenomenon is dependent on tlie activation of synaptic AMPA and NMDA receptors (see main text), (b) Depolaiization suppression of inliibition (DSI). Diagram sliows how endocannabinoids produce DSI in die liippocampus. Synaptic potentials recorded as hippocampal neurons ai e depressed following a tetanus.

Diagram of a synapse showing an enlarged axon terminal with vesicles containing neurotransmitter molecules... 

Figure 1.1. Diagram of synapse between an adrenergic neuron and its effector cell. NE, norepinephrine aR, a-adrenoceptor )3R, /3-adrenoceptor.

Fig. U. Diagram of the interaction of Purkinje cell dendrite with a climbing fiber and several parallel fibers. A proximal Purkinje cell dendrite (pd) shows stubby thorns contacted by a climbing fiber (cf), whereas parallel fibers (pO synapse on spines protruding from a spiny branchlet (sb). Rossi et al. (1991).

Figure 1.4 This is a diagram of the neuronal synapse. Neurotransmitters (black dots) are released into the synaptic cleft and bind to receptors on the adjacent neuron. The neurotransmitters are then recycled back into the neuron from where they were originally released. Antidepressants often work by preventing this recycling (by blocking reuptake transporters).

Figure 2.2 Diagram of a noradrenergic (NA) synapse. After an NA neurotransmitter is recycled back into a neuron, the MAO enzyme breaks it down. MAOIs block the MAO enzyme, causing a buildup of NA neurotransmitters inside the neuron, so that more are released into the synapse. Tricyclics block the recycling of NA neurotransmitters back into the neuron.

Figure 4.4 Remeron blocks alpha-2 receptors on neurons that make serotonin and norepinephrine (noradrenaline). Alpha-2 autoreceptors are found on neurons that make norepinephrine. When norepinephrine is released in the synapse, some of it binds to autoreceptors, which tells the neuron to stop releasing neurotransmitters. Alpha-2 heteroreceptors are receptors found on neurons that do not make norepinephrine. Heteroreceptors also provide negative feedback to the neuron releasing a neurotransmitter (serotonin in this diagram).

Figure 4.5 Diagram of a norepinephrine neuronal synapse. Norepinephrine (NE) is made from another neurotransmitter, dopamine. Wellbutrin acts on norepinephrine by blocking the norepinephrine transporter (NET). This results in the accumulation of norepinephrine within the synaptic cleft, which causes repeated activation of norepinephrine receptors. Normally norepinephrine is taken into the neuron and broken down by either MAO or COMT enzymes. Wellbutrin also blocks uptake of dopamine and serotonin.

Figure 6.3 A simplified diagram of some of the events that happen in an axon and at the synapse when an impulse is passing. At one location (P) of the axon the following events occur when an impulse passes ...

A FIGURE 13-22 Human rod cell, (a) Schematic diagram of an entire rod cell. At the synaptic body, the rod cell forms a synapse with one or more bipolar Interneurons. Rhodopsin, a light-sensitive G protein-coupled receptor, Is located In the flattened membrane disks of the outer segment, (b) Electron micrograph of the region... 

Within the nervous system neurons make connections with each other called synapses. At the synapse, the neurons do not touch each other but are separated by a microscopic gap, the synaptic cleft. When a nerve impulse arrives at a synapse, chemical substances are released. These are neurotransmitters, which are stored in pre-synaptic vesicles. On release they cross the synaptic cleft and bind to receptors on the post-synaptic neuron. Binding of neurotransmitter with its receptor is very brief, but it brings about stimulation or inhibition of the post-synaptic neuron. See Figure 11.2 for a diagram of synaptic transmission. 

Schematic diagram of the synapse at the neuromuscular junction. The nerve impulse causes acetylcholine (ACh) to be released from synaptic vesicles. Acetylcholine diffuses across the synaptic cleft and binds to a specific receptor protein (R) on the postsynaptic membrane. A channel opens that allows Na ions to flow into the cell and ions to flow out of the cell. This results in muscle contraction. Any ACh remaining in the synaptic cleft is destroyed by acetylcholinesterase (AChE) to terminate the stimulation of the muscle cell.

Fig. 5.5. A schematic diagram of the olfactory bulb neuronal model architecture which we have implemented in programmable logic (Guerrero and Pearce 2007) and aVLSI (Koickal et al. 2007) for real-time odour signal processing, showing receptor and principal neurons (triangles) and synapses (circles unfilled - excitatory, filled - inhibitory). There are 25 M/T cells in total and 75 ORNs. M/T mitral/tufted cells, ORN olfactory receptor neurons. LOT lateral olfactory tract.

Figure 5. Schematic diagram of synaptic multiprotem complexes. Post-synaptic complexes of proteins associated with the NMDA receptor and PSD-95, found at excitatory mammalian synapses, are shown. Individual proteins are illustrated with arbitrary shapes and known interactions indicated. Proteins shown in colour are those found in a proteomic screen, whereas those shown in grey are inferred from bioinformatic studies. The specific protein-protein interactions are predicted, based on published reports from yeast two-hybrid studies. Membrane proteins (such as receptors, channels and adhesion molecules) are attached to a network of intracellular scaffold, signaling and cytoskeletal proteins, as indicated.

A neuron, or nerve cell, is an example of an excitable cell. These cells have cell bodies (or soma) containing the nucleus and elongated processes called axons and dendrites. These cells form a complex web with many connections. Figure 11 shows a schematic diagram of a connection between two such nerve cells. The presynaptic neuron is separated from the postsynaptic neuron by a small gap known as the synapse, typically 2-800 A wide. Presynaptic nerve endings contain small sacs or vesicles filled with one of several compounds called neurotransmitters. The postsynaptic neuron has receptor sites for specific neurotransmitters located on the cell membrane. When appropriately stimulated, and area of a presynaptic neuron membrane becomes depolarized (the transmembrane potential becomes more positive). The depolarized area propagates down the axon very rapidly. This wave-like movement of depolarization is called the action potential. When the depolarized areas reaches the nerve ending, the vesicles move to the cell wall, fuse with it, and dump their contents into the synaptic cleft—a process called exocytosis. (Exocytosis is accepted as the mechanism of neurotransmitter release in the peripheral nervous system, but it has not yet been demonstrated... 

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