Terminal bouton

Figure 4.2 The neuron consists of several parts dendrite, soma (body), axon, and terminal bouton (or synaptic bouton). A gap, or synapse, separates one neuron from another. A chemical messenger, or neurotransmitter, must passively diffuse across the synapse in order to transmit information from one neuron to the next. Information travels from the soma, along the axon, and to the terminal bouton, stimulating the Ca -mediated release of a neurotransmitter.

Typically, the presynaptic ending is further distinguished from the postsynaptic component by the conspicuous presence of neurotransmitter-filled vesicles. In response to presynaptic membrane depolarization, the vesicles exocytose their contents into the cleft through complicated membrane-trafficking events. The presynaptic axon terminal (bouton) of the presynaptic component also contains other organelles such as mitochondria, smooth endoplasmic reticulum, microtubules, and neurofilaments. The presynaptic membrane is variably populated by docking/fusion apparatus, ion channels, and other protein constituents. The 20-30 nM wide synaptic cleft separates the pre- and postsynaptic membranes and generally contains a dense plaque of intercellular material that includes microfilaments. 

The function of the nervous system depends on communication between nerve cells (neurons). Structurally, all neurons are composed of a cell body, dendrites, axon, and terminal boutons (see figure 3-C). Dendrites are short, terminally branched structures projecting out from the cell body. They receive and conduct information to the cell body there may be one or several dendrites on each cell. Extremely fine projections on the dendrites are called dendritic spines. The axon is a single long fiber that ends in enlarged structures called terminal boutons. The axon serves to conduct impulses away from the cell body. 

Fig. 79. Photomicrograph of camera lucida drawing (inset) of anterogradely labelled axons and terminal boutons in the crus I ansiform lobule of rat cerebellum after cholera toxin (b fragment) injection into the contralateral ventral tegmental area. Arrows point to rosettes characteristic of mossy fiber endings in the granular layer (G). P, Purkinje cell layer WM, white matter. Scale bar = 40 ixm. Ikai et al. (1992).

Cyclic GMP and cyclic AMP were localised at the ultrastructural level using horseradish peroxidase immunocytochemistry (Ariano and Matus 1981). In the rat caudate-putamen both of the cyclic nucleotides were detected within postsynaptic terminal boutons and within astroglial processes. cGMP postsynaptic staining was stronger than glial staining, whereas the localisation pattern was reversed for cAMP. 

Histochemical fluorescent techniques have revealed the existence in most mammalian species of a nigro-striatal neuron system, containing dopamine, with cell bodies in the substantia nigra and axon terminations in the striatum [99-104]. These structures are confirmed by electron microscopic studies of the terminal boutons in the striatum which contain dense dopamine vesicles [105]. Striatal dopamine levels were reduced after experimental brain stem lesions which resulted in nigral degeneration [106-108], while removal of the caudate and putamen produced similar decreases together with nigral... 

BoTx acts at the nerve terminal of cholinergic synapses and blocks the release of ACh (see Chap. 6), after being taken up into the vesicles and translocated to the cytoplasm where the toxin catalyses proteolysis of components involved in the calcium-mediated exocytosis of ACh. The inhibition is permanent, and recovery occurs only after the creation of new terminal boutons. The toxin thus blocks neurotransmission, parasympathetic synapses and peripheral ganglia. Conventionally... 

The superfusion of isolated nerve terminals ( synaptosomes ) is a widely used technique for interrogating the pharmacological properties of presynaptic receptors and their biochemical mechanisms. Physiological buffer continuously flows over a layer of synaptosomes loaded with radiolabelled transmitter, such that released transmitter is removed in the perfusate and collected. A key feature of this methodology is that it eliminates transmitter crosstalk between different boutons, enabling presynaptic events to be studied in isolation (Raiteri and Raiteri 2000). 

The anatomy of autonomic synapses and junctions determines the localization of transmitter effects around nerve endings. Classic synapses such as the mammalian neuromuscular junction and most neuron-neuron synapses are relatively "tight" in that the nerve terminates in small boutons very close to the tissue innervated, so that the diffusion path from nerve terminal to postsynaptic receptors is very short. The effects are thus relatively rapid and localized. In contrast, junctions between autonomic neuron terminals and effector cells (smooth muscle, cardiac muscle, glands) differ from classic synapses in that transmitter is released from a chain of varicosities in the postganglionic nerve fiber in the region of the smooth muscle cells rather than boutons, and autonomic junctional clefts are wider than somatic synaptic clefts. Effects are thus slower in onset and often involve many effector cells. 

It is noteworthy that some attempts have been made to visualize synaptic vesicles at an ultrastructural level in the brains of individuals with schizophrenia. In one study, tissue obtained from a temporal lobe biopsy of an individual with schizophrenia (Ong and Garey, 1993) showed many unusual asymmetric synapses, including clumped but numerous, synaptic vesicles located at short synaptic active zones. In another study, electron microscopic examination of the postmortem caudate nucleus revealed swelling of some axon terminals, shrinkage of some axon boutons and fewer synaptic vesicles (Uranova et al., 1996). These observations are similar to a series of prior postmortem electron microscopic studies, where... 

The ultrastructural organization of dopaminergic boutons in the striatum has been extensively investigated (see, inter alia, the reviews of Smith and Bolam, 1990 Sesack, 2003). Extrastriatal inputs, including the dopaminergic one, terminate mainly on the more distal part of the dendritic tree of medium spiny neurons, while intrinsic inputs terminate mainly on the proximal parts of the dendritic shaft and on the cell body. A small proportion of dopaminergic axons also contact the cell body of striatal projection neurons (Fig. 18B). 

At variance with the ultrastructural features observed in the NAc shell, dopaminergic axon terminals and boutons of thalamocortical axons deriving from the thalamic paraventricular nucleus were not found to converge on the same structures, such as dendritic shafts or spines (Pinto et al., 2003). Also the terminals of hippocampal fibers did not show obvious synaptic relationship with dopaminergic terminals in the prefrontal cortex (Carr and Sesack, 1996), indicating a segregation of different sets of cortical inputs. 

The nerve fibers in the cochlea can be classified as afferent fibers (toward the brain) or efferent fibers (toward the periphery). The afferent fibers that terminate on IHCs constitute approximately 90-95% of all afferent fibers in the cochlea. These afferent fibers originate from type I ganglion cells and are coated with a thick myelin sheath. Each fiber is connected to only one IHC, but each IHC is innervated by 2-10 individual afferent fibers. The principal neurotransmitter released by IHCs, glutamate, activates the afferent fibers in a quantal manner. The remaining 5-10% of afferent fibers are connected to OHCs and are unmyelinated. They originate from type II ganglion cells. Each afferent fiber is highly branched and is connected to 6-100 OHCs. OHCs are innervated mainly by efferent fibers, which are derived from the medial olivocochlear bundle. Efferent fibers release acetylcholine (ACh) as their principal neurotransmitter. Each OHC is in contact with 2-5 efferent synaptic boutons at its base. IHCs receive axodendritic efferent innervation onto afferent fibers from the lateral olivocochlear bundle (reviewed by Raphael and Altschuler, 2003). 

Earlier investigations focused on peptides and other slow-acting agents as the principal neuroactive substances in neuronal circuits of the hypothalamus (Swanson, 1987). However, Van den Pol (1991) examined the presence Glu in several medial hypothalamic nuclei (the suprachiasmatic, arcuate, ventromedial, supraoptic and parvocellular and magnocellular periventricular nuclei) and detected a population of boutons displaying strong immunoreactiv-ity for Glu. Decavel and Van den Pol (1992) similarly found Glu-enriched terminals forming synapses with hypothalamic neurosecretory neurons (labeled by intravenous injections of... 

Fig. 5A-C. CBi expression on GABAergic terminals in rat somatosensory cortex. CBi receptors [arrowheads] were detected with an antibody directed againsttheC terminusof rat CBi using pre-embedding immunogold with silver enhancement. The boutons are forming symmetric synapses [arrows), characteristic of cortical GABAergic axon terminals. CBi -positive terminals form synapses with pyramidal cell bodies (A), main apical dendrites (B), and fine-caliber dendrite branches [C).Scalebar = 0.5 pm. (Original photomicrograph provided byTamas Freund and Agnes Bodor)...

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