Neuron axon terminal

Konopaske GT, Sweet RA, Wu Q, Sampson A, Lewis DA. 2006. Regional specificity of chandelier neuron axon terminal alterations in schizophrenia. Neuroscience 138(1) 189-196. 

Pierri JN, Chaudry AS, Woo TU, Lewis DA. 1999. Alterations in chandelier neuron axon terminals in the prefrontal cortex of schizophrenic subjects. Am J Psychiatry 156 1709-1719. 

At the axon terminus, neurotransmitters are released into the synaptic gap. Through aptic gaps, a typical neuron may intercormect with thousands and tens of thousands of other neurons. Axon terminals have knob-like swellings at the very end called synaptic knobs or end buttons. Each synaptic knob communicates with a dendrite or cell body of another neuron, the point of contact being a apse. Under very high magnification, a very tiny space, the aptic clefl or gap (about one millionth of an irKh, or mm), can be delected between the synaptic knob and dendrite or cell body. Synaptic knobs contain hundreds of neurovesicles that contain a transmitter substance (or neurotransmitter). 

Neurons have three parts the cell body and dendrites, the axon, and axon terminals. The cell body contains the nucleus and the organelles needed for metabolism, growth, and repair. The dendrites are branched extensions of the cell body membrane. The axon is a long, thin structure which transfers electrical impulses down to the terminals. The axon divides into numerous axon terminals and it is in this specialized region that neurotransmitters are released to transmit information from one neuron to its neighbors. The synapse has been defined as the space between two subsequent interrelated neurons. ... 

Neuromuscular junction (NMJ) is the synapse or junction of the axon terminal of motoneurons with the highly excitable region of the muscle fibre s plasma membrane. Neuronal signals pass through the NMJ via the neurotransmitter ACh. Consequent initiation of action potentials across the muscle s cell surface ultimately causes the muscle contraction. 

Synaptic vesicles are the organelles in axon terminals that store neurotransmitters and release them by exocytosis. There are two types, the large dense-core vesicles, diameter about 90 nm, that contain neuropeptides, and the small synaptic vesicles, diameter about 50nm, that contain non-peptide transmitters. About ten vesicles per synapse are docked to the plasma membrane and ready for release, the readily releasable pool . Many more vesicles per synapse are stored farther away from the plasma membrane, the resting pool . When needed, the latter vesicles may be recruited into the readily releasable pool. Neuronal depolarization and activation of voltage-sensitive Ca2+... 

Synaptic transmission. Transmission through the junction across which a nerve impulse passes from an axon terminal to a neuron, muscle cell, or gland cell. 

The axon terminals of one neuron synapse with other neurons either on the dendrites (axo-dendritic synapse) or soma (axo-somatic synapse). Synapses on another axon... 

Figure 1.6 Presynaptic inhibition of the form seen in the dorsal horn of the spinal cord, (a) The axon terminal (i) of a local neuron is shown making an axo-axonal contact with a primary afferent excitatory input (ii). (b) A schematic enlargement of the synapse, (c) Depolarisation of the afferent terminal (ii) at its normal resting potential by an arriving action potential leads to the optimal release of neurotransmitter, (d) When the afferent terminal (ii) is already partially depolarised by the neurotransmitter released onto it by (i) the arriving acting potential releases less transmitter and so the input is less effective...

Dendro-dendritic synapses have also been deseribed whieh show eharaeteristie synaptie eonneetions and we need to abandon the belief that one neuron ean only influenee another through its axon terminals. Dendro-dendritie synapses ean also be reeiproeal, i.e. one dendrite ean make synaptie eontaet with another and apparently be both pre- and postsynaptie to it. 

These are basically neurons whose cell body and axon terminals are both found in the same part of the CNS (Fig. 1.2). They are not concerned with transmitting information from one part of the CNS to another but in controlling activity in their own area. They can be excitatory but are more often inhibitory. They may act postsynaptically through conventional IPSPs (or slower potential changes) or presynaptically by modifying NT... 

To achieve their different effects NTs are not only released from different neurons to act on different receptors but their biochemistry is different. While the mechanism of their release may be similar (Chapter 4) their turnover varies. Most NTs are synthesised from precursors in the axon terminals, stored in vesicles and released by arriving action potentials. Some are subsequently broken down extracellularly, e.g. acetylcholine by cholinesterase, but many, like the amino acids, are taken back into the nerve where they are incorporated into biochemical pathways that may modify their structure initially but ultimately ensure a maintained NT level. Such processes are ideally suited to the fast transmission effected by the amino acids and acetylcholine in some cases (nicotinic), and complements the anatomical features of their neurons and the recepter mechanisms they activate. Further, to ensure the maintenance of function in vital pathways, glutamate and GABA are stored in very high concentrations (10 pmol/mg) just as ACh is at the neuromuscular junction. 

There is much evidence (e.g. Cheramy, Leviel and Glowinski 1981) from both in vitro and in vivo perfusion studies that DA is released from the dendrites of DA neurons in both A9 and AlO even though those dendrites do not contain many vesicles compared with axon terminals. The release and changes in it may also be slower and longer than that at axon terminals and the synaptic arrangement between the releasing dendrites and postsynaptic target is not clear. DA receptors also appear to be on neurons other than dopamine ones and on the terminals of afferent inputs to A9 (and AlO). It seems that the activation of the DA neurons may partly be controlled by the effects of the dendritically released DA on such inputs. 

Figure 15.9 Peptide modulation of striatal input to the globus pollidus. Enkephalin released from axon terminals of neurons of the indirect pathway (see Fig. 15.2 for details) is thought to inhibit GABA release from the same terminals so that feedback (auto) inhibition is reduced. This will free the neurons to inhibit the subthalamic nucleus (SThN) and its drive to GPint and SNr which in turn will have less inhibitory effect on cortico-thalamic traffic and possibly reduce akinesia. Dynorphin released from terminals of neurons of the direct pathway may also reduce glutamate release and excitation in the internal globus pallidus and further depress its inhibition of the cortico-thalamic pathway. High concentrations of these peptides may, however, result in dyskinesias. (See Henry and Brotchie 1996 and Maneuf et al. 1995)...

Of course, cholinergic neurons are not the only ones with axon terminals in the cortex and if their degeneration does originate in the cortex then other afferants and their neurons could also be affected. This contention is supported by reported reductions in the number of NA neurons in the locus coeruleus, and 5-HT neurons in dorsal raphe but these are less marked (approximately 50%) than the loss of cholinergic neurons. Accompanying reductions in cortical NA and 5-HT are also seen but are again lower than those for ChAT but 5-HT2 receptors are reduced (43%). 

Lamina IV is composed of heterogeneous sized cells and is less densely packed than lamina III due to the number of nerve axons passing in this layer. At least three types of neurons have been identified in lamina IV, based on different dendritic projection patterns and these include SCT and PSDC cells. Another cell type has been described which has a dendritic pattern similar to SCT and PSDC, but with local axon terminations. Somas of STT cells are also found in lamina IV. 

Herve, D. Pickel, V.M. Joh, T.H. and Beaudet, A. Serotonin axon terminals in the ventral tegmental area of the rat Fine strueture and synaptie input to dopaminergic neurons. Brain Res 435 71-83, 1987. 

The function of a neuron is to communicate or relay information to another cell by way of an electrical impulse. A synapse is the site at which the impulse is transmitted from one cell to the next. A neuron may terminate on a muscle cell, glandular cell, or another neuron. The discussion in this chapter will focus on neuron-to-neuron transmission. At these types of synapses, the presynaptic neuron transmits the impulse toward the synapse and the postsyn-aptic neuron transmits the impulse away from the synapse. Specifically, it is the axon terminal of the presynaptic neuron that comes into contact with the cell body or the dendrites of the postsynaptic neuron. Most neurons, particularly in the CNS, receive thousands of inputs. As will become evident, the transmission of the impulse at the synapse is unidirectional and the presynaptic neuron influences activity of the postsynaptic neuron only. 

Figure 5.1 Mechanism of action at a chemical synapse. The arrival of an action potential at the axon terminal causes voltage-gated Ca++ channels to open. The resulting increase in concentration of Ca++ ions in the intracellular fluid facilitates exocytosis of the neurotransmitter into the synaptic cleft. Binding of the neurotransmitter to its specific receptor on the postsynaptic neuron alters the permeability of the membrane to one or more ions, thus causing a change in the membrane potential and generation of a graded potential in this neuron.

Convergence occurs when the axon terminals of many presynaptic neurons all synapse with a single postsynaptic neuron. As discussed previously, spatial summation of nerve impulses relies on the presence of convergence. Divergence occurs when the axon of a single presynaptic neuron branches and synapses with multiple postsynaptic neurons. In this way, activity in a... 

These symptoms are alleviated by administering levodopa (L-dopa), a precursor for dopamine. L-dopa is taken up by the axon terminals of dopaminergic neurons and used to form dopamine. Interestingly, in some patients, a side effect of dopamine replacement therapy is the development of symptoms characteristic of schizophrenia. (Recall that this mental disorder is caused by overactive dopaminergic neurons.) On the other hand, drugs used to treat schizophrenia — dopamine receptor antagonists — may elicit symptoms of Parkinson s disease. 

Afferent neurons that transmit sensory information toward the spinal cord are referred to as first-order sensory neurons. The cell bodies of these neurons are found in the dorsal root ganglia. These ganglia form a swelling in each of the dorsal roots just outside the spinal cord. The portion of the axon between the distal receptor and the cell body is referred to as the peripheral axon and the portion of the axon between the cell body and the axon terminal within the CNS is referred to as the central axon. 

Morphine may be administered orally, intravenously, or epidurally. An advantage of epidural administration is that it provides effective analgesia while minimizing the central depressant effects associated with systemic administration. The mechanism of action with the epidural route of administration involves opioid receptors on the cell bodies of first-order sensory neurons in the dorsal root ganglia as well as their axon terminals in the dorsal hom. Stimulation of these receptors inhibits release of substance P and interrupts transmission of the pain signal to the second-order sensory neuron. 

Synapses between the autonomic postganglionic neuron and effector tissue — the neuroeffector junction — differ greatly from the neuron-to-neuron synapses discussed previously in Chapter 5 (see Table 9.1). The postganglionic fibers in the ANS do not terminate in a single swelling like the synaptic knob, nor do they synapse directly with the cells of a tissue. Instead, the axon terminals branch and contain multiple swellings called varicosities that lie across the surface of the tissue. When the neuron is stimulated, these varicosities release neurotransmitter over a large surface area of the effector tissue. This diffuse release of the neurotransmitter affects many tissue cells simultaneously. Furthermore, cardiac muscle and most smooth muscle have gap junctions between cells. These specialized intercellular communications... 

As discussed previously, the neurohypophysis has a direct anatomical connection to the hypothalamus. Therefore, the hypothalamus regulates the release of hormones from the neurohypophysis by way of neuronal signals. Action potentials generated by the neurosecretory cells originating in the hypothalamus are transmitted down the neuronal axons to the nerve terminals in the neurohypophysis and stimulate the release of the hormones into the blood. The tracts formed by these axons are referred to as hypothalamic-hypophyseal tracts (see Figure 10.2). The action potentials are initiated by various forms of sensory input to the hypothalamus. Specific forms of sensory input that regulate the release of ADH and oxytocin are described in subsequent sections in this chapter. 

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