Synaptic distribution

Brandstatter JH, Koulen P, Wiissle H (1997) Selective synaptic distribution of kainate receptor subunits in the two plexiform layers of the rat retina. J Neurosci 77 9298-9307. 

Rubio ME, Juiz JM (1998) Chemical anatomy of excitatory endings in the dorsal cochlear nucleus of the rat differential synaptic distribution of aspartate aminotransferase, glutamate, and vesicular zinc. J Comp Neurol 399 341-358. 

Kharazia VN, Weinberg RJ (1997) Tangential synaptic distribution of NMDA and AMPA receptors in rat neocortex. Neurosci Lett 258 41-44. 

Valtschanoff JG, Burette A, Wenthold RJ, Weinberg RJ (1999) Expression of NR2 receptor subunit in rat somatic sensory cortex synaptic distribution and colocalization with NRl and PSD-95. J Comp Neurol 470 599-611. 

Fig. 48. Electron micrograph of the synaptic distribution of immunoreactivity for the GluRl subunit of the AMPA receptor in rat cerebellum as detected by an antibody against the carboxy-terminal (intracellular) region of GluRl. A. A spine (s) emerging from a Purkinje cell dendrite (Pd) establishes an immunopositive type 1 synapse (solid arrows) with a parallel fiber terminal (pft). Intra-cellular immunoreactivity is present inside Bergmann glial cell processes along dendritic elements (e.g., open arrow). B. The peroxidase reaction end-product labels the postsynaptic density (psd) at the intracellular face of the postsynaptic membrane (pom) and not the synaptic cleft between the presyaptic (pem) and postsynaptic (pom) membranes. Scale bars in A = 0.5 /xm, in B = 0.1 jum. Baude et al. (1994).

Heimer, L. (1968) Synaptic distribution of centripetal and centrifugal nerve fibres in the olfactory system of the rat. An experimental anatomical study. J. Anat., 103, 413 32. 

Populations of receptors that are excluded from synaptic junctions. These may be distributed over neuronal cell bodies or located around but not directly beneath synapses (perisynaptic). Some receptors have become specialised to setve an extrasynaptic function producing a tonic level of activity in response to ambient levels of neurotransmitter. This tonic current can be used to maintain homeostatic control over neuronal excitation. 

Due to their physicochemical properties trace amines can pass the cell membrane to a limited extent by passive diffusion, with the more lipophilic PEA and TRP crossing membranes more readily than the more polar amines TYR. and OCT. In spite of these features, trace amines show a heterogeneous tissue distribution in the vertebrate brain, and for TYR. and OCT storage in synaptic vesicles as well as activity-dependent release have been demonstrated. So far, trace amines have always been found co-localized with monoamine neurotransmitters, and there is no evidence for neurons or synapses exclusively containing trace amines. 

Zenisek D, Steyer JA, Eeldman ME, Aimers W (2002) A membrane marker leaves synaptic vesicles in nulliseconds after exocytosis in retinal bipolar cells. Neuron 35 1085-1097 Zhang L, He T, Talal A, Wang G, Frankel SS, Ho DD (1998) In vivo distribution of the human immunodeficiency virus/simian immunodeficiency virus coreceptors CXCR4, CCR3, and CCR5. J Virol 72 5035-5045... 

Parkinsonism is unique among diseases of the CNS, in that it results from the known loss of a particular NT, i.e. DA, resulting from the degeneration of a particular pathway, the nigrostriatal. Dopamine also has a relatively limited distribution in the brain and few peripheral effects. It should therefore be amenable to therapy based on augmenting its function. Also since the role of DA appears to be to maintain a tonic inhibitory control on GABA output pathways from the striatum, possibly in part by an extra synaptic action (Chapter 6), it may not be necessary for it to be released physiologically from nerve terminals. Thus it may be adequate to just provide DA extracellularly. 

The action of catecholamines released at the synapse is modulated by diffusion and reuptake into presynaptic nerve terminals. Catecholamines diffuse from the site of release, interact with receptors and are transported back into the nerve terminal. Some of the catecholamine molecules may be catabolized by MAO and COMT. The cate-cholamine-reuptake process was originally described by Axelrod [18]. He observed that, when radioactive norepinephrine was injected intravenously, it accumulated in tissues in direct proportion to the density of the sympathetic innervation in the tissue. The amine taken up into the tissues was protected from catabolic degradation, and studies of the subcellular distribution of catecholamines showed that they were localized to synaptic vesicles. Ablation of the sympathetic input to organs abolished the ability of vesicles to accumulate and store radioactive norepinephrine. Subsequent studies demonstrated that this Na+- and Cl -dependent uptake process is a characteristic feature of catecholamine-containing neurons in both the periphery and the brain (Table 12-2). 

The postsynaptic receptors on any given neuron receive information from transmitters released from another neuron. Typically, postsynaptic receptors are located on dendrites or cell bodies of neurons, but may also occur on axons or nerve terminals in the latter case, an axoaxonic synaptic relationship may cause increases or decreases in transmitter release. In contrast, autoreceptors are found on certain neurons and respond to transmitter molecules released from the same neuron. Autoreceptors may be widely distributed on the surface of the neuron. At the nerve terminal, they respond to transmitter molecules released into the synaptic cleft on the cell body, they may respond to transmitter molecules released by dendrites. Functionally, most autoreceptors appear to decrease further transmitter release in a kind of negative feedback loop. Autoreceptors have been identified for all the catecholamines, as well as for several other neurotransmitters. a2-adrenergic receptors are often found on noradrenergic nerve terminals of postganglionic sympathetic nerves, as well as on noradrenergic neurons in the CNS [36], and activation of these receptors decreases further norepinephrine release. Dopamine autoreceptors,... 

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