Neuron-scattering

The diffuse part of the TMN consists of a small group of neurons scattered within the lateral hypothalamic area, the posterior hypothalamic region, the perifornical area, the supramammillary nucleus, and the dorsomedial hypothalamic nucleus. 

These results led to the suggestion that the functional unit of reward is a population of individual neurons ( hedonistic neurons ) scattered around reward areas of the brain which are specifically responsive to certain transmitters and are presumably connected to pathways controlling motivated behaviour. Phillips and Fibiger (1989) demonstrated an increase in dopamine metabolism, synthesis and release in the ventral tegmental area and nucleus accumbens during ICSS in rats, an increase proportional to the stimulation rate and intensity. 

In addition to pyramidal cells, a population of smaller neurons scattered in strata oriens and radiatum of the hippocampus are found to contain dysbindin-1 in truly optimal immunohistochemical preparations. They remain uncharacterized, but their distribution suggests that they include the subset of GABAergic hippocampal interneurons expressing the calcium-binding protein calbindin mapped by Freund and Buzsaki (1996). 

Figure 4.05 The neuron scattering length, as a function of atomic number, Z, showing the value for the natural element ( ) and the range of isotopic variation (bar). A dashed bar denotes elements with complex b and only the variation in the real part of at a wavelength of 1 A (From Wright, 1993).

Neutron scattering studies of setal hydrogen systems The palladium hydrogen system Ab Initio calculations of metal hydrogen systems Experimental measurements of the inelastic neuron scattering form factors for scattering to excited states in PdH... 

Smith, J. C. (1991). Protein dynamics comparison of simulations with inelastic neuron scattering experiments. Quarterly Reviews of Biophysics, 24, 227-92. 

Hepatocyte growth factor (HGF), also known as scatter factor, has been shown to support the survival of sympathetic neuroblasts and subpopulations of spinal motor neurons. In the former case this is apparently an autocrine effect since these cells have been shown to synthesize HGF. 

R. A. Stepnowski, J. A. LaPorta, F. Raccuia-Behling, G. E. Blonder, R. E. Slusher, and D. Kleinfeld. Noninvasive detection of changes in membrane potential in cultured neurons by light scattering. Proceedings of National Academy of Science USA, 88 9382-9386, 1991. 

How precisely does cocaine achieve these effects in the brain As described in Chapter i, once a neurotransmitter is released from its neuronal terminal, its actions within the synapse are ended principally by reuptake into the presynaptic terminal. Cocaine primarily blocks the reuptake of dopamine but also acts similarly on norepinephrine and serotonin reuptake. If your neuronal terminals can be seen as acting like little vacuum cleaners, then cocaine essentially clogs the vacuum nozzle. As a consequence of this blockade, the concentrations of dopamine, norepinephrine, and serotonin within the synaptic cleft between two neurons increases dramatically. Withinmillions of synapses in the brain, these neurotransmitters are now free to continue to stimulate their receptors over and over, again and again. There are neuronal terminals for dopamine, norepinephrine, and serotonin scattered throughout the entire brain, and thus the consequences of cocaine on brain function are also widespread. 

Fig. 4.1. Frequency maps of two types of ischemic damage complete infarction (left) and scattered neuronal injury (right). Histology was obtained 24 h after left MCA occlusion in rats. Total number of animals was 9. Pseudocolor representation denotes the number of animals that showed the respective type of injury at this pixel. Note the widespread distribution of incomplete infarction over the affected left hemisphere. [Adapted from Alexis et al. (1996)]...

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