Terminal lesions

D2 Mostly in striatum, nucleus accumbens and olfactory tubercle but also on neuron cell bodies in substantia nigra and ventral tegmentum where they are the autoreceptors for locally (dendritic) released DA. The loss of specific D2 antagonist binding in the striatum after lesions of the afferent nigro-striatal tract indicates their presynaptic autoreceptor role on terminals there. Other lesion studies have also established D2 receptors on other inputs such as the cortico striatal tract. 

Pycock, CJ, Kerwin, RW and Carter, CJ (1980) Effect of lesion of cortical dopamine terminals on subcortical dopamine receptors in rats. Nature 286 74-77. 

The motor activation produced by psychomotor stimulants has been long associated with the midbrain dopamine systems. While focused stereotyped behavior produced by high doses of indirect sympathomimetics is blocked by removal of dopamine terminals in the corpus striatum (Creese and Iversen 1975), the locomotor activation produced by low doses of indirect sympathomimetics is blocked by removal of dopamine terminals in the region of the nucleus accumbens (Kelly et al. 1975). This dopaminergic substrate for psychostimulant effects appears selective for the indirect sympathomimetics in that dopamine lesions to the region of the nucleus... 

Fuxe 1965) and throughout the brain stem and spinal cord. A series of studies employing small intracerebral lesions (Anden et al. 1966 Ungerstedt 1971) indicated that most 5-HT nerve terminals in the forebrain arise from raphe nuclei in the midbrain and that the axons ascend through the lateral hypothalamus within the medial forebrain bundle (Moore and Heller 1967 Azmitia 1978 Conrad et al. 1974). 

Neuritic (senile) plaques Microscopic lesions composed of fragmented axon terminals and dendrites surrounding a core of amyloid seen in the cerebral cortex in Alzheimer s disease. 

Acatalasemia is a rare hereditary deficiency of tissue catalase and is inherited as an autosomal recessive trait (03). This enzyme deficiency was discovered in 1948 by Takahara and Miyamoto (Tl). Two different types of acatalasemia can be distinguished clinically and biochemically. The severe form, Japanese-type acatalasemia, is characterized by nearly total loss of catalase activity in the red blood cells and is often associated with an ulcerating lesion of the oral cavity. The asymptomatic Swiss-type acatalasemia is characterized by residual catalase activity with aberrant biochemical properties. In four unrelated families with Japanese-type acatalasemia, a splicing mutation due to a G-to-A transition at the fifth nucleotide in intron 4 was elucidated (K20, W5). We have also determined a single base deletion resulting in the frameshift and premature translational termination in the Japanese patient (HI6). 

Neuronal histamine can be methylated outside of histaminergic nerve terminals. In contrast to the striking regional distribution of histamine and HDC, HMT shows a more even distribution [14], suggesting a widespread HMT localization. In support of this, lesions that destroy... 

They have many of the morphological and ultrastructural characteristics of disease filaments [11, 12] (Fig. 45-5). Assembly is a nucleation-dependent process that occurs through its amino-terminal repeats. The carboxy-terminal region, in contrast, is inhibitory. Assembly is accompanied by the transition from random coil to a [3-pleated sheet. By electron diffraction, a-synuclein filaments show a conformation characteristic of amyloid fibers. Under the conditions of these experiments, P- and y-synucleins failed to assemble, consistent with their absence from the filamentous lesions of the human diseases. When incubated with a-synuclein, P- and y-synucleins inhibit the fibrillation of a-synuclein, suggesting that they may indirectly influence the pathogenesis of Lewy body diseases and multiple system atrophy. 

No remarkable changes or lesions were present in treated mice at either the end of exposure or at terminal sacrifice compared with the control groups. 

Cardiovascular Effects. Cardiovascular effects as terminal events were reported in patients dying after dermal and inhalation exposure to 1,2-dibromoethane. One individual also had acute myocardial lesions (Letz et al. 1984). Cardiovascular effects were not identified in humans who died after 1,2-dibromoethane ingestion. These findings in humans were not supported by studies in experimental animals exposed by inhalation, oral, or dermal routes. It is unlikely that humans exposed to low levels of 1,2-dibromoethane will experience adverse cardiovascular effects. 

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