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Partial lesions

QUESTION Do you get bigger effects on some of the behavioral parameters after the amphetamine treatments if you pretreat the animals with a low dose of alpha methyltyrosine during that period, during the postamphetamine period In the old days, when we had a partial lesion, we gave a low dose of AMFT, and it would reexpose the lesion. Have you tried that ... [Pg.154]

Didn t that require a partial lesion in the animals first ... [Pg.71]

Differentiation and migration of long term expanded human neural progenitors in a partial lesion model of Parkinson s disease. Int JBiochem Cell Biol, 36, 702-13. [Pg.40]

As synaptic contacts are being reestablished, it is likely that the high-affinity DAT is down regulated to maintain dopamine concentrations in the synaptic cleft. With time, and as the number of contacts normalize, normal transport may also be restored. This however, requires a lengthy process and would not be completed in animals with extensive lesions, even after 16 weeks. Blanchard et al. (1996) observed growth cones entering the striatum seven months after partial lesions, suggesting that 12 months or more may be required for normalization of synaptic function (Blanchard et al., 1996). [Pg.182]

Blanchard V, Anglade P, Dziewczapolski G, Savasta M, Agid Y, Raisman-Vozari R (1996) Dopaminergic sprouting in the rat striatum after partial lesion of the substantia nigra. Brain Res 709 319-325. [Pg.185]

Dravid A, Jaton AL, Enz A, Frei P (1984) Spontaneous recovery from motor asymmetry in adult rats with 6-hydroxydopamine-induced partial lesions of the substantia nigra. Brain Res 577 361-365. [Pg.187]

Hansen JT, Sakai K, Greenamyre JT, Moran S (1995) Sprouting of dopaminergic fibers from spared mesencephalic dopamine neurons in the unilateral partial lesioned rat. Brain Res 670 197-204. [Pg.189]

Hefti F, Melamed E, Wurtman RJ (1980) Partial lesions of the dopaminergic nigrostriatal system in rat brain biochemical characterization. Brain Res 795 123-137. [Pg.189]

Stanic D, Parish CL, Zhu WM, Krstew EV, Lawrence AJ, Drago J, Finkelstein DI, Horne MK (2003b) Changes in function and ultrastructure of striatal dopaminergic terminals that regenerate following partial lesions of the SNpc. J Neurochem 56 329 343. [Pg.195]

Fig. 6. Proposed hypothetical mechanisms of pre- and post-synaptic plasticity that might underlie recovery of function following partial lesions of the nigrostriatal dopamine neurones. A. Schematic illustration of two intact dopamine terminals making synaptic contact with a post-synaptic striatal neurone. B. Following partial lesion, spared terminals up-regulate to restore normal levels of postsynaptic activation by a combination of processes that include (1) increased firing, (2) increased dopamine synthesis, (3) increased dopamine release, (4) reduced dopamine uptake, (5) diffusion to deafferented synapses, and (6) supersensitivity of all post-synaptic synapses. (Redrawn from Zigmond and Sticker (1984), with permission.)... Fig. 6. Proposed hypothetical mechanisms of pre- and post-synaptic plasticity that might underlie recovery of function following partial lesions of the nigrostriatal dopamine neurones. A. Schematic illustration of two intact dopamine terminals making synaptic contact with a post-synaptic striatal neurone. B. Following partial lesion, spared terminals up-regulate to restore normal levels of postsynaptic activation by a combination of processes that include (1) increased firing, (2) increased dopamine synthesis, (3) increased dopamine release, (4) reduced dopamine uptake, (5) diffusion to deafferented synapses, and (6) supersensitivity of all post-synaptic synapses. (Redrawn from Zigmond and Sticker (1984), with permission.)...
Kirik D, Rosenblad C, Bjorklund A (1998) Characterization of behavioral and neurodegenerative changes following partial lesions of the nigrostriatal dopamine system induced by intrastriatal 6-hydroxydopamine in the rat. Exp Neurol 752 259-277. [Pg.290]

This proposition was tested using a well-studied animal model of Parkinson s disease in which partial lesions of the nigrostriatal system are created by unilateral microinjection of the catecholamin-ergic-specific neurotoxin 6-hydroxydopamine (6-... [Pg.259]

Buda R, Ferruzzi A, Vannini F, Zambelli L, Di Caprio F (2006) Augmentation technique with semitendinosus and gracilis tendons in chronic partial lesions of the ACL clinical and arthrometric analysis. Knee Surg Sports Traumatol Arthrosc 14 1101-1107... [Pg.346]

Some have questioned the specificity of DWI in delineating particular areas of the brain that are destined for infarction, noting that some DWI lesions resolve at least partially in follow-up studies. However, it appears that reversibility of DWI lesions is quite unusual and typically involves only a small portion of initially abnormal tissue. One study found that reversal of a DWI abnormality occurred in 33% of patients following intra-arterial thrombolysis. However, in this study, the areas of reversal nevertheless went on to infarction in the majority of patients. ... [Pg.7]

Complex partial seizures manifest themselves as bizarre behaviours which are also known as psychomotor or temporal lobe epilepsy, since a lesion (focus) is often found in that brain area. Repetitive and apparently purposeful movements vary from simple hand clenching or rubbing to more bizarre hand movements and walking. These can last a few minutes, often disrupt other ongoing activity or speech and the patient has no subsequent memory of them. Complex seizures may develop from simple ones. [Pg.325]

Abe, K, Takeyama, C and Yoshimura, K (1998) Effects of S-8510, a novel benzodiazepine receptor partial inverse agonist, on basal forebrain lesioning-induced dysfunction in rats. Eur. J. Pharmacol. 347 145-152. [Pg.421]

Partial response (PR) At least a 30% decrease in the sum of the longest diameter of target lesions from baseline... [Pg.1338]

So we are still left with two models of the stereochemistry of DNA alkylated by a PAH diol epoxide the PAH either lies in a groove of DNA or else tries to intercalate between the bass of DNA. Since it is covalently bonded to a base it must cause considerable distortion if it tries to lie between the bases. However, the stacking observed in the crystalline state seems to argue for partial intercalation. We will need crystal structures of at least one appropriately alkylated polynucleotide before this problem can be resolved. And when this is done it will be just the beginning of the answer to the problem of alkylation of DNA by activated carcinogens. The subsequent question is, what is the lesion in DNA that is important in carcinogenesis, and then what does it cause to happen so that tumor formation is initiated ... [Pg.181]

Table 3. Antimicrobial and mechanical bowel preparation in patients with partially obstructing intestinal lesions... Table 3. Antimicrobial and mechanical bowel preparation in patients with partially obstructing intestinal lesions...
The goal of therapy is to achieve resolution of lesions, but partial clearing using regimens with decreased toxicity and increased patient acceptability... [Pg.200]


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See also in sourсe #XX -- [ Pg.175 , Pg.177 , Pg.181 , Pg.182 , Pg.249 ]




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