Striatal, ventral mesencephalic and cortical transplants into the intact rat striatum: A neuroanatomical study

Lu, Sunny Y.; Shipley, Michael T.; Norman, Andrew B.; Sanberg, Paul R.

doi:10.1016/0014-4886(91)90168-c

Cited by 34 publications

(9 citation statements)

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“…4B). Although diverse markers of activated microglia are present in ventral mesencephalic grafts in rat striatum (Lu et al, 1991), we note that there was a tendency for [ 11 C]PK11195 binding to decline after mesencephalic grafting, relative to the V d measured in the earlier acute MPTP intoxication scans (Fig. 4C).…”

Section: Discussionmentioning

confidence: 75%

Distribution of PK11195 binding sites in porcine brain studied by autoradiography in vitro and by positron emission tomography

Cumming

Pedersen

Minuzzi

et al. 2006

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The cerebral distribution of peripheral-type benzodiazepine binding sites (PBBS) in human brain has been investigated by positron emission tomography (PET) with the specific radioligand [11C]PK11195 in diverse neuropathological conditions. However, little is known about the pattern of PK11195 binding sites in healthy brain. Therefore, we used quantitative autoradiography to measure the saturation binding parameters for [3H]PK11195 in cryostat sections from young Landrace pigs. Specific binding was lowest in the cerebellar white matter (85 fmol mg(-1)) and highest in the caudate nucleus (370 fmol mg(-1)), superior colliculus (400 fmol mg(-1)), and anterior thalamic nucleus (588 fmol mg(-1)). The apparent affinity was in the range of 2-6 nM in vitro, predicting high specific binding in PET studies of living brain. However, the distribution volume (V(d), ml g(-1)) of high specific activity [11C]PK11195 was nearly homogeneous (3 ml g(-1)) throughout brain of healthy Landrace pigs, and was nearly identical in studies with lower specific activity, suggesting that factors in vivo disfavor the detection of PBBS in Landrace pigs with this radioligand. In young, adult Göttingen minipig brain, the magnitude of V(d) for [11C]PK11195 was in the range 5-10 ml g(-1), and had a heterogeneous distribution resembling the in vitro findings in Landrace pigs. There was a trend toward globally increased V(d) in a group of minipigs with acute MPTP-induced parkinsonism, but no increase in V(d) was evident in the same pigs rescanned at 2 weeks after grafting of fetal mesencephalon to the partially denervated striatum. Thus, [11C]PK11195 binding was not highly sensitive to constituitively expressed PBBS in brain of young Landrace pigs, and did not clearly demonstrate the expected microglial activation in the MPTP/xenograft model of minipigs.

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Section: Discussionmentioning

confidence: 75%

Distribution of PK11195 binding sites in porcine brain studied by autoradiography in vitro and by positron emission tomography

Cumming

Pedersen

Minuzzi

et al. 2006

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“…This means that there may not be adequate survival signals to keep the graft alive as well as the surrounding `normal' tissue. Previous studies of fetal grafts, or marrow stromal cells into normal brain tissue do show some evidence of detrimental effects [7,18,30] and therefore it may be interesting to see whether HUCB cell survival is enhanced following transplantation into lesioned NOD SCID mice. Coyne et al [7] found that marrow stromal cell transplants induced an inflammatory response which led to loss of the transplanted cells by 14 days, and Hagenmeyer-Houser and Sanberg [18] showed a time-dependent decrease in striatal transplant size of embryonic striatal tissue at 10 weeks compared to 3 weeks, though they still had a surviving graft at the later time point.…”

Section: Discussionmentioning

confidence: 99%

Long-term cultured human umbilical cord neural-like cells transplanted into the striatum of NOD SCID mice

Walczak¹,

Chen²,

Eve³

et al. 2007

Brain Research Bulletin

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The use of stem cells and other cells as therapies is still in its infancy. One major setback is the limited survival of the grafts, possibly due to immune rejection. Studies were therefore performed with human umbilical cord blood cells (HUCB) to determine the ability of these cells to survive in vivo and the effect of the immune response on their survival by transplantation into the normal striatum of immunodeficient NOD SCID mice.Long-term culture of HUCB cells resulted in several different populations of cells, including one that possessed fine processes and cell bodies that resembled neurons. Their neuronal phenotype was confirmed by immunohistochemical staining for the early neuronal marker TuJ1 and the potentially neural marker Nestin. Five days after cell transplantation of this neuronal phenotype, immunohistochemical staining for human mitochondria confirmed the presence of living HUCB cells in the mouse striatum, with cells localized at the site of injection, expressing early neural and neuronal markers (Nestin and TuJ1) as well as exhibiting neuronal morphology. However, no evidence of surviving cells was apparent 1 month postgrafting. The absence of signs of T cell-mediated rejection, such as CD4 and CD8 lymphocytes and minimal changes in microglia and astrocytes, suggest that cell loss was not due to a T cell-mediated immune response. In conclusion HUCB cells can survive long-term in vitro and undergo neuron-like differentiation. In mice, these cells do not survive a month. This may relate to the differentiated state of the cells transplanted into the unlesioned striatum, rather than T cell-mediated immunological rejection.

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“…However, it has also been shown that the survival of embryonic neurons and the formation of reciprocal connections between grafted and host tissue is also possible in several previously unlesioned brain areas (Gage and Bjorklund, 1986;Kawamura et al, 1988;Zhou et al, 1989;Busziki et al, 1991;Lu et al, 1991). Nevertheless, in these reports embryonic cells have been transplanted intraparenchymally, a procedure that itself induces an injury in the host brain, which could affect the survival of grafted neurons by enhanced production of neurotrophic substances at the lesion site (Nieto-SamNro et al, 1982;Needels et al, 1986).…”

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confidence: 98%

Embryonic Purkinje Cells Grafted on the Surface of the Cerebellar Cortex Integrate in the Adult Unlesioned Cerebellum

Rossi

Borsello

Strata

1992

Eur J of Neuroscience

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The presence of an injury or the selective degeneration of specific neuronal populations is commonly assumed to be a necessary prerequisite for the survival and the integration of grafted neurons in the recipient brain. In the present study we have placed solid grafts of cerebellar anlage in the fourth ventricle of adult rats, in close contact with the host cerebellar cortex, to assess the capacity of embryonic Purkinje cells to interact with adult neurons and integrate in the unlesioned cerebellar cortex. Numerous grafted Purkinje cells are indeed able to leave the implant and migrate into the host molecular layer, where they develop adult structural features. In addition, such cells are able to elicit the growth of host climbing fibre sprouts which end in newly formed arborizations impinging upon their dendritic trees. Climbing fibre collateral branches also penetrate the implant to innervate Purkinje cells which have not migrated in the host cerebellum. These results show that embryonic Purkinje cells are able to survive and integrate in an adult unlesioned cerebellar cortex. In addition, adult olivary axons respond to the increased size of the target population by expanding their terminal domain to innervate grafted Purkinje cells.

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Striatal, ventral mesencephalic and cortical transplants into the intact rat striatum: A neuroanatomical study

Cited by 34 publications

References 50 publications

Distribution of PK11195 binding sites in porcine brain studied by autoradiography in vitro and by positron emission tomography

Distribution of PK11195 binding sites in porcine brain studied by autoradiography in vitro and by positron emission tomography

Long-term cultured human umbilical cord neural-like cells transplanted into the striatum of NOD SCID mice

Embryonic Purkinje Cells Grafted on the Surface of the Cerebellar Cortex Integrate in the Adult Unlesioned Cerebellum

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