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PubMed1982

The generation of 'cytotoxic' macrophages in mice during infection with influenza A or Sendai virus.

Injection of infectious but not of non-infectious influenza A virus or of infectious or non-infectious Sendai virus intraperitoneally into mice induces the generation of plastic-adherent cells that are able to effect release of 51Cr from labelled virus-infected target cells but not from labelled, uninfected cells. Their activity is greatly diminished by exposure to silica or carrageenan but not by anti-Thy 1 antibody and complement treatment. Similarly, the activity of the cell preparation cannot be explained by contamination with natural killer or 'K' cells. Thus, the effector cells were identified as macrophages and for convenience are called 'cytotoxic macrophages'. The maximum cytotoxic activity was recovered from the peritoneal cavity 5 days after virus injection and declined thereafter. Although the effector cells are cross-reactive in that cells activated by an influenza A strain virus lyse target cells infected with the same or other A strain viruses or with Sendai virus, there is preferential lysis of cells infected with the homologous virus. The action of the effector cells is not h-2-restricted. Preliminary experiments showed that similar effector cells can be recovered from the lungs of mice 5 days after intranasal inoculation of infectious influenza virus, so they may contribute to the host control of the disease.

Animals↗
PubMed2002

Impairment of hippocampal CA1 heterosynaptic transformation and spatial memory by beta-amyloid(25-35).

In Alzheimer's disease, the cholinergic damage (reduced neurotransmission) and cognitive impairment occur long before beta-amyloid (Abeta) plaque formation. It has not been established whether the link between soluble Abeta and cholinergic functions contributes to synaptic dysfunction that underlies the cognitive impairment. Here, we report that Abeta(25-35), an active form of Abeta, inhibited long-term synaptic modification that depends on the associative activation of cholinergic and GABAergic inputs when bilaterally injected intracerebroventricularly (icv; 200 microg/site). The Abeta microinjections did not affect single-pulse-evoked glutamatergic and GABAergic synaptic transmission onto the hippocampal CA1 pyramidal cells, while cholinergic intracellular theta; was dramatically reduced by the Abeta(25-35) injection. Spatial memory of the water maze task was also impaired by the bilateral icv Abeta(25-35) injections, while bilateral microinjections of the same dose of Abeta(35-25) was ineffective in affecting the long-term synaptic modification evoked by associative activation of cholinergic and GABAergic inputs, the cholinergic intracellular theta;, or producing memory impairments. Thus restoring the synaptic plasticity involved in this associative activation of cholinergic and GABAergic inputs may offer an important therapeutic target in the treatment of early Abeta-induced memory decline.

Amyloid beta-Peptides↗
PubMed2006

Dendritic mRNAs encode diversified functionalities in hippocampal pyramidal neurons.

BACKGROUND: Targeted transport of messenger RNA and local protein synthesis near the synapse are important for synaptic plasticity. In order to gain an overview of the composition of the dendritic mRNA pool, we dissected out stratum radiatum (dendritic lamina) from rat hippocampal CA1 region and compared its mRNA content with that of stratum pyramidale (cell body layer) using a set of cDNA microarrays. RNAs that have over-representation in the dendritic fraction were annotated and sorted into function groups. RESULTS: We have identified 154 dendritic mRNA candidates, which can be arranged into the categories of receptors and channels, signaling molecules, cytoskeleton and adhesion molecules, and factors that are involved in membrane trafficking, in protein synthesis, in posttranslational protein modification, and in protein degradation. Previously known dendritic mRNAs such as MAP2, calmodulin, and G protein gamma subunit were identified from our screening, as were mRNAs that encode proteins known to be important for synaptic plasticity and memory, such as spinophilin, Pumilio, eEF1A, and MHC class I molecules. Furthermore, mRNAs coding for ribosomal proteins were also found in dendrites. CONCLUSION: Our results suggest that neurons transport a variety of mRNAs to dendrites, not only those directly involved in modulating synaptic plasticity, but also others that play more common roles in cellular metabolism.

Animals↗
PubMed1992

Promoter for the regulatory type I beta subunit of the 3',5'-cyclic adenosine monophosphate-dependent protein kinase directs transgene expression in the central nervous system.

Cyclic AMP-dependent protein kinase (cAPK) modulates synaptic transmission and influences memory and learning. Among the various isoforms of regulatory and catalytic subunits that comprise mammalian cAPK, only the regulatory type I beta (RI beta) subunit is unique to nervous tissue. The requirement for RI beta in neurons is presently unknown. Previous studies demonstrate that holoenzyme containing RI beta activates at lower concentrations of cAMP compared to other forms of cAPK. Thus, neurons that induce RI beta expression may become more sensitive to subsequent hormonal signals and maintain more long-term phosphorylation events. To further elucidate the function of this novel protein, we have begun to investigate its gene. Here we report the isolation of the mouse RI beta promoter as determined by S1 nuclease analysis and transgenic mouse expression. A beta-galactosidase fusion gene containing 1.5 kilobases of 5'-nontranscribed RI beta DNA and 2 kilobases of intron 1 was expressed preferentially in the cortex and hippocampus of the brain and within the spinal cord. In addition to mimicking the location of endogenous RI beta expression, the transgene was activated at a similar time (embryonic day 11.5) during mouse fetal development. Isolation of the RI beta promoter will help identify the elements that direct transcription in a subset of neurons and illuminate the physiological conditions that may regulate RI beta expression. This promoter can also be used to target the expression of wild type and mutant cAPK subunit genes in order to investigate synaptic plasticity in animals.

Animals↗
PubMed2005

Heptaspanning membrane receptors and cytoskeletal/scaffolding proteins: focus on adenosine, dopamine, and metabotropic glutamate receptor function.

Most cellular functions are mediated by multiprotein complexes. In neurons, these complexes are directly involved in the proper neuronal transmission, which is responsible for phenomena like learning, memory, and development. In recent years studies based on two-hybrid screens and proteomic, biochemical, and cell biology approaches have shown that intracellular domains of G protein-coupled receptors (GPCRs) or heptaspanning membrane receptors (HSMRs) interact with intracellular proteins. These interactions are the basis of a protein network associated with these receptors, which includes scaffolding proteins containing one or several PDZ (postsynaptic-density-95/discs-large/zona occludens-1) domains, signaling proteins, and proteins of the cytoskeleton. The present article is focused on the emerging evidence for interactions of adenosine, dopamine, and metabotropic glutamate receptors, with scaffolding and cytoskeletal proteins that play a role in the targeting and anchoring of these receptors to the plasma membrane, thus contributing to neuronal development and plasticity. Finally, given the complexity of neurological disorders such as ischemic stroke, Alzheimer's disease, and epilepsy, exploitation of these HSMR-associated interactions might prove to be efficient in the treatment of such disorders.

Animals↗
PubMed1989

[Detection of donor specific cytotoxic T lymphocyte activity in lung grafted mongrel dogs].

Cytotoxic activity against donor skin fibroblasts in peripheral blood mononuclear cells was evaluated by using 10 mongrel dogs with left lung allografts and the results obtained herein were as follows. 1) Culture of skin fibroblasts primarily separated with collagenase and disperse was feasible to grow monolayers within several days to 1 weeks. Four hour responding time of mononuclear cells to targets was superior to 18 hour responding time, with the reproducibility of this assay under the 4 hour cocultivation between effectors and targets. 2) The effectors in this assay established in our laboratory were the cells nonadherent on plastics and nylon wool, suggesting T lymphocytes and donor specificity was confirmed by cold competition. 3) This donor specific cytotoxic activity derived from T lymphocytes was steeply elevated 4 to 8 days postoperatively with the average of 6 days in rejecting lung allografts and histologic examination revealed edema and fibrin-like substance in alveolar space. Cyclosporin A, however, could remarkably suppress its activity and grafted lung maintained function. In conclusion, the effectors in cytotoxic activity against donor skin fibroblasts in lung allografted mongrel dogs developed in our laboratory revealed as donor specific cytotoxic T lymphocytes and this assay is very useful to demonstrate rejection, the effect of immunosuppressive drugs and the differentiation between rejection and infection.

Animals↗
PubMed1998

Neurite outgrowth from bipolar and horizontal cells after experimental retinal detachment.

PURPOSE: To study the responses of horizontal cells and rod bipolar cells, the second-order neurons in the retina, to the degeneration induced by experimental retinal detachment. METHODS: Retinas from the eyes of domestic cats were examined 1, 3, 7, and 28 days after detachment using immunocytochemical and electron microscopic analyses. Retinal sections were labeled with antibodies to synaptophysin, calbindin D, and protein kinase C (PKC), proteins that serve as markers for synaptic terminals, horizontal cells, and rod bipolar cells, respectively. RESULTS: Beginning 1 day after detachment, the outer plexiform layer becomes disorganized and synaptophysin-labeled photoreceptor terminals are detected among the cell bodies of photoreceptors in the outer nuclear layer (ONL). At the same time, horizontal and rod bipolar cell processes grow into the ONL. In some cases, these processes contact photoreceptor terminals that have withdrawn deep into the ONL. Double-labeling experiments with antibodies to glial fibrillary acidic protein (Müller cell labeling) and phosphodiesterase gamma (cone labeling) demonstrate that the calbindin D- and PKC-positive neurite outgrowths are not derived from either Müller cells or cone photoreceptors. CONCLUSIONS: Horizontal and rod bipolar cell processes lengthen after retinal detachment, perhaps in response to a withdrawal of their presynaptic targets, the photoreceptor synaptic terminals. This apparent attempt to maintain synaptic contact after injury demonstrates a plasticity in the adult retina that may be of importance for the recovery of vision in human patients.

Animals↗
PubMed1998

Induction of interleukin-1 associated with compensatory dopaminergic sprouting in the denervated striatum of young mice: model of aging and neurodegenerative disease.

Young mice challenged with the neurotoxin 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP), which selectively destroys the substantia nigra dopaminergic neurons in the midbrain, exhibit spontaneous recovery of dopaminergic nerve terminals. However, such recovery becomes attenuated with age. Here we report that newly sprouted fibers originate from spared dopaminergic neurons in the ventral tegmental area. We found that interleukin-1 (IL-1), an immune response-generated cytokine that can enhance dopaminergic sprouting when exogenously applied, increased dramatically in the denervated striatum of young mice (2 months) compared with middle-aged mice (8 months) after MPTP treatment. Young mice displayed a maximal 500% induction of IL-1alpha synthesis that remained elevated for several weeks in the dorsal and ventral striatum, whereas middle-aged mice exhibited a modest 135% induction exclusively in the dorsal striatum for a week. IL-1alpha immunoreactivity was localized in GFAP-immunoreactive hypertrophied astrocytes and neurons within the denervated striatum of young mice. However, no induction of IL-1alpha mRNA was seen in the midbrain in either age group despite glial activation. Because we have reported that IL-1 can regulate astroglia-derived dopaminergic neurotrophic factors, it was surprising that no changes were observed in acidic and basic fibroblast growth factor or glial cell line-derived neurotrophic factor mRNA levels associated with MPTP-induced plasticity of dopaminergic neurons in the striatum of young mice. Interestingly, we found that dopaminergic neurons express IL-1 receptors, thus suggesting that IL-1alpha could directly act as a target-derived dopaminergic neurotrophic factor to initiate or enhance the sprouting of dopaminergic axonal terminals. These findings strongly suggest that IL-1alpha could play an important role in MPTP-induced plasticity of dopaminergic neurons.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1997

Increased expression of neuronal nitric oxide synthase in bladder afferent and spinal neurons following spinal cord injury.

Changes in the distribution of neuronal nitric oxide synthase immunoreactivity (NOS-IR) after chronic (5-6 weeks) spinal cord injury (SCI) were examined in bladder afferent and spinal neurons in the region of the sacral parasympathetic nucleus (SPN) in the L6-S1 spinal segments. Bladder afferent neurons in the L1, L2, L6 and S1 dorsal root ganglia (DRG) were identified by retrograde axonal transport following injection of fluorogold (FG) into the urinary bladder. A differential distribution of NOS-IR was detected in DRG cells at different segmental levels of spinal cord intact animals with significantly greater numbers of NOS-IR cells present in thoracic (T8, T12; 30-40 NOS-IR cell profiles/section) and rostral lumbar (L1) DRGs (18 NOS-IR cell profiles/ section) compared to caudal lumbosacral (L5-S1) DRGs (0.2-0.4 NOS-IR cell profiles/section). A significant increase in the number of NOS-IR cells was detected in the L6-S1 DRG (p < or = 0.001; 12-20 NOS-IR cell profiles/section) and in the L1-L2 DRG (15-40 NOS-IR cell profiles/section) but not in the L5 DRG following SCI. In these ganglia, an average of 41.2 +/- 7.8% (L6) and 36.3 +/- 0.9% (S1) of FG-labeled bladder afferent neurons were NOS-IR. In contrast, in spinal cord intact animals, no FG-labeled bladder afferent neurons were NOS-IR. Following SCI, NOS-IR fibers were detected along the lateral edge of the dorsal horn extending from Lissauer's tract to the region of the SPN (lateral collateral pathway of Lissauer) of the L6 and S1 spinal segments. These NOS-IR fibers were not detected in adjacent spinal segments (L5, S2). SCI also significantly (p < or = 0.001) increased the number of spinal neurons in the region of the SPN (presumptive preganglionic neurons) in the L6-S1 spinal segments exhibiting NOS-IR. These results indicate that NOS-IR in bladder afferent and spinal neurons is plastic and can be up-regulated by chronic SCI. Changes in the neurochemical properties of these neurons after SCI may be mediated by pathological changes in the target organ (i.e., urinary bladder) and/or spinal cord.

Animals↗
PubMedDate not supplied

Insulin-like growth factors as mediators of functional plasticity in the adult brain.

Insulin-like growth factors (IGFs) are present in the brain throughout life. While their role as modulators of brain growth and differentiation during development is becoming apparent, their possible involvement in adult brain function is less known. Nevertheless, accumulating evidence indicates a role for IGFs in brain plasticity processes. Specifically, IGFs modulate synaptic efficacy by regulating synapse formation, neurotransmitter release and neuronal excitability. IGFs also provide constant trophic support to target cells in the brain and in this way maintain appropriate neuronal function. Pathological dearrangement of this trophic input may lead to brain disease. Molecular targets of the IGFs in the adult brain may include pre- and post-synaptic proteins involved in synaptic contacts, membrane channels, neurite-guiding molecules, extracellular matrix components and glial-derived intercellular messengers. Future studies on the role of IGFs in the adult brain may help unravel the relationship between neuronal plasticity and brain disease.

Adult↗
PubMed2005

Conformational constraint as a means for understanding RNA-aminoglycoside specificity.

The lack of high RNA target selectivity displayed by aminoglycoside antibiotics results from both their electrostatically driven binding mode and their conformational adaptability. The inherent flexibility around their glycosidic bonds allows them to easily assume a variety of conformations, permitting them to structurally adapt to diverse RNA targets. This structural promiscuity results in the formation of aminoglycoside complexes with diverse RNA targets in which the antibiotics assume distinct conformations. Such differences suggest that covalently linking individual rings in an aminoglycoside could reduce its available conformations, thereby altering target selectivity. To explore this possibility, conformationally constrained neomycin and paromomycin analogues designed to mimic the A-site bound aminoglycoside structure have been synthesized and their affinities to the TAR and A-site, two therapeutically relevant RNA targets, have been evaluated. As per design, this constraint has minimal deleterious effect on binding to the A-site. Surprisingly, however, preorganizing these neomycin-class antibiotics into a TAR-disfavored structure has no deleterious effect on binding to this HIV-1 RNA sequence. We rationalize these observations by suggesting that the A-site and HIV TAR possess inherently different selectivities toward aminoglycosides. The inherent plasticity of the TAR RNA, coupled to the remaining flexibility within the conformationally constrained analogues, makes this RNA site an accommodating target for such polycationic ligands. In contrast, the deeply encapsulating A-site is a more discriminating RNA target. These observations suggest that future design of novel target selective RNA-based therapeutics will have to consider the inherent "structural" selectivity of the RNA target and not only the selectivity patterns displayed by the low molecular weight ligands.

Aminoglycosides↗
PubMed2006

Synapse formation and plasticity: recent insights from the perspective of the ubiquitin proteasome system.

The formation of synaptic connections during the development of the nervous system requires the precise targeting of presynaptic and postsynaptic compartments. Furthermore, synapses are continually modified in the brain by experience. Recently, the ubiquitin proteasome system has emerged as a key regulator of synaptic development and function. The modification of proteins by ubiquitin, and in many cases their subsequent proteasomal degradation, has proven to be an important mechanism to control protein stability, activity and localization at synapses. Recent work has highlighted key questions of the UPS during the development and remodeling of synaptic connections in the nervous system.

Animals↗
PubMedDate not supplied

Estrogen: a multifunctional messenger to nigrostriatal dopaminergic neurons.

Gonadal steroids affect a wide variety of functions in the mammalian brain ranging from the regulation of neuroendocrine systems and the modulation of behavior to the stimulation of differentiation and plasticity of distinct neuronal populations and circuits. The last decades have also demonstrated that estrogen serves as a neuroprotective factor for distinct neurodegenerative disorders. Such neuroprotective effects of estrogen are most obvious for Parkinson's and Alzheimer's disease. Despite this knowledge, little is known about the mechanisms and cellular targets by that estrogen might elicit its protective influence. In the past, we have intensively studied the effects of estrogen on midbrain dopaminergic neurons which represent the most affected cell population during Parkinson's disease. These studies were mainly performed on developing dopaminergic cells and revealed that estrogen is an important regulator of plasticity and function of this neuronal phenotype. Precisely, we found that dopaminergic neurons are direct targets for estrogen and that estrogen stimulates neurite extension/branching and the expression of tyrosine hydroxylase, the key enzyme in dopamine synthesis. Together with other in vivo studies, we might draw the conclusion that estrogen is required for the plasticity and activity of the developing and adult nigrostriatal system. The presence of the estrogen-synthesizing enzyme aromatase within the nigrostriatal system further supports this idea. Surprisingly, estrogen effects on nigrostriatal cell function are not only transmitted by classical nuclear estrogen receptors but also depend on nonclassical estrogen actions mediated through putative membrane receptors coupled to diverse intracellular signaling cascades. In the future, it has to be elucidated whether nonclassical mechanisms besides genomic actions also contribute to estrogen-mediated neuroprotection in the adult CNS.

Animals↗
PubMed2005

A modular concept of phenotypic plasticity in plants.

Based on empirical evidence from the literature we propose that, in nature, phenotypic plasticity in plants is usually expressed at a subindividual level. While reaction norms (i.e. the type and the degree of plant responses to environmental variation) are a property of genotypes, they are expressed at the level of modular subunits in most plants. We thus contend that phenotypic plasticity is not a whole-plant response, but a property of individual meristems, leaves, branches and roots, triggered by local environmental conditions. Communication and behavioural integration of interconnected modules can change the local responses in different ways: it may enhance or diminish local plastic effects, thereby increasing or decreasing the differences between integrated modules exposed to different conditions. Modular integration can also induce qualitatively different responses, which are not expressed if all modules experience the same conditions. We propose that the response of a plant to its environment is the sum of all modular responses to their local conditions plus all interaction effects that are due to integration. The local response rules to environmental variation, and the modular interaction rules may be seen as evolving traits targeted by natural selection. Following this notion, whole-plant reaction norms are an integrative by-product of modular plasticity, which has far-reaching methodological, ecological and evolutionary implications.

Adaptation, Physiological↗
PubMed2002

H-channels in epilepsy: new targets for seizure control?

Hyperpolarization-activated cation channels (h-channels) are key regulators of neuronal excitation and inhibition, and have a rich diversity of subunit composition, distribution, modulation and function. Recent results indicate that the behavior of h-channels can be altered significantly by seizures. The activity-dependent, short-term and long-term plasticity of h-channels can, in turn, modulate neuronal excitability. The reciprocal interactions between neuronal activity and h-channels indicate that these ion channels could be promising novel targets for anti-epileptic therapies.

Anticonvulsants↗
PubMed1999

Metabolic and morphological stability of motoneurons in response to chronically elevated neuromuscular activity.

The purpose of this study was to determine the plasticity of spinal motoneuron size and succinate dehydrogenase activity in response to increased levels of neuromuscular activation and/or increased target size. The plantaris muscles of adult rats were functionally overloaded for one or 10 weeks via the removal of the soleus and gastrocnemius muscles bilaterally. In addition, one group of functionally overloaded rats at each time period was trained daily (1 h/day) on a treadmill. The plantaris muscle on one side in each rat was injected with the fluorescent tracer Nuclear Yellow two days prior to the end of the study to retrogradely label the associated motor pool. At one week, the plantaris weight was increased compared to control, whereas there was no change in motoneuron size. Succinate dehydrogenase activity was unaffected in either the muscle or motoneurons. At 10 weeks, the plantaris muscle weight was larger and the succinate dehydrogenase activity lower in the functionally overloaded rats compared to age-matched controls. Training further increased the hypertrophic response, whereas the succinate dehydrogenase activity returned to control levels. In contrast, mean motoneuron size and succinate dehydrogenase activity were similar among the three groups. These data indicate that overload of a specific motor pool, involving both an increase in activation and an increase in target size, had a minimal effect on the size or the oxidative potential of the associated motoneurons. Thus, it appears that the spinal motoneurons, unlike the muscle fibers, are highly stable over a wide range of levels of chronic neuromuscular activity.

Animals↗
PubMed2002

Testing the role of the cell-surface molecule Thy-1 in regeneration and plasticity of connectivity in the CNS.

Thy-1 is a cell-surface signaling molecule of the Ig superfamily implicated in the regulation of neurite outgrowth, synaptic function and plasticity. There is, however, no consensus as to its precise function in the nervous system, and it remains unclear or untested as to what its role is in the development, maintenance and plasticity of neuronal connectivity in the intact brain and whether it is essential for any of the purported functions which have been attributed to it based largely on in vitro bioassays. Here, we have engineered transgenic mice with a targeted deletion of the Thy-1 gene and, after characterizing the development of their corticospinal and thalamocortical pathways, subjected them at adulthood to paradigms of axonal regeneration and plasticity which can be readily induced during development. Quantitative analyses of the brains and spinal cords of adult null mutants showed normal cellular organization, normal anatomical features of the corticospinal and thalamocortical pathways, and basic neurophysiological properties of thalamocortical synaptic transmission which were quantitatively indistinguishable from wild-type mice. Despite the absence of Thy-1, corticospinal axons in adult mutants failed to exhibit overt regeneration following spinal cord lesion; likewise, the terminal arbors of ventrobasal thalamocortical axons also failed to reorganize in adult barrel cortex in response to whisker cautery, although they did so during a developmental critical period identical to that displayed by wild-type mice.Taken together, these results suggest that Thy-1 is not essential for the normal development and maintenance of major axon pathways and functional synaptic connections, nor would it appear to be critically important for inhibiting or promoting axonal growth, regeneration and plasticity in the developing and mature CNS.

Afferent Pathways↗
PubMed2002

Pluripotent stem cells--model of embryonic development, tool for gene targeting, and basis of cell therapy.

Embryonic stem (ES) cells are pluripotent cell lines with the capacity of self-renewal and a broad differentiation plasticity. They are derived from pre-implantation embryos and can be propagated as a homogeneous, uncommitted cell population for an almost unlimited period of time without losing their pluripotency and their stable karyotype. Murine ES cells are able to reintegrate fully into embryogenesis when returned into an early embryo, even after extensive genetic manipulation. In the resulting chimeric offspring produced by blastocyst injection or morula aggregation, ES cell descendants are represented among all cell types, including functional gametes. Therefore, mouse ES cells represent an important tool for genetic engineering, in particular via homologous recombination, to introduce gene knock-outs and other precise genomic modifications into the mouse germ line. Because of these properties ES cell technology is of high interest for other model organisms and for livestock species like cattle and pigs. However, in spite of tremendous research activities, no proven ES cells colonizing the germ line have yet been established for vertebrate species other than the mouse (Evans and Kaufman, 1981; Martin, 1981) and chicken (Pain et al., 1996). The in vitro differentiation capacity of ES cells provides unique opportunities for experimental analysis of gene regulation and function during cell commitment and differentiation in early embryogenesis. Recently, pluripotent stem cells were established from human embryos (Thomson et al., 1998) and early fetuses (Shamblott et al., 1998), opening new scenarios both for research in human developmental biology and for medical applications, i.e. cell replacement strategies. At about the same time, research activities focused on characteristics and differentiation potential of somatic stem cells, unravelling an unexpected plasticity of these cell types. Somatic stem cells are found in differentiated tissues and can renew themselves in addition to generating the specialized cell types of the tissue from which they originate. Additional to discoveries of somatic stem cells in tissues that were previously not thought to contain these kinds of cells, they also appear to be capable of developing into cell types of other tissues, but have a reduced differentiation potential as compared to embryo-derived stem cells. Therefore, somatic stem cells are referred to as multipotent rather than pluripotent. This review summarizes characteristics of pluripotent stem cells in the mouse and in selected livestock species, explains their use for genetic engineering and basic research on embryonic development, and evaluates their potential for cell therapy as compared to somatic stem cells.

Animals↗