The response of the brachial ventral horn of Xenopus laevis to forelimb amputation during development

Development ◽  
1976 ◽  
Vol 36 (3) ◽  
pp. 453-468
Author(s):  
Joanne E. Fortune ◽  
Antonie W. Blackler
Keyword(s):  
Xenopus Laevis ◽  
Normal Development ◽  
Developmental Stages ◽  
Neuronal Degeneration ◽  
Neuronal Loss ◽  
Cell Loss ◽  
Cell Number ◽  
Ventral Horn ◽  
Cell Degeneration ◽  
Cell Numbers

The normal development of the brachial ventral horn of the frog Xenopus laevis and the response of the brachial ventral horn to complete forelimb extirpation at five developmental stages were assessed histologically. Differentiation of brachial ventral horn neurons occurred in pre-metamorphic tadpoles between stages 52/53 and 57. Mean cell number in the brachial ventral horn reached a peak of 2576 (S.E.M. = ±269, n = 2) per side of the spinal cord at stage 55 and decreased to 1070 (S.E.M. = ± 35, n =7) by the end of metamorphosis. Cell degeneration was presumed to be the mode of cell loss since it was most prevalent during the period of rapid decrease in cell numbers. The response of the ventral horn to forelimb removal varied with the stage of the animal at amputation. Following amputation at stage 52/53 or 54 the ipsilateral ventral horn neurons appeared less differentiated than those on the controlside and a rapid cell loss of about 80 % occurred on the operated side. These effects occurred more rapidly after ablation at stage 54 than at stage 52/53. Amputation at stage 58, 61, or 66 caused chromatolysis in the ventral horn, a period of relative cell excess on the operated side, and a delayed neuronal loss of 32–66%. It was concluded that excess cell degeneration accounted for cell loss and that suppression of normal neuronal degeneration caused the relative cell excess on the operated side. The data indicate that the brachial ventral horn was indifferent to the periphery before stage 54, was quickly affected by limb removal between stages 54 and 58, and by stage 58 had entered a phase in which a delay preceded cell death. No forelimb regeneration occurred.

A quantitative study of the growth and development of the ventral root in normal and experimental conditions

Development ◽  
1974 ◽  
Vol 32 (3) ◽  
pp. 819-833
Author(s):  
M. C. Prestige ◽  
Margaret A. Wilson
Keyword(s):  
Normal Development ◽  
Cell Number ◽  
Ventral Horn ◽  
Ventral Root ◽  
Limb Bud ◽  
Experimental Conditions ◽  
Collateral Sprouting ◽  
Cell Counts ◽  
Ventral Roots ◽  
Fibre Loss

1. The development of the ventral root (VR) in Xenopus has been studied by electron microscopy. Total fibre counts, and counts of classes of fibres were made from large photomontages of the whole of VR 9 at × 15000. 2. The total number of fibres in the root shows the same pattern of initial rise, peak, and subsequent decline that previous ventral horn (VH) cell counts had shown, The two curves overlay each other initially, but after the decline, there were apparently more cells than fibres. 3. Promyelin and myelin formation was seen at the time of the decline. There was no evidence that dying axons had started to myelinate. 4. In some animals the limb-bud was removed at the time of its first penetration by nerve fibres. The ventral roots developed normally for a week, but thereafter fibre loss was accentuated, advanced and more profound, so that after another week, no fibres were left. In these roots, no promyelin or myelin was formed. 5. In other animals, it was shown that there is no evidence for collateral sprouting in the ventral roots during normal development. 6. It is argued that the axons which die in normal development have already reached the limb-bud. 7. The correspondence between axon and cell number is discussed.

scholarly journals Lovastatin reduces neuronal cell death in hippocampal CA1 subfield after pilocarpine-induced status epilepticus: preliminary results

2005 ◽  
Vol 63 (4) ◽  
pp. 972-976 ◽  
Author(s):  
Pauline Rangel ◽  
Roberta Monterazzo Cysneiros ◽  
Ricardo Mario Arida ◽  
Marly de Albuquerque ◽  
Diego Basile Colugnati ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Seizure Activity ◽  
Hippocampal Formation ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neuronal Loss ◽  
Cell Loss ◽  
Cell Number ◽  
Control Group ◽  
Cell Counts

OBJECTIVE: To further characterize the capacity of lovastatin to prevent hippocampal neuronal loss after pilocarpine-induced status epilepticus (SE) METHOD: Adult male Wistar rats were divided into four groups: (A) control rats, received neither pilocarpine nor lovastatin (n=5); (B) control rats, received just lovastatin (n=5); (C) rats that received just pilocarpine (n=5); (D) rats that received pilocarpine and lovastatin (n=5). After pilocarpine injection (350mg/kg, i.p.), only rats that displayed continuous, convulsive seizure activity were included in our study. Seizure activity was monitored behaviorally and terminated with an injection of diazepam (10 mg/kg, i.p.) after 4 h of convulsive SE. The rats treated with lovastatin received two doses of 20mg/kg via an oesophagic probe immediately and 24 hours after SE induction. Seven days after pilocarpine-induced SE, all the animals were perfused and their brains were processed for histological analysis through Nissl method. RESULTS: The cell counts in the Nissl-stained sections performed within the hippocampal formation showed a significant cell loss in rats that received pilocarpine and presented SE (CA1= 26.8 ± 13.67; CA3= 38.1 ± 7.2; hilus= 43.8 ± 3.95) when compared with control group animals (Group A: CA1= 53.2 ± 9.63; CA3= 63.5 ± 13.35; hilus= 59.08 ± 10.24; Group B: CA1= 74.3 ± 8.16; CA3= 70.1 ± 3.83; hilus= 70.6 ± 5.10). The average neuronal cell number of CA1 subfield of rats that present SE and received lovastatin (44.4 ± 17.88) was statically significant increased when compared with animals that just presented SE. CONCLUSION: Lovastatin exert a neuroprotective role in the attenuation of brain damage after SE.

scholarly journals Loss of the golgin GM130 causes Golgi disruption, Purkinje neuron loss, and ataxia in mice

2016 ◽  
Vol 114 (2) ◽  
pp. 346-351 ◽  
Author(s):  
Chunyi Liu ◽  
Mei Mei ◽  
Qiuling Li ◽  
Peristera Roboti ◽  
Qianqian Pang ◽  
...  
Keyword(s):  
Golgi Apparatus ◽  
Purkinje Cell ◽  
Secretory Pathway ◽  
Neuronal Degeneration ◽  
Cell Loss ◽  
Cell Number ◽  
Causative Role ◽  
Neurodegenerative Process ◽  
And Function

The Golgi apparatus lies at the heart of the secretory pathway where it is required for secretory trafficking and cargo modification. Disruption of Golgi architecture and function has been widely observed in neurodegenerative disease, but whether Golgi dysfunction is causal with regard to the neurodegenerative process, or is simply a manifestation of neuronal death, remains unclear. Here we report that targeted loss of the golgin GM130 leads to a profound neurological phenotype in mice. Global KO of mouse GM130 results in developmental delay, severe ataxia, and postnatal death. We further show that selective deletion of GM130 in neurons causes fragmentation and defective positioning of the Golgi apparatus, impaired secretory trafficking, and dendritic atrophy in Purkinje cells. These cellular defects manifest as reduced cerebellar size and Purkinje cell number, leading to ataxia. Purkinje cell loss and ataxia first appear during postnatal development but progressively worsen with age. Our data therefore indicate that targeted disruption of the mammalian Golgi apparatus and secretory traffic results in neuronal degeneration in vivo, supporting the view that Golgi dysfunction can play a causative role in neurodegeneration.

scholarly journals SYSTEMIC KANAMYCIN TREATMENT HAS NO EFFECT ON CELL NUMBERS IN THE MOUSE UTRICULAR MACULA

2011 ◽  
Vol 24 (2) ◽  
pp. 69 ◽  
Author(s):  
Mette Kirkegaard ◽  
Stig Å Severinsen ◽  
Lise Wogensen ◽  
Jens R Nyengaard
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Caspase 3 ◽  
Cell Loss ◽  
Supporting Cell ◽  
Cell Number ◽  
Sensory Epithelium ◽  
Positive Staining ◽  
Survival Times ◽  
Cell Numbers

The aim of the present study is to estimate the total number of the sensory hair cells (chalice innervated and bouton innervated) and supporting cells in the mouse utricular sensory epithelium at two different time points after systemic kanamycin treatment. Mice were given two daily subcutaneous injections of kanamycin (600 or 900 mg/kg) for 15 consecutive days and allowed to survive either 1 or 3 weeks after end of treatment. Cell numbers were estimated using a physical fractionator. Paraffin-embedded tissue was immunohistochemically stained for active caspase-3 in order to detect apoptosis. There was no change in hair cell or supporting cell number after treatment with kanamycin and the survival time had no effect. Although no positive staining for caspase-3 was seen, hair cells with swollen chalices and dark stained nuclei were observed in the sensory epithelium of the treated animals, indicating some effect of the treatment. In conclusion, the dosing regime and survival times studied here are not sufficient to induce hair cell loss in the mouse utricle.

The control of cell number in the lumbar ventral horns during the development of Xenopus laevis tadpoles

Development ◽  
1967 ◽  
Vol 18 (3) ◽  
pp. 359-387
Author(s):  
M. C. Prestige
Keyword(s):  
Xenopus Laevis ◽  
Cell Number ◽  
Ventral Horn ◽  
Early Evidence ◽  
Motor Neurones

The developing limb has been amputated by many workers in several species and in each case the number of surviving motor neurones on the side of the operation was less than normal. This may be observed among the mammals (e.g. Barron, 1945), birds (e.g. Hamburger, 1934), urodeles (e.g. Stultz, 1942), and anurans (e.g. May, 1930). The loss of motor neurones after amputation in adults appears to have been first noticed by Vulpian (1868) and Johnson & Clarke (1868). The early evidence is reviewed by Sherrington (1893) and the later by Piatt (1948). The control that the developing leg has over proliferation, migration, maintenance and degeneration of ventral horn cells has been most completely analysed in the chick, notably by Hamburger (1934, 1939, 1958), Hamburger & Keefe (1944), Bueker (1943, 1944, 1945a), Barron (1946, 1948), Mottet (1952) and Mottet & Barron (1954). Less is known about this in Anura.

Experimental studies on the organization of the preimplantation mouse embryo

Development ◽  
1972 ◽  
Vol 28 (2) ◽  
pp. 255-261
Author(s):  
M. Susan Stern
Keyword(s):  
Normal Development ◽  
Developmental Stages ◽  
Experimental Studies ◽  
Subsequent Development ◽  
Cell Numbers ◽  
Preimplantation Mouse Embryo ◽  
Preimplantation Mouse ◽  
Partial Dissociation ◽  
Complete Dissociation ◽  
Regulative Capacity

The reaggregation and subsequent development of a range of disaggregated embryos has been examined: 1. Following complete dissociation embryos from 8-cell to late blastocyst reaggregated and developed to form morphologically normal blastocysts, even when blastomeres of two different developmental stages were present in the reaggregate. 2. Dissociated mid-blastocysts could also reaggregate to form blastocysts but more commonly they produced vesiculated masses, as did disaggregates of late blastocysts. 3. Successful fusion of pairs of mid or late blastocysts, with full cell numbers, was achieved following partial dissociation. These results are discussed in relation to blastocyst formation. It is suggested that even if the embryo derives polarity from the oocyte it is not functionally essential to normal development in view of the remarkable regulative capacity of the egg.

scholarly journals Role of MHC-I Expression on Spinal Motoneuron Survival and Glial Reactions Following Ventral Root Crush in Mice

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 483 ◽  
Author(s):  
Luciana Politti Cartarozzi ◽  
Matheus Perez ◽  
Frank Kirchhoff ◽  
Alexandre Leite Rodrigues de Oliveira
Keyword(s):  
Neuronal Degeneration ◽  
Neuronal Loss ◽  
Cell Loss ◽  
Surface Expression ◽  
Ventral Root ◽  
Synaptic Loss ◽  
Mhc I ◽  
Glial Reactions ◽  
Over Time

Lesions to the CNS/PNS interface are especially severe, leading to elevated neuronal degeneration. In the present work, we establish the ventral root crush model for mice, and demonstrate the potential of such an approach, by analyzing injury evoked motoneuron loss, changes of synaptic coverage and concomitant glial responses in β2-microglobulin knockout mice (β2m KO). Young adult (8–12 weeks old) C57BL/6J (WT) and β2m KO mice were submitted to a L4–L6 ventral roots crush. Neuronal survival revealed a time-dependent motoneuron-like cell loss, both in WT and β2m KO mice. Along with neuronal loss, astrogliosis increased in WT mice, which was not observed in β2m KO mice. Microglial responses were more pronounced during the acute phase after lesion and decreased over time, in WT and KO mice. At 7 days after lesion β2m KO mice showed stronger Iba-1+ cell reaction. The synaptic inputs were reduced over time, but in β2m KO, the synaptic loss was more prominent between 7 and 28 days after lesion. Taken together, the results herein demonstrate that ventral root crushing in mice provides robust data regarding neuronal loss and glial reaction. The retrograde reactions after injury were altered in the absence of functional MHC-I surface expression.

scholarly journals Intrathecal Magnesium Sulfate Administration at the Time of Experimental Ischemia Improves Neurological Functioning by Reducing Acute and Delayed Loss of Motor Neurons in the Spinal Cord

2008 ◽  
Vol 108 (1) ◽  
pp. 78-86 ◽  
Author(s):  
Walter S. Jellish ◽  
Xin Zhang ◽  
Kenneth E. Langen ◽  
Matthew S. Spector ◽  
Michael T. Scalfani ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Magnesium Sulfate ◽  
Motor Function ◽  
Neuronal Degeneration ◽  
Spinal Cord Ischemia ◽  
Recovery Period ◽  
Neuronal Loss ◽  
Ventral Horn ◽  
Lower Lumbar

Background In this study, the authors determined the effect of magnesium sulfate on intrathecal glutamate concentrations, hindlimb motor function, and histopathology after a transient episode of spinal cord ischemia. Methods Fifty-two New Zealand White rabbits underwent spinal cord ischemia for 30 min. Fifteen minutes before ischemia, animals received intrathecal magnesium sulfate (MgSO4) (3 mg/kg) or placebo (artificial cerebrospinal fluid). Intrathecal microdialysis samples were measured for glutamate using high-performance liquid chromatography. Neurologic function and spinal cord histopathology were assessed throughout the recovery period. Results Intrathecal glutamate levels in placebo-treated animals were higher after spinal cord ischemia compared with sham- and MgSO4-treated animals. MgSO4-treated animals had increased lower extremity motor function compared with the placebo group (64.7% vs 14.3%, P < 0.01). Histologic examination of placebo-treated animals revealed significant motor neuron cell loss at thoracolumbar levels by Day 7 (P < 0.05), whereas lower lumbar regions displayed significant neuron loss on Day 1. Spinal cords from MgSO4-treated animals exhibited less neuronal loss in lumbar regions. Similar effects were present in the thoracolumbar segments on Day 7. A significant correlation existed between diminished neuronal loss and hind leg movement (Tarlov score) and demonstrates that the neurologic outcome after MgSO4 treatment was related to lower lumbar ventral horn cell survival (r2 = 0.812, P < 0.001). Conclusions These results demonstrate that MgSO4 affords significant spinal cord motor neuron protection by diminishing acute neuronal loss at the foci of the ischemic injury (L3-L6) with delayed neuronal degeneration in adjacent spinal cord regions (T7-L2).

scholarly journals Neuroplastin expression is essential for hearing and hair cell PMCA expression

2021 ◽  
Author(s):  
Xiao Lin ◽  
Michael G. K. Brunk ◽  
Pingan Yuanxiang ◽  
Andrew W. Curran ◽  
Enqi Zhang ◽  
...  
Keyword(s):  
Hair Cell ◽  
White Noise ◽  
Hair Cells ◽  
Normal Development ◽  
Single Photon ◽  
Photon Emission ◽  
Auditory Brainstem ◽  
Outer Hair Cells ◽  
Emission Computed Tomography ◽  
Cell Degeneration

AbstractHearing deficits impact on the communication with the external world and severely compromise perception of the surrounding. Deafness can be caused by particular mutations in the neuroplastin (Nptn) gene, which encodes a transmembrane recognition molecule of the immunoglobulin (Ig) superfamily and plasma membrane Calcium ATPase (PMCA) accessory subunit. This study investigates whether the complete absence of neuroplastin or the loss of neuroplastin in the adult after normal development lead to hearing impairment in mice analyzed by behavioral, electrophysiological, and in vivo imaging measurements. Auditory brainstem recordings from adult neuroplastin-deficient mice (Nptn−/−) show that these mice are deaf. With age, hair cells and spiral ganglion cells degenerate in Nptn−/− mice. Adult Nptn−/− mice fail to behaviorally respond to white noise and show reduced baseline blood flow in the auditory cortex (AC) as revealed by single-photon emission computed tomography (SPECT). In adult Nptn−/− mice, tone-evoked cortical activity was not detectable within the primary auditory field (A1) of the AC, although we observed non-persistent tone-like evoked activities in electrophysiological recordings of some young Nptn−/− mice. Conditional ablation of neuroplastin in Nptnlox/loxEmx1Cre mice reveals that behavioral responses to simple tones or white noise do not require neuroplastin expression by central glutamatergic neurons. Loss of neuroplastin from hair cells in adult NptnΔlox/loxPrCreERT mice after normal development is correlated with increased hearing thresholds and only high prepulse intensities result in effective prepulse inhibition (PPI) of the startle response. Furthermore, we show that neuroplastin is required for the expression of PMCA 2 in outer hair cells. This suggests that altered Ca2+ homeostasis underlies the observed hearing impairments and leads to hair cell degeneration. Our results underline the importance of neuroplastin for the development and the maintenance of the auditory system.

Characterization of isolated bovine preantral follicles based on morphology, diameter and cell number

Zygote ◽  
2020 ◽  
Vol 28 (2) ◽  
pp. 154-159
Author(s):  
Juliana I. Candelaria ◽  
Anna C. Denicol
Keyword(s):  
Granulosa Cells ◽  
Developmental Stages ◽  
Assisted Reproductive Technologies ◽  
Reproductive Technologies ◽  
Cell Number ◽  
Culture Conditions ◽  
Preantral Follicles ◽  
Secondary Stage

SummaryPreantral follicles are a potential reservoir of oocytes to be used in assisted reproductive technologies. With the increasing interest in developing techniques to grow preantral follicles in vitro, and as the bovine emerges as an appropriate model species to understand human folliculogenesis, the establishment of an accurate classification of developmental stages is needed. Classification of bovine preantral follicles has been mostly based on histological analysis and estimation models, which may not translate well to correctly characterize preantral follicles isolated from the ovary. In this study, we classified bovine preantral follicles by morphology upon isolation, determined diameter and number of granulosa cells by direct counting, and compared our results with previous studies reporting bovine preantral follicle classification. Follicles were isolated via homogenization of ovary tissue and classified into primary, early secondary and secondary stage based on morphology and number of layers of granulosa cells. Diameter was individually measured and Hoechst 33342 was used as a nuclear stain to count granulosa cells. We found that follicles classified by morphology into primary, early secondary, and secondary had different mean diameter and cell number (P < 0.01); cell number and diameter were positively correlated, as were cell density and cell number in each developmental stage (P < 0.01). Results obtained here were mostly in agreement with previous classifications based on histological sections and on isolated follicles, with some discrepancies. The present data add accuracy to classification of bovine preantral follicles that is critical to optimize culture conditions to produce developmentally competent oocytes.

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