scholarly journals Chronic, episodic nicotine alters hypoglossal motor neuron function at a critical developmental time point in neonatal rats

eNeuro ◽  
2021 ◽  
pp. ENEURO.0203-21.2021
Author(s):  
Lila Buls Wollman ◽  
Ralph F. Fregosi
Keyword(s):  
Motor Neuron ◽  
Developmental Time ◽  
Neonatal Rats ◽  
Developmental Time Point ◽  
Neuron Function ◽  
Time Point

scholarly journals Sensitive periods in cognitive development: A mutualistic perspective

2020 ◽  
Author(s):  
Rogier Kievit
Keyword(s):  
Cognitive Development ◽  
Cognitive Abilities ◽  
Developmental Time ◽  
General Cognitive Ability ◽  
Small Individual ◽  
Cognitive Domains ◽  
Sensitive Periods ◽  
Developmental Time Point ◽  
Time Point ◽  
Do So

The theory of mutualism posits that general cognitive ability emerges, at least in part, due to positive reciprocal interaction between distinct cognitive abilities during development. In other words, cognitive abilities at a given developmental time point govern the rate of growth in other cognitive abilities. Moreover, this emerging field of work finds that the strength as well as the nature of these interactions differs during developmental time: In other words, there are sensitive periods when small individual differences may have especially pronounced, long-lasting consequences for cognitive development. Here I review the literature on mutualistic effects, and show how it can shed new light on sensitive periods. I do so by considering sensitive periods as periods where interactions between (cognitive) domains differ in strength and/or in kind.

scholarly journals Omega-3 Hastens and Omega-6 Delays the Progression of Neuropathology in a Murine Model of Familial ALS

2017 ◽  
Vol 11 (1) ◽  
pp. 84-91 ◽  
Author(s):  
Edward F. Boumil ◽  
Rishel Brenna Vohnoutka ◽  
Yuguan Liu ◽  
Sangmook Lee ◽  
Thomas B Shea
Keyword(s):  
Quality Of Life ◽  
Motor Neuron ◽  
Motor Function ◽  
Motor Neurons ◽  
Omega 3 ◽  
Self Medication ◽  
Familial Als ◽  
Neuron Function ◽  
The Impact

Background: Amyotrophic lateral sclerosis (ALS) is a progressive disease of motor neurons that has no cure or effective treatment. Any approach that could sustain minor motor function during terminal stages would improve quality of life. Objective: We examined the impact of omega-3 (Ω-3) and Ω-6, on motor neuron function in mice expressing mutant human superoxide dismutase-1 (SOD-1), which dominantly confers familial ALS and induces a similar sequence of motor neuron decline and eventual death when expressed in mice. Method: Mice received standard diets supplemented with equivalent amounts of Ω-3 and Ω-6 or a 10x increase in Ω-6 with no change in Ω-3 commencing at 4 weeks of age. Motor function and biochemical/histological parameters were assayed by standard methodologies. Results: Supplementation with equivalent Ω-3 and Ω-6 hastened motor neuron pathology and death, while 10x Ω-6 with no change in Ω-3 significantly delayed motor neuron pathology, including preservation of minor motor neuron function during the terminal stage. Conclusion: In the absence of a cure or treatment, affected individuals may resort to popular nutritional supplements such as Ω-3 as a form of “self-medication”. However, our findings and those of other laboratories indicate that such an approach could be harmful. Our findings suggest that a critical balance of Ω-6 and Ω-3 may temporarily preserve motor neuron function during the terminal stages of ALS, which could provide a substantial improvement in quality of life for affected individuals and their caregivers.

scholarly journals Identification of measures predictive of age of puberty onset in gilts

2019 ◽  
Vol 4 (1) ◽  
pp. 285-292 ◽  
Author(s):  
Kody L Graves ◽  
Bethany R Mordhorst ◽  
Elane C Wright ◽  
Benjamin J Hale ◽  
Kenneth J Stalder ◽  
...  
Keyword(s):  
Ovarian Development ◽  
Age At Onset ◽  
Developmental Time ◽  
Follicle Development ◽  
Central Hypothesis ◽  
Estrus Detection ◽  
The Mean ◽  
Puberty Onset ◽  
Time Point ◽  
Follicular Activity

Abstract A potential indicator of female lifetime productivity in swine is age of puberty, when a gilt achieves her first behavioral estrus. Follicular activity, as determined by tertiary follicle development, in prepubertal gilts begins during postnatal day (PND) 75 to 115. The central hypothesis of this study is that gilts demonstrating tertiary follicle development earlier in life, assessed using vulva size as a proxy, achieve puberty earlier in life compared with counterparts of a similar age and weight that lack tertiary follicle development. The objectives of this project were to identify a developmental time point when variation in ovarian development exists and to determine whether a relationship between the age prepubertal ovarian development and the age at onset of puberty exists. To accomplish this, 155 gilts of similar age (± 2 d) were weighed and vulva size measured on PND 75, 85, 95, 105, and 115. Vulva measures, including vulva width (VW), vulva length (VL), and vulva area (VA), were utilized as developmental proxies for follicular activity. At each time point, gilts (n = 10) were sacrificed and ovarian follicular activity recorded. In a subset of gilts (n = 105), estrus detection was conducted daily on PND days 126 to 200. Mean VA on PND 75, 85, 95, 105, and 115 was 596 ± 206, 683 ± 190, 864 ± 212, 1014 ± 228, and 1265 ± 252 mm2, respectively. Of the gilts demonstrating behavioral estrus, 28 were within PND 140 to 160, 36 between PND 161 to 180, 15 between PND 181 to 200, and 26 did not demonstrate estrus behavior within 200 d of age. All gilts euthanized at PND 75 lacked follicular activity as defined by having a minimum of 2 antral follicles per ovary, whereas 60%, 80%, 90%, and 100% demonstrated follicular activity on PND 85, 95, 105, and 115, respectively. Body weight at PND 75 and VW at PND 115 were correlated to age at first estrus (P < 0.05). Of the gilts whose VA was less than 1 SD from the mean on PND 95 (i.e., <652 mm2), 31% and 50% demonstrated their first behavioral estrus by PND 180 and 200, respectively. However, of gilts whose VA was within or greater than 1 SD of the mean (i.e., ≥652 mm2), 66% and 79% exhibited estrus prior to PND 180 and 200, respectively. These data support utilization of VA changes between 95 and 115 d of age as a useful tool to identify replacement gilts prior to puberty for inclusion into the sow herd.

scholarly journals Assessing Rat Forelimb and Hindlimb Motor Unit Connectivity as Objective and Robust Biomarkers of Spinal Motor Neuron Function

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Markus E. Harrigan ◽  
Angela R. Filous ◽  
Andrew P. Tosolini ◽  
Renee Morris ◽  
Jan M. Schwab ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Motor Unit ◽  
Compound Muscle Action Potential ◽  
Motor Units ◽  
Longitudinal Assessment ◽  
Muscle Contractility ◽  
Cross Sectional ◽  
Muscle Action Potential ◽  
Experimental Findings ◽  
Neuron Function

Abstract Sensitive and objective biomarkers of neuronal injury, degeneration, and regeneration can help facilitate translation of experimental findings into clinical testing. Whereas measures of upper motor neuron connectivity have been readily established, functional assessments of lower motor neuron (LMN) innervation of forelimb muscles are lacking. Compound muscle action potential (CMAP) and motor unit (MU) number estimation (MUNE) are well-established methods that allow longitudinal MU integrity monitoring in patients. In analogy we refined CMAP and MUNE methods for assessing spinal MU input in the rat forelimb and hindlimb. Repeated CMAP and MUNE recordings are robust (coefficients of variability: 4.5–11.3%), and MUNE measurements from forelimb wrist flexor muscles (415 ± 8 [SEM]) align with back-traced anatomical LMN counts (336 ± 16 [SEM]). For disease validation, cross-sectional blinded electrophysiological and muscle contractility measurements were obtained in a cohort of G93A SOD1 mutant overexpressing rats and compared with controls. Longitudinal assessment of mutant animals demonstrated progressive motor unit decline in the hindlimb to a greater extent than the forelimb. Hindlimb CMAP and MUNE demonstrated strong correlations with plantarflexion muscle contractility. Cross-species assessment of upper/fore- limb and lower/hind- limb motor units using objective electrophysiological CMAP and MUNE values as biomarkers will guide and improve bi-directional translation.

Mechanistic Insights of Astrocyte-Mediated Hyperactive Autophagy and Loss of Motor Neuron Function in SOD1L39R Linked Amyotrophic Lateral Sclerosis

2020 ◽  
Vol 57 (10) ◽  
pp. 4117-4133
Author(s):  
Chetan Singh Rajpurohit ◽  
Vivek Kumar ◽  
Arquimedes Cheffer ◽  
Danyllo Oliveira ◽  
Henning Ulrich ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Motor Neuron ◽  
Neuron Function ◽  
Lateral Sclerosis

scholarly journals Progressive Loss of Motor Neuron Function in Wasted Mice: Effects of a Spontaneous Null Mutation in the Gene for the eEF1A2 Translation Factor

2005 ◽  
Vol 64 (4) ◽  
pp. 295-303 ◽  
Author(s):  
Helen J. Newbery ◽  
Thomas H. Gillingwater ◽  
Permphan Dharmasaroja ◽  
Josephine Peters ◽  
Stephen B. Wharton ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Null Mutation ◽  
Translation Factor ◽  
Progressive Loss ◽  
Neuron Function

scholarly journals Identification of Novel Compounds That Increase SMN Protein Levels Using an Improved SMN2 Reporter Cell Assay

2012 ◽  
Vol 17 (4) ◽  
pp. 481-495 ◽  
Author(s):  
Jonathan J. Cherry ◽  
Matthew C. Evans ◽  
Jake Ni ◽  
Gregory D. Cuny ◽  
Marcie A. Glicksman ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Neurodegenerative Disorder ◽  
Muscular Atrophy ◽  
Full Length ◽  
Reporter Cell ◽  
Protein Levels ◽  
Smn2 Gene ◽  
Smn Protein ◽  
Neuron Function ◽  
Survival Of Motor Neuron

Spinal muscular atrophy (SMA) is a neurodegenerative disorder that is characterized by progressive loss of motor neuron function. It is caused by the homozygous loss of the SMN1 ( survival of motor neuron 1) gene and a decrease in full-length SMN protein. SMN2 is a nearly identical homolog of SMN1 that, due to alternative splicing, expresses predominantly truncated SMN protein. SMN2 represents an enticing therapeutic target. Increasing expression of full-length SMN from the SMN2 gene might represent a treatment for SMA. We describe a newly designed cell-based reporter assay that faithfully and reproducibly measures full-length SMN expression from the SMN2 gene. This reporter can detect increases of SMN protein by an array of compounds previously shown to regulate SMN2 expression and by the overexpression of proteins that modulate SMN2 splicing. It also can be used to evaluate changes at both the transcriptional and splicing level. This assay can be a valuable tool for the identification of novel compounds that increase SMN2 protein levels and the optimization of compounds already known to modulate SMN2 expression. We present here preliminary data from a high-throughput screen using this assay to identify novel compounds that increase expression of SMN2.

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