Influence of Physical Activity on Human Sensory Long-Term Potentiation

2015 ◽  
Vol 21 (10) ◽  
pp. 831-840 ◽  
Author(s):  
Nicola Smallwood ◽  
Meg J. Spriggs ◽  
Christopher S. Thompson ◽  
Carolyn C. Wu ◽  
Jeff P. Hamm ◽  
...  
Keyword(s):  
Physical Activity ◽  
Physical Fitness ◽  
High Activity ◽  
Long Term Potentiation ◽  
Self Report ◽  
Activity Group ◽  
Term Potentiation ◽  
The Impact ◽  
Low Activity

AbstractA growing body of literature has explored the influence of physical activity on brain structure and function. While the mechanisms of this relationship remain largely speculative, recent research suggests that one of the effects of physical exercise is an increase in synaptic long-term potentiation (LTP). This has not yet been explored directly in humans due to the difficulty of measuring LTP non-invasively. However, we have previously established that LTP-like changes in visual-evoked potentials (VEPs) can be measured in humans. Here, we investigated whether physical fitness status affects the degree of visual sensory LTP. Using a self-report measure of physical activity, participants were split into two groups: a high-activity group, and a low-activity group. LTP was measured and compared between the two groups using the previously established electroencephalography-LTP paradigm, which assesses the degree to which the N1b component of the VEP elicited by a sine grating is potentiated (enhanced) following a rapid “tetanic” presentation of that grating. Both groups demonstrated increased negativity in the amplitude of the N1b component of the VEP immediately after presentation of the visual “tetanus,” indicating potentiation. However, after a 30-min rest period, the N1b for the high-activity group remained potentiated while the N1b for the low-activity group returned to baseline. This study presents the first evidence for the impact of self-reported levels of physical activity on LTP in humans, and sheds light on potential neurological mechanisms underlying the relationship between physical fitness and cognition. (JINS, 2015, 21, 831–840)

scholarly journals Physical Activity Trajectories and Associated Changes in Physical Performance in Older Men: The MrOS Study

2020 ◽  
Vol 75 (10) ◽  
pp. 1967-1973
Author(s):  
Deepika R Laddu ◽  
Neeta Parimi ◽  
Katie L Stone ◽  
Jodi Lapidus ◽  
Andrew R Hoffman ◽  
...  
Keyword(s):  
Physical Activity ◽  
Grip Strength ◽  
High Activity ◽  
Physical Performance ◽  
Gait Speed ◽  
Functional Independence ◽  
Performance Measure ◽  
Least Square ◽  
Activity Group ◽  
Low Activity

Abstract Background Physical activity (PA) is important to maintaining functional independence. It is not clear how patterns of change in late-life PA are associated with contemporaneous changes in physical performance measures. Methods Self-reported PA, gait speed, grip strength, timed chair stand, and leg power were assessed in 3,865 men aged ≥ 65 years at baseline (2000–2002) and Year 7 (2007–2009). Group-based trajectory modeling, using up to four PA measures over this period, identified PA trajectories. Multivariate linear regression models (adjusted least square mean [95% confidence interval {CI}]) described associations between-PA trajectories and concurrent changes in performance. Results Three discrete PA patterns were identified, all with declining PA. Linear declines in each performance measure (baseline to Year 7) were observed across all three PA groups, but there was some variability in the rate of decline. Multivariate models assessing the graded response by PA trajectory showed a trend where the high-activity group had the smallest declines in performance while the low-activity group had the largest (p-for trend < .03). Changes in the high-activity group were the following: gait speed (−0.10 m/s [−0.12, −0.08]), grip strength (−3.79 kg [−4.35, −3.23]), and chair stands (−0.38 [−0.50, −0.25]), whereas changes in the low-activity group were the following: gait speed (−0.16 [−0.17, −0.14]), grip strength (−4.83 kg [−5.10, −4.55]), and chair stands (−0.53 [−0.59, −0.46]). Between-group differences in leg power trajectories across PA patterns were not significant. Conclusions Declines in functional performance were higher among those with lower PA trajectories, providing further evidence for the interrelationship between changes in PA and performance during old age.

scholarly journals Relationship between the intention–behavior gap and self-efficacy for physical activity during childhood

2018 ◽  
Vol 23 (1) ◽  
pp. 79-86 ◽  
Author(s):  
Tsunenori Isa ◽  
Yuya Ueda ◽  
Ryo Nakamura ◽  
Shogo Misu ◽  
Rei Ono
Keyword(s):  
Physical Activity ◽  
High Activity ◽  
Self Efficacy ◽  
Self Report ◽  
Physically Active ◽  
Education Interventions ◽  
Relationship Of ◽  
The Relationship ◽  
Low Activity ◽  
Actual Participation

This study investigated the relationship of a gap between the intent to be physically active and actual participation in physical activity (‘intention–behavior gap’) and self-efficacy for physical activity during childhood. A self-report questionnaire was used to collect information from 946 children from the fourth and sixth grades in Japan on self-efficacy, intention, and physical activity. Children with an intention–behavior gap (high intent–low activity or low intent–high activity) had higher self-efficacy scores than those with low intent and low activity (27.66 or 27.65 vs. 21.69; p < .001). They had lower self-efficacy scores than those with high intent and high activity (27.66 or 27.65 vs. 30.56; p < .001). Children with an intention–behavior gap had lower self-efficacy for physical activity than those who intended to be and were physically active. Such children may benefit from education interventions that focus on improving self-efficacy.

A comparison of physical activity, physical fitness levels, BMI and blood pressure of adults with intellectual disability, who do and do not take part in Special Olympics Ireland programmes: Results from the SOPHIE study

2017 ◽  
Vol 22 (2) ◽  
pp. 154-170 ◽  
Author(s):  
Denise Walsh ◽  
Sarahjane Belton ◽  
Sarah Meegan ◽  
Kirsty Bowers ◽  
Deidre Corby ◽  
...  
Keyword(s):  
Physical Activity ◽  
Blood Pressure ◽  
Intellectual Disability ◽  
Physical Fitness ◽  
Vigorous Physical Activity ◽  
Well Being ◽  
Self Report ◽  
Special Olympics ◽  
The Impact ◽  
Fitness Levels

People with an intellectual disability are less physically active, live more sedentary lives, have lower fitness levels and are more likely to be overweight or obese than the general population. No evidence exists on the impact of participation in Special Olympics Ireland (SOI) on physical activity and physical fitness levels. Adults with intellectual disabilities (16–64 years) were recruited from services and SOI clubs. Physical measures included waist circumference, height, weight, blood pressure, heart rate and 6-min walking test. Self-report questionnaires gathered data on physical activity levels. Actigraph (GT3X) accelerometers were used to gain an objective measure of physical activity. SOI participants accumulated more moderate to vigorous physical activity per day, had higher fitness levels and more positive health profile scores than those not taking part in SOI. SOI has the potential to make a positive difference to people’s physical health and subsequently their overall health and well-being.

scholarly journals Early low-level developmental arsenic exposure impacts mouse hippocampal synaptic function

2021 ◽  
Author(s):  
Karl F Foley ◽  
Daniel Barnett ◽  
Deborah A Cory-Slechta ◽  
Houhui Xia
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Arsenic Exposure ◽  
Long Term Potentiation ◽  
Epidemiological Studies ◽  
Synaptic Function ◽  
Learning Deficits ◽  
Term Potentiation ◽  
The Impact

Background: Arsenic is a well-established carcinogen known to increase all-cause mortality, but its effects on the central nervous system are less well understood. Recent epidemiological studies suggest that early life exposure to arsenic is associated with learning deficits and behavioral changes, and increased arsenic exposure continues to affect an estimated 200 million individuals worldwide. Previous studies on arsenic exposure and synaptic function have demonstrated a decrease in synaptic transmission and long-term potentiation in adult rodents, but have relied on in vitro or extended exposure in adulthood. Therefore, little is known about the effect of arsenic exposure in development. Objective: Here, we studied the effects of gestational and early developmental arsenic exposure in juvenile mice. Specifically, our objective was to investigate the impact of arsenic exposure on synaptic transmission and plasticity in the hippocampus. Methods: C57BL/6 females were exposed to arsenic (0, 50ppb, 36ppm) in their drinking water two weeks prior to mating and continued to be exposed to arsenic throughout gestation and after parturition. We then performed field recordings in acute hippocampal slices from the juvenile offspring prior to weaning (P17-P23). In this paradigm, the juvenile mice are only exposed to arsenic in utero and via the mothers milk. Results: High (36ppm) and relatively low (50ppb) arsenic exposure both lead to decreased basal synaptic transmission in the hippocampus of juvenile mice. There was a mild decrease in paired-pulse facilitation in juvenile mice exposed to high, but not low, arsenic, suggesting the alterations in synaptic transmission are primarily post-synaptic. Finally, high developmental arsenic exposure led to a significant increase in long-term potentiation. Discussion: These results suggest that indirect, ecologically-relevant arsenic exposure in early development impacts hippocampal synaptic transmission and plasticity that could underlie learning deficits reported in epidemiological studies.

scholarly journals Astrocytes dystrophy in ageing brain parallels impaired synaptic plasticity

2020 ◽  
Author(s):  
Alexander Popov ◽  
Alexey Brazhe ◽  
Pavel Denisov ◽  
Oksana Sutyagina ◽  
Natalia Lazareva ◽  
...  
Keyword(s):  
Volume Fraction ◽  
Long Term Potentiation ◽  
Two Photon Microscopy ◽  
Two Photon ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Age Dependent ◽  
And Function ◽  
The Impact

Little is known about age-dependent changes in structure and function of astrocytes and of the impact of these into the cognitive decline in the senescent brain. The prevalent view on age-dependent increase in reactive astrogliosis and astrocytic hypertrophy requires scrutiny and detailed analysis. Using two-photon microscopy in conjunction with 3D reconstruction, Sholl and volume fraction analysis we demonstrate a significant reduction in the number and the length of astrocytic processes, in astrocytic territorial domains and in astrocyte-to-astrocyte coupling in the aged brain. Probing physiology of astrocytes with patch-clamp and Ca2+ imaging revealed deficits in K+ and glutamate clearance, and spatiotemporal reorganization of Ca2+ events in old astrocytes. These changes paralleled impaired synaptic long-term potentiation (LTP) in hippocampal CA1 in old mice. Our findings may explain astroglial mechanisms of age-dependent decline in learning and memory.

scholarly journals Short- and long-term plasticity in CA1 neurons from mice lacking h-channel auxiliary subunit TRIP8b

2013 ◽  
Vol 110 (10) ◽  
pp. 2350-2357 ◽  
Author(s):  
Darrin H. Brager ◽  
Alan S. Lewis ◽  
Dane M. Chetkovich ◽  
Daniel Johnston
Keyword(s):  
Long Term Potentiation ◽  
Perforant Path ◽  
Membrane Properties ◽  
Oscillatory Activity ◽  
Calcium Stores ◽  
Wild Type ◽  
Term Potentiation ◽  
H Channels ◽  
The Impact

Hyperpolarization-activated cyclic nucleotide-gated nonselective cation channels (HCN or h-channels) are important regulators of neuronal physiology contributing to passive membrane properties, such as resting membrane potential and input resistance ( RN), and to intrinsic oscillatory activity and synaptic integration. The correct membrane targeting of h-channels is regulated in part by the auxiliary h-channel protein TRIP8b. The genetic deletion of TRIP8b results in a loss of functional h-channels, which affects the postsynaptic integrative properties of neurons. We investigated the impact of TRIP8b deletion on long-term potentiation (LTP) at the two major excitatory inputs to CA1 pyramidal neurons: Schaffer collateral (SC) and perforant path (PP). We found that SC LTP was not significantly different between neurons from wild-type and TRIP8b-knockout mice. There was, however, significantly more short-term potentiation in knockout neurons. We also found that the persistent increase in h-current ( Ih) that normally occurs after LTP induction was absent in knockout neurons. The lack of Ih plasticity was not restricted to activity-dependent induction, because the depletion of intracellular calcium stores also failed to produce the expected increase in Ih. Interestingly, pairing of SC and PP inputs resulted in a form of LTP in knockout neurons that did not occur in wild-type neurons. These results suggest that the physiological impact of TRIP8b deletion is not restricted to the integrative properties of neurons but also includes both synaptic and intrinsic plasticity.

scholarly journals Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala

2019 ◽  
Vol 20 (17) ◽  
pp. 4310 ◽  
Author(s):  
Susanne Meis ◽  
Thomas Endres ◽  
Thomas Munsch ◽  
Volkmar Lessmann
Keyword(s):  
Synaptic Transmission ◽  
Long Term Potentiation ◽  
Fear Learning ◽  
Inhibitory Synapses ◽  
Lateral Amygdala ◽  
Term Potentiation ◽  
Gabaergic Synapses ◽  
Bdnf Signaling ◽  
The Impact

Brain-derived neurotrophic factor (BDNF) has previously been shown to play an important role in glutamatergic synaptic plasticity in the amygdala, correlating with cued fear learning. While glutamatergic neurotransmission is facilitated by BDNF signaling in the amygdala, its mechanism of action at inhibitory synapses in this nucleus is far less understood. We therefore analyzed the impact of chronic BDNF depletion on GABAA-mediated synaptic transmission in BDNF heterozygous knockout mice (BDNF+/−). Analysis of miniature and evoked inhibitory postsynaptic currents (IPSCs) in the lateral amygdala (LA) revealed neither pre- nor postsynaptic differences in BDNF+/− mice compared to wild-type littermates. In addition, long-term potentiation (LTP) of IPSCs was similar in both genotypes. In contrast, facilitation of spontaneous IPSCs (sIPSCs) by norepinephrine (NE) was significantly reduced in BDNF+/− mice. These results argue against a generally impaired efficacy and plasticity at GABAergic synapses due to a chronic BDNF deficit. Importantly, the increase in GABAergic tone mediated by NE is reduced in BDNF+/− mice. As release of NE is elevated during aversive behavioral states in the amygdala, effects of a chronic BDNF deficit on GABAergic inhibition may become evident in response to states of high arousal, leading to amygdala hyper-excitability and impaired amygdala function.

scholarly journals Misaligned feeding impairs memories

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Dawn H Loh ◽  
Shekib A Jami ◽  
Richard E Flores ◽  
Danny Truong ◽  
Cristina A Ghiani ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Molecular Clock ◽  
Food Access ◽  
Long Term Potentiation ◽  
Sleep Time ◽  
Circadian System ◽  
Term Potentiation ◽  
Dependent Learning ◽  
The Impact

Robust sleep/wake rhythms are important for health and cognitive function. Unfortunately, many people are living in an environment where their circadian system is challenged by inappropriate meal- or work-times. Here we scheduled food access to the sleep time and examined the impact on learning and memory in mice. Under these conditions, we demonstrate that the molecular clock in the master pacemaker, the suprachiasmatic nucleus (SCN), is unaltered while the molecular clock in the hippocampus is synchronized by the timing of food availability. This chronic circadian misalignment causes reduced hippocampal long term potentiation and total CREB expression. Importantly this mis-timed feeding resulted in dramatic deficits in hippocampal-dependent learning and memory. Our findings suggest that the timing of meals have far-reaching effects on hippocampal physiology and learned behaviour.

scholarly journals Deletion of ErbB4 Disrupts Synaptic Transmission and Long-Term Potentiation of Thalamic Input to Amygdalar Medial Paracapsular Intercalated Cells

2021 ◽  
Vol 13 ◽  
Author(s):  
Douglas Asede ◽  
James Okoh ◽  
Sabah Ali ◽  
Divyesh Doddapaneni ◽  
M. McLean Bolton
Keyword(s):  
Synaptic Transmission ◽  
Critical Role ◽  
Inhibitory Neuron ◽  
Long Term Potentiation ◽  
Learning Mechanisms ◽  
Disease Etiology ◽  
Term Potentiation ◽  
And Function ◽  
The Impact

Identification of candidate risk genes and alteration in the expression of proteins involved in regulating inhibitory neuron function in various psychiatric disorders, support the notion that GABAergic neuron dysfunction plays an important role in disease etiology. Genetic variations in neuregulin and its receptor kinase ErbB4, expressed exclusively by GABAergic neurons in the CNS, have been linked with schizophrenia. In the amygdala, ErbB4 is highly expressed in GABAergic intercalated cell clusters (ITCs), which play a critical role in amygdala-dependent behaviors. It is however unknown whether ErbB4 deletion from ITCs affects their synaptic properties and function in amygdala circuitry. Here, we examined the impact of ErbB4 deletion on inhibitory and excitatory circuits recruiting medial paracapsular ITCs (mpITCs) using electrophysiological techniques. Ablation of ErbB4 in mpITCs suppressed NMDA receptor-mediated synaptic transmission at thalamo-mpITC synapses and enhanced thalamic driven GABAergic transmission onto mpITCs. Furthermore, long-term potentiation (LTP) at thalamo-mpITC synapses was compromised in ErbB4 mutant mice, indicating that ErbB4 activity is critical for LTP at these synapses. Together, our findings suggest that ErbB4 deletion from mpITCs disrupts excitation-inhibition balance and learning mechanisms in amygdala circuits.

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