https://perso.univ-rennes1.fr/francois.tiaho/L3-physio.%20G-tiaho/Bibliographie/glucose/2002-Routh_review++.pdf

Glucose-sensing neurons: are they physiologically relevant?

Adequate fluid intake is critical for survival. While adults are at liberty to drink fluids as wanted, children and infants are dependent upon caregivers for food and fluid. Children are at greater risk for dehydration than adults due to their higher surface-to-mass ratio. Additionally, children have different thirst sensitivities and body cooling mechanisms than adults. Children differ from adults in total body water content, and boys and girls differ in body water content with maturation. Research in young adults shows that mild dehydration corresponding to only 1% to 2% of body weight loss can lead to significant impairment in cognitive function. Dehydration in infants is associated with confusion, irritability, and lethargy; in children, it may produce decrements in cognitive performance.

Hydration and Cognitive Function in Children

Krause MP, Riddell MC, Hawke TJ. Effects of type 1 diabetes mellitus on skeletal muscle: clinical observations and physiological mechanisms.

Effects of type 1 diabetes mellitus on skeletal muscle: clinical observations and physiological mechanisms

No matter how mild, dehydration is not a desirable condition because there is an imbalance in the homeostatic function of the internal environment. This can adversely affect cognitive performance, not only in groups more vulnerable to dehydration, such as children and the elderly, but also in young adults. However, few studies have examined the impact of mild or moderate dehydration on cognitive performance. This paper reviews the principal findings from studies published to date examining cognitive skills. Being dehydrated by just 2% impairs performance in tasks that require attention, psychomotor, and immediate memory skills, as well as assessment of the subjective state. In contrast, the performance of long-term and working memory tasks and executive functions is more preserved, especially if the cause of dehydration is moderate physical exercise. The lack of consistency in the evidence published to date is largely due to the different methodology applied, and an attempt should be made to standardize methods for future studies. These differences relate to the assessment of cognitive performance, the method used to cause dehydration, and the characteristics of the participants.

Cognitive Performance and Dehydration

Does diabetes mellitus target motor neurons

Background

Peripheral neuropathy of both motor and sensory nerves has been well documented in diabetes mellitus, but the evidence for physiological and correlated morphological changes during the pathogenesis of myopathy is scarce. In the present report, we have chosen the dorsiflexor muscle of adult male mice as a model for studying in situ muscle contraction and neuromuscular ultrastructure during the pathogenesis of streptozotocin-induced diabetes.



Methods

Thirty mice (30 g bodyweight) were injected once i.p. with streptozotocin solution (200 mg/kg) to induce experimental diabetes mellitus. Comparative analyses of in situ muscle isometric contractile characteristics were studied (at 1 Hz, 5 Hz, and 30 Hz nerve stimulation) in urethane-anesthetized (2 mg/g, i.p.) control and diabetic mice at three time points, 2 weeks, 4 weeks, and 8 weeks postinjection. Synaptic delay was also recorded in diabetic and age-matched control mice.



Results

There was a significant increase in synaptic delay in both 4-week and 8-week diabetic mice compared with control mice (8.9 ± 1.2 msec and 7.6 ± 0.6 msec, respectively, compared with 6.1 ± 0.5 msec). At all three stimulation frequencies, diabetes did not affect muscle contractile speed but significantly reduced the twitch tension after 8 weeks, with no changes at 2 weeks or 4 weeks. The recorded single-twitch tension values were 2.6 ± 0.3 g, 2.1 ± 0.6 g, 2.2 ± 0.7 g, and 1.2 ± 0.1 g for control, 2 weeks, 4 weeks, and 8 weeks, respectively. At 30 Hz, the recorded tension values were 4.6 ± 1.6 g, 3.1 ± 1.2 g, 3.1 ± 1.1 g, and 2.1 ± 1.0 g for control, 2 weeks, 4 weeks, and 8 weeks, respectively. Ultrastructural changes in neuromuscular junctions were similar to those that have been described in disuse and aging. These changes were observed after 8 weeks and included severe loss of synaptic vesicles, electron-dense bodies, and myelin-like figures as well as degeneration of mitochondria.



Conclusions

The results reveal that streptozotocin-induced diabetes affects presynaptically the neuromuscular junction as well as muscle itself. Actions at both sites may contribute to the functional alterations seen in muscle contractile properties and may play a role in the pathogenesis of diabetic neuromyopathy. Anat. Rec. 251:240–244, 1998. © 1998 Wiley-Liss, Inc.

https://anatomypubs.onlinelibrary.wiley.com/doi/pdf/10.1002/%28SICI%291097-0185%28199806%29251%3A2%3C240%3A%3AAID-AR13%3E3.0.CO%3B2-O

Muscle contractility decrement and correlated morphology during the pathogenesis of streptozotocin‐diabetic mice

The effect of 24 hrs. water deprivation on spontaneous and evoked transmitter release was studied at flexor nerve terminals of control and lead-treated male C57BL mice. Miniature endplate potentials (MEPPs) and endplate potentials (EPPs) were recorded intracellularly from urethane-anesthetized (2 mg/g, i.p.) control and lead exposed mice in both hydrated and dehydrated conditions. Exposure to lead was made by i.p. injection of lead acetate (1.0 mg/kg) dissolved in a 5% glucose solution 24 hrs. prior to the experiment. Unimodal and bimodal MEPP frequencies decreased with dehydration, while small mode MEPPs remained unchanged and large mode MEPPs increased in frequency. EPP amplitude and quantal content were unchanged by dehydration. Lead treatment by itself reduced the frequency of unimodal and bimodal MEPPs but had no effect on the amplitude of EPPs or of quantal content. However a combination of dehydration and acute lead treatment reduced the frequency of unimodal, bimodal and large mode MEPPs and significantly reduced both EPP amplitude and quantal content. Dehydration apparently reveals an underlying neurotoxic action of lead at the neuromuscular junction. This raises a health concern that people subjected to both lead pollution and dehydration are at greater risk to lead poisoning of the neuromuscular junction.

Dehydration affects synaptic transmission at flexor muscle in acute lead-treated mice

The effect of increasing extracellular calcium concentration on spontaneous transmitter release was studied at both soleus (slow) and fast extensor digitorum longus (EDL) nerve terminals of control and streptozotocin-induced diabetic (STZ-D) young C57 BL mice (7 months old) depolarized by high (20 mM) extracellular potassium [K]o. Diabetes was induced by i.p. injection with a single dose of streptozotocin (200 mg/kg) at the age 5 months and the electrophysiological studies were carried out after 8 more weeks. By using intracellular recording, miniature endplate potentials (MEPPs) were first recorded in a normal [K]o Krebs solution. Subsequently, MEPPs were recorded in high [K]o Krebs solution with 4 different Ca concentrations: Ca-free/ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetra acetic acid (EGTA), 0.5, 1.5 and 2 mM Ca. MEPP frequency was lower at STZ-D than control nerve terminals in EDL but not soleus. However, MEPP frequency was progressively higher at both EDL and soleus of STZ-D than control with increasing Ca concentration in Krebs that contained 20 mM [K]o. In STZ-D slow soleus muscle, depolarization produced 0.7, 4.3, 41.6 and 62.7 vs 1.4, 2.8, 20.7 and 31.6 Hz for control in the 4 different Ca concentrations. In STZ-D fast EDL muscle, depolarization produced 0.5, 4.9, 48.2 and 66.8 vs 1.2, 2.5, 27 and 35.4 Hz for control in the 4 different Ca concentrations. Bimodal and unimodal MEPP amplitude were present at both slow and fast nerve terminals. However, depolarization increased the percentage of bimodal MEPP amplitude in STZ-D compared to control (p<0.01) mice in EDL but not soleus. The results revealed that these changes in muscle firing pattern may provide a protective effect against diabetes-induced neuropathy at the neuromuscular junction.

N Davidson

Papers

Muscle contractility decrement and correlated morphology during the pathogenesis of streptozotocin‐diabetic mice

Dehydration affects synaptic transmission at flexor muscle in acute lead-treated mice

Depolarization affects neuromuscular junction of streptozotocin-diabetic mice.