Brain volume regulation in response to changes in osmolality

Department of Medicine, 232 Building D, Georgetown University Medical Center, 4000 Reservoir Road NW, Washington, DC 20007, USA.
Neuroscience (Impact Factor: 3.33). 07/2010; 168(4):862-70. DOI: 10.1016/j.neuroscience.2010.03.042
Source: PubMed

ABSTRACT Hypoosmolality and hyperosmolality are relatively common clinical problems. Many different factors contribute to the substantial morbidity and mortality known to occur during states of altered osmotic homeostasis. The brain is particularly vulnerable to disturbances of body fluid osmolality. The most serious complications are associated with pathological changes in brain volume: brain edema during hypoosmolar states and brain dehydration during hyperosmolar states. Studies in animals have elucidated many of the mechanisms involved with brain adaptation to osmotic stresses, and indicate that it is a complex process involving transient changes in water content and sustained changes in electrolyte and organic osmolyte contents. Appreciation of the nature of the adaptation process, and conversely the deadaptation processes that occur after recovery from hypoosmolality and hyperosmolality, enables a better understanding of the marked variations in neurological sequelae that characterize hyperosmolar and hypoosmolar states, and provides a basis for more rational therapies.

  • Source
    • "Body fluid volume homoeostasis and osmolality are key factors for organism survival (Bourque, 2008; Verbalis, 2010). In different stress conditions, many regulatory mechanisms act simultaneously for the achievement of their maintenance (Morimoto and Itoh, 1998; Cheuvront et al., 2010). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Many studies have demonstrated the physiological effects of oxytocin (OT), atrial natriuretic peptide (ANP) and vasopressin (VP) in the homoeostasis of body fluids during physical exercise. However, a little information is available about the related immunohistochemical changes in hypothalamic magnocellular neurosecretory system during and after the training. The aim of the present work was to study the immunohistochemical changes in OT, ANP and VP levels in the hypothalamic paraventricular nucleus during and after resistance exercise protocol. Three groups of Wistar rats were trained by a rung ladder protocol for 15, 30 and 45 days, respectively; a fourth group was left to rest for 15 days after the training. Finally, four sedentary groups were used as controls. The results show that resistance training induces a significant reduction in the percentage of OT-positive neurons, compared with sedentary controls. In contrast, this protocol did not induce any change in VP levels, and ANP levels did not change significantly. However, VP increased after the resting period of 15 days. Our work shows that neurons of the paraventricular nucleus are involved in body fluid homoeostasis during and after resistance exercise. The functional significance of these changes in OT and VP levels, during and after the protocol, needs to be further investigated.
    Anantomia Histologia Embryologia 04/2013; DOI:10.1111/ahe.12051 · 0.74 Impact Factor
  • Source
    • "In this chronic, allostatic state, brain solute losses are sustained over long periods (Verbalis & Gullans, 1991). Of particular importance, the ongoing loss of brain glutamate (up to 30%) particular to CHN (Verbalis & Gullans) suggests the possibility of decreased synaptic release of excitatory neurotransmitters (Verbalis, 2010). This could have significant negative effects on neuronal synaptic transmission (Verbalis; Verbalis & Gullans). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Chronic hyponatremia (CHN) has traditionally been considered asymptomatic. If symptoms are observed, they are often mistakenly attributed to the underlying disorder. However, in recent studies neuropsychological deficits have been associated with CHN. The authors sought to determine the association between CHN and motor deficits. They used previously collected data, and 41 subjects with hyponatremia were included. An exploratory factor analysis with principal component analysis (PCA) was performed (eigenvalues >1.0). Factor scores were generated for each subject based on the resultant PCA factor structure. Finally, partial correlations were computed to measure the degree of association between baseline serum sodium concentration [Na+] and individual neuropsychological factor scores with the effect of age removed. All significance tests were performed using 2-tailed comparisons with alpha level of p ≤ .05. A 3-factor model emerged accounting for 70.17% of the total variance, including 1 factor that loaded primarily with motor speed and reaction time. A significant correlation was observed between this motor factor and serum [Na+] (r = -.477, p = .002). These findings add to previous observations suggesting that CHN is associated with subtle yet harmful motor deficits.
    Journal of Motor Behavior 06/2012; 44(4):255-9. DOI:10.1080/00222895.2012.688895 · 1.41 Impact Factor
  • Source
    • "Brain swelling can be caused by either intracellular ionic overload (e.g., hyperexcitability, hypoglycemia, status epilepticus, ischemia, acute ammonia toxicity, and anoxia) or by decreases in the extracellular ionic concentration (e.g., hyponatremia) (reviewed by Pasantes- Morales and Martin del Rio 1990; Verbalis, 2010). In response to such osmotic disturbances the concentrations of amino acids are altered, notably of taurine (Huxtable 1992). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Luminal and abluminal plasma membranes were isolated from bovine brain microvessels and used to identify and characterize Na(+)-dependent and facilitative taurine transport. The calculated transmembrane potential was -59 mV at time 0; external Na(+) (or choline under putative zero-trans conditions) was 126 mM (T=25 °C). The apparent affinity constants of the taurine transporters were determined over a range of taurine concentrations from 0.24 μM to 11.4 μM. Abluminal membranes had both Na(+)-dependent taurine transport as well as facilitative transport while luminal membranes only had facilitative transport. The apparent K(m) for facilitative and Na(+)-dependent taurine transport were 0.06±0.02 μM and 0.7±0.1 μM, respectively. The Na(+)-dependent transport of taurine was voltage dependent over the range of voltages studied (-25 to -101 mV). The transport was over 5 times greater at -101 mV compared to when V(m) was -25 mV. The sensitivity to external osmolality of Na(+)-dependent transport was studied over a range of osmolalities (229 to 398 mOsm/kg H(2)O) using mannitol as the osmotic agent to adjust the osmolality. For these experiments the concentration of Na(+) was maintained constant at 50mM, and the calculated transmembrane potential was -59 mV. The Na(+)-dependent transport system was sensitive to osmolality with the greatest rate observed at 229 mOsm/kg H(2)O.
    Experimental Neurology 11/2011; 233(1):457-62. DOI:10.1016/j.expneurol.2011.11.019 · 4.62 Impact Factor
Show more