A novel function of anti-diuretic hormone vasopressin in the brain

ScienceDaily (Jan. 20, 2011) — The anti-diuretic hormone "vasopressin" is released from the brain, and known to work in the kidney, suppressing the diuresis. Now, a Japanese research team led by Professor Yasunobu Okada, Director-General of National Institute for Physiological Sciences (NIPS), and Ms. Kaori Sato, a graduate student of The Graduate University for Advanced Studies, has clarified the novel function of "vasopressin" that works in the brain, as well as in the kidney via the same type of the vasopressin receptor, to maintain the size of the vasopressin neurons.

See Also:Health & MedicineNervous SystemBrain TumorPsychology ResearchMind & BrainBrain InjuryNeuroscienceDisorders and SyndromesReferenceVasopressinHypothalamusSensory neuronAstrocyte

It might be a useful result for clarification of the condition of cerebral edema which swells along with the brain trauma or the cerebral infarction, and for its treatment method development. This result of the study is reported in the Science Signaling magazine.

The research team focused on the vasopressin neurons which exist in a hypothalamus of the brain. The vasopressin is essentially released from the vasopressin neurons into blood circulation and acts on the kidney as anti-diuretic, when the blood plasma becomes more concentrated. In contrast, they ascertained that the vasopressin neurons release the vasopressin into the brain, not in blood, when the surrounding body fluid becomes more diluted than usual. Usually, the more diluted the body fluid becomes, the bigger the neuronal cell swells. However, their finding shows that the vasopressin in the brain maintains the size of the vasopressin neurons even when the body fluid becomes more diluted. In addition, it was clarified that the vasopressin sensor protein (receptor) which was currently considered to be only in the kidney, was related to this function in the brain.

This study became possible by labeling vasopressin neurons of the rat brain hypothalamus with green fluorescent protein (GFP)．(The transgenic rat was developed by Professor Yoichi Ueta; University of Occupational and Environmental Health, Japan.)

Professor Okada says that "It is a surprising result that the same type of the vasopressin receptor as the kidney exists in the brain and the vasopressin works on it. It can be expected to clarify the condition of cerebral edema which swells along with the brain trauma or the cerebral infarction, and to develop its treatment method.

This result is supported by Grants-in-Aid for Scientific Research, the MEXT, Japan.

Email or share this story:

Self-administered light therapy may improve cognitive function after traumatic brain injury

ScienceDaily (Mar. 18, 2011) — At-home, daily application of light therapy via light-emitting diodes (LEDs) placed on the forehead and scalp led to improvements in cognitive function and post-traumatic stress disorder in patients with a traumatic brain injury (TBI), according to a groundbreaking study published in Photomedicine and Laser Surgery, a peer-reviewed journal published by Mary Ann Liebert, Inc.

See Also:Health & MedicineToday's HealthcareGene TherapyMental Health ResearchMind & BrainDisorders and SyndromesBrain InjuryIntelligenceReferenceBrain damageOccupational therapyTraumatic brain injuryAmnesia

Margaret Naeser, PhD, LAc, VA Boston Healthcare System, Boston University School of Medicine, and colleagues from Massachusetts General Hospital, and Harvard-MIT Division of Health Sciences and Technology, in Boston, and MedX Health Inc. (Mississauga, ON, Canada), report on the use of transcranial LED-based light therapy to treat two patients with longstanding traumatic brain injury (TBI). Each patient applied LEDs nightly and demonstrated substantial improvement in cognitive function, including improved memory, inhibition, and ability to sustain attention and focus. One patient was able to discontinue medical disability and return to full-time work. These cognitive gains decreased if the patients stopped treatment for a few weeks and returned when treatment was restarted. Both patients are continuing LED treatments in the home. The findings are presented in "Improved Cognitive Function After Transcranial, Light-Emitting Diode Treatments in Chronic, Traumatic Brain Injury: Two Case Reports."

Low-level light therapy using lasers or externally placed LEDs to deliver red and near-infrared (NIR) light energy has been shown in cell-based studies to improve cellular metabolism and to produce beneficial physiological effects. In acute stroke in humans, for example, transcranial NIR light therapy applied less than 24 hours post-stroke was associated with improved outcomes.

"The results of this study will provide a basis for future therapeutic use of phototherapy to improve recovery after injury and facilitate management of other CNS disorders. The development of novel therapies to restore function after neurologic injury, stroke, or disease is an increasingly important goal in medical research as a result of an increase in non-fatal traumatic wounds and the increasing prevalence of dementias and other degenerative disorders in our aging population," says Raymond J. Lanzafame, MD, MBA, Editor-in-Chief of the Journal.

Email or share this story:

Improved recovery of motor function after stroke

ScienceDaily (Apr. 20, 2011) — After the acute treatment window closes, the only effective treatment for stroke is physical/occupational therapy. Now scientists from Children's Hospital Boston report a two-pronged molecular therapy that leads to significant recovery of skilled motor function in a rat model of stroke. Their findings are reported April 20 in the Journal of Neuroscience.

See Also:Health & MedicineNervous SystemDisabilityStroke PreventionMind & BrainBrain InjuryNeuroscienceCaregivingReferencePhantom limbSensory neuronBrain damagePupillary reflex

By combining two molecular therapies -- each known to promote some recovery on its own -- the researchers achieved more nerve growth and a greater recovery of motor function than with either treatment alone. One therapy, inosine, is a naturally-present molecule that promotes nerve growth; the other is NEP1-40, an agent that counteracts natural inhibitors of nerve growth.

"When you put these two together, you get much stronger growth of new circuits than either one alone, and very striking functional improvements," says senior author Larry Benowitz, PhD, of the Children's Department of Neurosurgery.

Strokes in humans often damage the motor cortex on one side of the brain, interfering with skilled motor functions on the opposite side of the body. Led by Laila Zai, PhD, a postdoctoral fellow in Benowitz's lab and the study's first author, the researchers modeled this scenario by inducing strokes on one side of the rats' brains -- specifically in a part of the motor cortex that controls forelimb movement. They then examined the rats' ability to perform a skilled reaching task -- retrieving food -- with the forelimb on the opposite side.

After 3 to 4 weeks, rats treated with both inosine and NEP1-40 could perform the task -- which required coordinated movements of the paw and digits -- with success rates equivalent to those before the stroke. Benowitz likens the complexity of this task to a person eating with utensils or operating a joystick.

Benowitz has three issued US patents and several US and foreign patent applications pending for the use of inosine to treat stroke, spinal cord injury and traumatic brain injury, and a pending patent application for the inosine/NEP1-40 combined treatment of CNS injury. Earlier studies from his lab, including one published in 2002 and another published last year, demonstrated that inosine encourages nerve fibers to grow from the uninjured side of the brain into regions of the spinal cord that have lost nerve fibers due to stroke. This compensatory rewiring of neural circuits was matched by functional improvements. A separate 2007 study from the University of Cambridge also found that inosine promotes recovery of skilled motor function following traumatic brain injury in rats.

Inosine works by activating a key regulator of nerve growth (an enzyme known as Mst3b). It has a history of safe usage in humans -- it is widely available as a nutritional supplement, and is currently being investigated in clinical trials for the treatment of multiple sclerosis and Parkinson's disease.

NEP1-40 complements inosine's effects by counteracting molecules outside of nerve cells that inhibit nerve growth. Specifically, it blocks signaling through the Nogo receptor, shown by a number of studies to promote the rewiring of neural circuits and to improve functional recovery after stroke.

Benowitz believes circuit rewiring is a promising approach to treating stroke because that is what is thought to underlie the recovery that happens naturally. People with strokes often do regain some function that correlates with shifts in activity to the uninjured parts of the brain. In animal studies, these shifts in brain activity correlate with the growth of new branches from uninjured nerve fibers.

The researchers also found that inosine administered together with environmental enrichment (a model for physical/occupational therapy in humans) led to greater recovery of both nerve growth and motor function. "Physical/occupational therapy should always be part of the strategy," Benowitz says.

The study was funded by the National Institutes of Health, Alseres Pharmaceuticals and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation (AMRF).

Email or share this story: