Lab Notes
Check out recent research developments at UF Health
UF RESEARCHERS IDENTIFY WAY TO LOWER “REWARD EFFECTS” OF METHAMPHETAMINE
UF neuroscientists have identified a way to decrease the reward effects of methamphetamine on the brain using on-the-market medicines. A multi-university team led by UF’s Habibeh Khoshbouei, Ph.D., PharmD, associate professor of neuroscience, demonstrated in a rodent model how preventive use of medications known as sigma-1 receptor agonists — a group including the antidepressant Prozac — decreases the euphoria that normally results from methamphetamine intake. In mice, a low dose of a sigma-1 receptor agonist thwarts the expected increase in firing activity of dopamine neurons in the brain that goes with meth use. Dopamine is a chemical messenger released during pleasurable activities such as eating and sex.
FAT LOSS CAN BE TRIGGERED THROUGH THE BRAIN IN ANIMAL MODEL, RESEARCHERS FIND
Activating a part of the central nervous system triggers fat loss and reduces body mass in rat models independent of dieting, UF Health researchers have found. Using a drug that was developed to prevent skin cancer and is known to activate two molecular signaling pathways in the brain, the researchers found that when Melanotan II stimulated the central melanocortin system, the rat models lost body mass independent of a reduction in caloric intake. After 19 days, rat models that did not receive Melanotan II gained body weight while those receiving the drug lost weight. All three groups, including one that was given a low dose of the drug, were restricted to the same amount of food during the study.
UF RESEARCH OPENS NEW AVENUE FOR TREATMENT OF ALZHEIMER’S DISEASE
UF neuroscientists have validated a potential pathway to halt the progression of Alzheimer’s disease. Protein pieces called amyloid beta, or Abeta, play a role in triggering Alzheimer’s disease and scientists say the accumulation of Abeta 42 is key in promoting the disease. A class of compounds developed to treat Alzheimer’s disease known as gamma-secretase modulators have been shown to lower levels of Abeta 42 but raise levels of shorter Abeta peptides. The researchers report the Abeta peptides were not toxic in two animal models and were protective from the toxic effects of Abeta 42. The findings hold the potential for a drug therapy to be tested in humans to stop Alzheimer’s progression.
