Brain-Derived Neurotrophic Factor Potentiates Entorhinal-Dentate but not Hippocampus CA1 Pathway in Adult Male Rats: A Mechanism of Taurine-Modulated BDNF on Learning and Memory.

Taurine plays an important role in neural growth and function from early to adult life, particularly in learning and memory via BDNF action. This study tested the hypothesis that BDNF differentially potentiates entorhinal-hippocampal synaptic transmission in vivo in adult rats. In anesthetized male Sprague-Dawley rats, a stainless steel recording electrode with an attached microinjector was placed into CA1 and the dentate gyrus to record fEPSP, and a paired stainless steel electrode was inserted into entorhinal cortex for continuous paired-pulse stimulation of that brain region. In the dentate gyrus, microinjection of BDNF resulted in a gradual increase in the peak slope of the fEPSP. Following the infusion, the peak fEPSP began to rise in about 8 min, reached a maximum of 120 ± 2% (from baseline) by about 20 min, and remained near peak elevation (~115%) for more than 30 min. In contrast, the same dose of BDNF when injected into CA1 had no consistent effect on fEPSP slopes in the CA1. Further, an equimolar cytochrome C (horse heart) infusion had no significant effect on fEPSP slopes in either the dentate gyrus or CA1. The potentiation effect of BDNF in the dentate gyrus is consistent with a significant increase in power spectral density of dentate gyrus field potentials at 70-200 Hz, but not at frequencies below 70 Hz. In addition, the CA1 power spectral density was not affected by BDNF (compared to cytochrome C). These data indicate that in vivo BDNF potentiates entorhinal-hippocampal synaptic transmission in dentate gyrus, but not in CA1.

Creating a Sustainable Partnership Between a Science Center, University, and Local School Districts: A Retrospective on Over 20 Years of Successful Programming and Partnership.

The University of Alabama at Birmingham (UAB) and the McWane Science Center have partnered for over 20 years to provide secondary students in Alabama opportunities to conduct inquiry-based, standards-aligned science labs. LabWorks (middle school) and GENEius (high school) programs offer multiple research laboratory experiences in which students explore molecular biology, physical science, genetics, engineering, anatomy, and forensic science, with associated summer professional development for teachers: BioTeach and GeoTeach. These programs each attract 3,000-4,000 participants annually. This partnership has been synergistic, allowing the science center to offer high-level secondary science programming, while giving the university a conduit into the K-12 world. Originally, these programs were developed through Howard Hughes Medical Institute funding, and then expanded through support from the National Institutes of Health, the National Science Foundation, and the US Department of Education. These programs have excited secondary students and teachers about science education and careers, provided authentic science experiences, and given teachers the opportunity to experience a model of learning that engages students in "real science" closely linked to their curriculum. For over 20 years, this unique, evolving partnership has increased the understanding of over 90,000 students and teachers relative to the opportunities that science and STEM careers hold.

Inhibition of Renin-Angiotensin System from Conception to Young Mature Life Induces Salt-Sensitive Hypertension via Angiotensin II-Induced Sympathetic Overactivity in Adult Male Rats.

Previous studies indicate that perinatal compromise of taurine causes cardiovascular disorders in adults via the influence of taurine on renin-angiotensin system (RAS). This study tested whether perinatal inhibition of the RAS would itself alter the adult cardiovascular system in a similar way. Female Sprague-Dawley rats were fed normal rat chow and given water alone (Control) or water containing captopril (400 mg/l) from conception until weaning. Then, the male offspring drank water or water containing captopril until 5 weeks of age followed by normal rat chow and water alone until 7 weeks of age. Thereafter, they drank water alone (Control, Captopril) or 1% NaCl solution (Control+1%, Captopril+1%). At 9 weeks of age, all animals were implanted with femoral arterial and venous catheters. Forty-eight hours later, blood chemistry, glucose tolerance, and hemodynamic parameters were determined in freely moving conscious rats. Then, the same experiments were repeated 2 days after captopril treatment. Body weights, kidney and heart to body weight ratios, fasting and non-fasting blood sugar, glucose tolerance, and heart rates were not significantly different among groups. Further, plasma sodium, mean arterial pressure, and sympathetic activity significantly increased whereas baroreflex sensitivity decreased in Captopril+1% compared to other groups. These changes were normalized by acute captopril treatment and the arterial pressure differences also by acute ganglionic and central adrenergic blockade. The present study suggests that inhibition of the RAS in the early life induces RAS overactivity, leading to salt-sensitive hypertension via sympathetic nervous system overactivity and depressed baroreflex sensitivity in adult male rats.

Taurine Supplementation Inhibits Cardiac and Systemic Renin-Angiotensin System Overactivity After Cardiac Ischemia/Reperfusion in Adult Female Rats Perinatally Depleted of Taurine Followed by High Sugar Intake.

Perinatal taurine depletion and high sugar intake from weaning onward worsen cardiac damage and arterial pressure control after ischemia/reperfusion (IR) in adult male and female rats, which can be ameliorated by high taurine diets or inhibition of renin-angiotensin system. This study tests if taurine supplementation ameliorates cardiac damage and arterial pressure control in adult female rats via alterations of both cardiac and systemic renin-angiotensin system. Female Sprague-Dawley rats were fed normal rat chow and drank water alone (control, C) or water containing 3% beta-alanine (taurine depletion, TD) from conception to weaning, and female offspring were subjected to high sugar intake (normal rat chow and 5% glucose in water; CG and TDG) or the normal rat diet (CW and TDW). At 7 weeks of age, half of the rats in each group received 3% taurine in water (CW+T, CG+T, TDW+T, and TDG+T). One week later, rats were subjected to IR or Sham procedures followed by renal nerve recording, plasma and cardiac angiotensin II measurements. Cardiac angiotensin II levels significantly elevated in CG, TDW, and TDG. Further, plasma angiotensin II concentrations were significantly elevated only in the TDG, in consistent with a significant increase in renal nerve activity to juxtaglomerular cells, but not renal vessels and tubules. These abnormalities were ameliorated by short-term taurine supplementation. Thus, in adult female rats that are perinatally depleted of taurine followed by high sugar intake after weaning, taurine supplementation decreases the adverse effects of cardiac IR via inhibition of both cardiac and systemic renin-angiotensin system overactivity.

Blunted Nighttime Sympathetic Nervous System Response to Stress Among Thai Men with Positive Family History of Sudden Unexplained Nocturnal Death Syndrome.

Sudden unexplained nocturnal death syndrome (SUNDS) is prominent among northeast Thai men. This study tests the hypothesis that Thai men with positive family history of SUNDS display abnormal diurnal, autonomic nervous system responses to stress. Healthy northeast Thai men (20-49 years old) lived in the same rural area were divided into two groups based on their positive (PF) or negative family (NF1) history of SUNDS. A second control included Thai men with an NF history of SUNDS from a non-endemic area (NF2). All data were collected at 4:00-6:00 AM (nighttime) and 4:00-6:00 PM (daytime). All three groups displayed nighttime decreases in mean arterial pressure, heart rate, and blood glucose. Furthermore, all subjects displayed similar glucose tolerance and electrolyte balance. The tachycardic responses to a four-minute step test were similar among groups in the daytime, but the nighttime responses were significantly blunted in the PF group compared to either control group (about 20 bpm less). Tachycardic responses to a cold pressor test tended to decrease more during the nighttime in the PF compared to NF1 and NF2 groups, but the difference was not significant. Arterial pressure responses to the exercise were similar among the three groups during the nighttime, whereas in the NF2, daytime mean arterial pressures increased more than those in the other groups. The present data suggest that Thai men with a PF history of SUNDS display blunted sympathetic nervous system responses to stress during the nighttime, a potential factor that may trigger cardiac arrhythmias and contribute to SUNDS.

Perinatal taurine exposure affects adult oxidative stress.

Perinatal exposure to taurine (a ß-amino acid) can alter adult physiological functions, including arterial pressure, hormonal and renal functions. Whereas perinatal taurine supplementation appears to have only minor effects on adult physiology, perinatal taurine depletion is associated with multiple adverse health effects, especially in animals postnatally exposed to other insults. New studies indicate that the mechanism for many of the physiological effects of taurine is related to the antioxidant activity of taurine. Thus the perinatal taurine depletion leads to oxidative stress in adult animals. It is likely that perinatal taurine depletion increases oxidative stress throughout life and that the early life taurine depletion leads to perinatal, epigenetic programming that impacts adult physiological function.

Impaired renal response to portal infusion of hypertonic saline in adriamycin-treated rats.

1. The hepatorenal reflex plays an important role in water and salt homeostasis by matching renal excretion to gastrointestinal absorption. This homeostatic mechanism is impaired in nephrotic rats. The present study tested the hypothesis that, in nephrotic rats, the renal sodium excretion response to hypertonic saline infusion is impaired due to decreased sensitivity of the hepatoportal sodium-sensing mechanism. 2. The present study was performed in control and adriamycin (ADR)-induced nephrotic syndrome rats. After baseline data collection, urinary sodium (U(Na)V) and potassium (U(K)V) excretion responses were tested following continuous infusion of hypertonic NaCl solution (20 µL/min for 30 min) into either the femoral or mesenteric vein. A second series of experiments tested hepatic and renal nerve responses to continuous mesenteric vein infusion of hypertonic NaCl (10 µL/s for 30 s). 3. Compared with control rats, nephrotic rats displayed significantly lower baseline U(Na)V and U(K)V excretion. In control rats, mesenteric compared with femoral vein infusion of hypertonic NaCl produced a more rapid and greater increase in U(Na)V. In contrast, in nephrotic rats, femoral and mesenteric vein infusion caused similar increases in U(Na)V and the maximum increases in U(Na)V to either route of infusion were much lower in nephrotic than control rats. Furthermore, portal hypertonic saline infusion caused greater increases in hepatic nerve activity and greater decreases in renal nerve activity in control compared with nephrotic rats. 4. These data suggest that, in rats, adriamycin treatment decreases hepatoportal sodium-sensing sensitivity, leading to marked impairment of hepatorenal reflex responses, potentially contributing to salt and water retention.