Perinatal Taurine Exposure Programs Patterns of Autonomic Nerve Activity Responses to Tooth Pulp Stimulation in Adult Male Rats

Abstract

Perinatal taurine excess or deficit influences adult health and disease, especially relative to the autonomic nervous system. This study tests the hypothesis that perinatal taurine exposure influences adult autonomic nervous system control of arterial pressure in response to acute electrical tooth pulp stimulation. Female Sprague-Dawley rats were fed normal rat chow with 3% β-alanine (taurine depletion, TD), 3% taurine (taurine supplementation, TS) or water alone (control, C) from conception to weaning. Their male offspring were fed normal rat chow and tap water throughout the experiment. At 8–10 weeks of age, blood chemistry, arterial pressure, heart rate and renal sympathetic nerve activity were measured in anesthetized rats. Age, body weight, mean arterial pressure, heart rate, plasma electrolytes, blood urea nitrogen, plasma creatinine and plasma cortisol were not significantly different among the three groups. Before tooth pulp stimulation, low (0.3–0.5 Hz) and high frequency (0.5–4.0 Hz) power spectral densities of arterial pressure were not significantly different among groups, while the power spectral densities of renal sympathetic nerve activity were significantly decreased in TD compared to control rats. Tooth pulp stimulation did not change arterial pressure, heart rate, renal sympathetic nerve and arterial pressure power spectral densities in the 0.3–4.0 Hz spectrum or renal sympathetic nerve firing rate in any group. In contrast, perinatal taurine imbalance disturbed very low frequency power spectral densities of both arterial pressure and renal sympathetic nerve activity (below 0.1 Hz), both before and after the tooth pulp stimulation. The power densities of TS were most sensitive to ganglionic blockade and central adrenergic inhibition, while those of TD were sensitive to both central and peripheral adrenergic inhibition. The present data indicate that perinatal taurine imbalance can lead to aberrant autonomic nervous system responses in adult male rats.

Taurine Depletion Causes ipRGC Loss and Increases Light-Induced Photoreceptor Degeneration

“…b-alanine is a competitive inhibitor of taurine to the taurine transporter activity. 1 Previous studies have shown that b-alanine treatment administered in the drinking water at a concentration of 3% causes a decline in taurine plasma levels [34][35][36] and in tissues such as the hippocampus, posterior cortex, and retina, as well as in cellular taurine content 13,14,[37][38][39][40] and also that taurine depletion causes loss of retinal neurons 6,41-43 (see below). [50][51][52] Light is a risk factor for some retinal degenerations, [53][54][55][56] and it accelerates photoreceptor degeneration in some inherited retinal degenerations.…”

Perinatal taurine exposure affects adult arterial pressure control

“…Maternal taurine deficiency leads to impaired development of central nervous system (particularly the autonomic nervous system control areas) and to impaired learning and memory in adult life. Perinatal taurine imbalance alters patterns of renal sympathetic nerve activity (Khimsuksri et al 2012). Perinatal taurine imbalance also alters autonomic nervous system control of arterial pressure in adult rats.…”

Glial Cell Activation and Oxidative Stress in Retinal Degeneration Induced by β-Alanine Caused Taurine Depletion and Light Exposure

“…One of the existing approaches to study the role of taurine in tissues such as the retina is to induce its systemic depletion using pharmacological treatments [ 1 , 4 , 5 ] and then studying the alterations triggered in the target tissue, i.e., the retina. It is well established that the administration of β-alanine on the drinking water of rats at a concentration of 3% causes a decline in taurine plasma levels [ 4 , 6 , 39 , 40 , 41 , 42 ] and loss of photoreceptors and retinal ganglion cells [ 27 , 43 ]. Moreover, light exposure has been shown to worsen the harmful effects of taurine depletion [ 4 , 6 ].…”