Hippocampal neurogenesis persists in adult mammals, but its rate declines dramatically with age. Evidence indicates that experimentally-reduced levels of neurogenesis (e.g., by irradiation) in young rats has profound influence on cognition as determined by learning and memory tests. In the present study we asked whether in middle-aged, 10- to 13-months-old rats, cell production can be restored toward the level present in young rats. To manipulate neurogenesis we induced bilateral carotid occlusion with hypotension. This procedure is known to increase neurogenesis in young rats, presumably in a compensatory manner, but until now, has never been tested in aging rats. Cell production was measured at 10, 35, and 90 days after ischemia. The results indicate that neuronal proliferation and differentiation can be transiently restored in middle-aged rats. Furthermore, the effects are more pronounced in the dorsal as opposed to ventral hippocampus thus restoring the dorso-ventral gradient seen in younger rats. Our results support previous findings showing that some of the essential features of the age-dependent decline in neurogenesis are reversible. Thus, it may be possible to manipulate neurogenesis and improve learning and memory in old age.
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http://dx.doi.org/10.3389/fnins.2010.00163 | DOI Listing |
Pflugers Arch
January 2025
Department of Neuroscience, Graduate School of Biomedical Sciences, Mayo Clinic College of Medicine, Phoenix, AZ, USA.
To examine the effect of DBS of the lateral hypothalamic area (LHA) on age-related memory changes, neuronal firing from CA1, oxidative stress, and the expression of Hsp70, BDNF, and synaptophysin. 72 male rats were randomly allocated into 6 equal groups: a) normal young group (8 W), b) sham young group, c) DBS young group, d) normal old group (24 months), e) sham old group and f) DBS old group. Memory tests (passive avoidance and Y maze), oxidative stress markers (MDA, catalase, and GSH) and expression of Nrf2, HO-1, Hsp70, BDNF, and synaptophysin were measured by the end of the experiment.
View Article and Find Full Text PDFBMC Gastroenterol
January 2025
Department of Anesthesiology, First Affiliated Hospital, Fujian Medical University, No. 20, Cha Zhong Road, Fuzhou, Fujian Province, People's Republic of China.
Background: Visceral pain sensitization and emotional reactions due to irritable bowel syndrome (IBS) occur frequently in the general population. Oxidative stress plays a crucial role in the pathogenesis of IBS. Previous studies have demonstrated that activation of peroxisome proliferator-activated receptor gamma (PPARγ) has analgesic effects.
View Article and Find Full Text PDFBiogerontology
January 2025
Department of Anatomy, College of Medicine, Tzu Chi University, No. 701, Section 3, Zhongyang Rd., Hualien, 970374, Taiwan.
Aging women experience a significant decline of ovarian hormones, particularly estrogen, following menopause, and become susceptible to cognitive and psychomotor deficits. Although the effects of estrogen depletion had been documented in the prefrontal and somatosensory cortices, its impact on somatomotor cortex, a region crucial for motor and cognitive functions, remains unclear. To explore this, we ovariectomized young adult female rats and fed subsequently with phytoestrogen-free diet and studied the effects of estrogen depletion on the somato-sensory and motor cortices.
View Article and Find Full Text PDFJ Physiol
January 2025
College of Medicine, Department of Pharmacology, University of Arizona, Tucson, AZ, USA.
The endocannabinoid system's significance in maintaining blood-brain barrier (BBB) integrity under physiological and pathological conditions is suggested by several reports, but the underlying molecular mechanisms are not well understood. In this paper, we investigated the effects of depletion of 2-arachidonoylglycerol (2-AG), one of the main endocannabinoids in the central nervous system, on BBB integrity using pharmacological tools. Female Sprague-Dawley rats were injected with the diacylglycerol lipase α (DAGLα) inhibitor LEI-106 (40 mg/kg, i.
View Article and Find Full Text PDFJ Transl Med
January 2025
Department of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.
Background: Sepsis is a systemic inflammatory syndrome that can cause coagulation abnormalities, leading to damage in multiple organs. Vascular endothelial cells (VECs) are crucial in the development of sepsis-induced coagulopathy (SIC). The role of Parthenolide (PTL) in regulating SIC by protecting VECs remains unclear.
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