Brain research
-
Comparative Study
Increases of antioxidants are related to more delayed neuronal death in the hippocampal CA1 region of the young gerbil induced by transient cerebral ischemia.
In age-related studies, young animals are resistant to ischemic damage. In present study, we investigated the neuronal death of pyramidal neurons and compared changes in the immunoreactivities and levels of antioxidants, Cu/Zn-SOD (SOD1), Mn-SOD (SOD2), catalase (CAT) and glutathione peroxidase (Gpx), in the hippocampal CA1 region between adult and young gerbils after 5 min of transient cerebral ischemia. In the adult ischemia-group, only a few (12%) of CA1 pyramidal neurons survived 4 days after ischemia-reperfusion (I-R); however, in the 4 days after I-R the young group, most of CA1 pyramidal neurons survived. ⋯ Four days after I-R in the adult groups, the levels of all the antioxidants were dramatically deceased; however, at this time in the young ischemia-groups, they were distinctively increased in the CA1 region. Seven days after I-R, all the antioxidants levels in the CA1 region were distinctively decreased. In brief, we conclude that the increased antioxidants levels were related to a less and much delayed neuronal death in the CA1 pyramidal neurons in the young group following I-R injury.
-
The presence of a proinflammatory environment in the sensory neuron axis in diabetes was tested by measuring levels of proinflammatory cytokines in lumbar dorsal root ganglia (DRG) and peripheral nerve from age matched control and streptozotocin (STZ)-induced diabetic rats. The levels of tumor necrosis factor-α (TNFα) and other cytokines were diminished in lumbar DRG from diabetic animals. Consequently, we tested the hypothesis that TNFα modulated axonal plasticity in adult sensory neurons and posited that impairments in this signal transduction pathway may underlie degeneration in diabetic sensory neuropathy. ⋯ Immunofluorescent staining for NF-κB subunit p50 within neuronal nuclei revealed that medium to large diameter neurons were most susceptible to NF-κB inhibition and was associated with decreased neurite outgrowth. The results demonstrating reduced cytokine expression in DRG confirm that diabetic sensory neuropathy does not involve a neuroinflammatory component at this stage of the disease in experimental animal models. In addition, it is hypothesized that reduced TNFα expression in the DRG and possibly associated deficits in anterograde transport may contribute to impaired collatoral sprouting and regeneration in target tissue in type 1 diabetes.
-
A conditioned taste aversion (CTA) is acquired when an animal consumes a novel taste (CS) and then experiences the symptoms of poisoning (US). Following CTA training, animals will avoid the taste that was previously associated with malaise. This defensive reaction to a learned fear can be extinguished by repeated exposure to the CS alone (CS-only; CSO-EXT). ⋯ However a detailed analysis of PAG c-Fos expression provided hints about some of the physiological changes evoked by these 2 extinction paradigms that produce very different behavioral outcomes. The findings are clinically relevant as we seek the development of treatments for deficits in fear extinction (e.g. PTSD, phobias).
-
Acute stress has been shown to modify hypothalamus-pituitary-gonadal (HPG) axis activity. Corticotropin-releasing hormone (CRH), the principal regulator of the hypothalamus-pituitary-adrenal (HPA) axis, has been implicated as a mediator of stress-induced effects on the reproductive axis. The role of the specific CRH receptor subtypes in this response is not completely understood. ⋯ In a similar manner, we observed a suppression of the afternoon surge in plasma FSH, a delay of E(2)-induced PRL secretion, and an increase in plasma P and CT. Antalarmin attenuated stress-induce LH increase, decreased CT and P secretion and blocked the stress effects on PRL secretion. These findings suggest that CRH-R(1) mediates, at least in part, the restraint stress effects on the HPA, PRL, and reproductive axes.