Investigations into mild electric foot shock stress-induced cognitive enhancement: possible role of angiotensin neuropeptides

Abstract

This study was designed to investigate the role of angiotensin neuropeptides in mild electric foot shock stress-induced cognitive enhancement in mice. Mild stress was induced by applying mild electric foot shocks of 0.15 mA intensity for 0.5 s. The stress-induced alteration in cognition was assessed using a Morris water maze test. The animals were subjected to mild electric foot shocks 5 min before we recorded escape latency time (ELT), an index of learning, during the first 4 days of a 5-day trial in the Morris water maze. The time spent in target quadrant (TSTQ), an index of retrieval, was noted on the fifth day without prior administration of electric foot shock. The angiotensin-converting enzyme inhibitor lisinopril (5, 10 and 20 mg/kg), and telmisartan (1, 2 and 5 mg/kg), an angiotensin II receptor blocker, were employed to assess the role of angiotensin neuropeptides. The application of mild electric shocks significantly decreased ELT and increased TSTQ, indicating enhancement in stress-induced learning and memory. However, administration of lisinopril and telmisartan significantly attenuated the stress-induced decrease in ELT and increase in TSTQ. It may be concluded that mild electric foot shock-induced stress triggers the release of angiotensin neuropeptides that may be responsible for memory enhancement.

Adaptogenic potential of royal jelly in liver of rats exposed to chronic stress

“…In the present study, restraint and cold stress not only augmented corticosterone levels, blood glucose levels and biomarkers of oxidative stress, but also diminished the glutathione antioxidant defense system in the liver tissues. Our results corroborate other studies that reported an increase of corticosterone levels under several stress models such as restraint and cold, immobilization and cold, besides other models of stress induction [ 2 , 4 – 6 , 20 , 29 ]. Besides that, we showed a decreased of the corticosterone level associated with RJ supplementation, even in absence of stress.…”

“…Physical and psychological stress activates the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system (ANS), increasing plasma glucocorticoid levels [ 3 ]. Increased corticosterone levels were observed in stress responses using the stress models, such as restraint and cold [ 2 ], immobilization [ 4 ], cold [ 5 ], cold water immersion [ 5 ], electric foot shock [ 6 ] and social isolation stress [ 7 ]. Corticosterone increases gluconeogenesis and hepatic glycogenolysis in rats, resulting in an increase in the availability of metabolic substrates [ 8 ].…”

Renin–angiotensin system in pain: Existing in a double life?

“…7 Our own studies have described the dual role of angiotensin neuropeptides in cognition. 8,135 There have been contradictory results, i.e. both pain attenuation and increased pain sensitivity with RAS blockers.…”

“…5,7,8 Studies based on pharmacological antagonism of RAS have mainly described the stress-inducing role of angiotensin. 9,132 On the other hand, studies employing TGR(ASrAOGEN)680, within an active central angiotensin system, have shown the stress-attenuating role of endogenous angiotensin.…”

“…[4][5][6] In contrast, studies from our laboratory and from others have described the learningfacilitating and memory-enhancing effects of angiotensin neuropeptides. 7,8 Furthermore, evidence from pharmacological studies suggests the dual role of RAAS in modulating stress and associated anxiety in different models of stress. [9][10][11] These effects have been mainly attributed to differential changes in AT 1 and AT 2 receptor expression in the stress-responsive brain areas, both inside and outside the blood-brain barrier.…”