1. Volume 25, Issue 1, Pages 41-50 (March 2018)
Glucocorticoid receptor activation selectively influence performance of Wistar rats in Y- maze 
Amin Abdulbasit, Fii Stephen Michael, Amusa Shukurat Onaopemipo, Alli-Oluwafuyi Abdulmusawwir, Imam Aminu, Asogwa Nnaemeka Tobechukwu, Abdulmajeed Wahab Imam, Adeyanju Oluwaseun Aremu, Olaseinde Folajimi, Abolarinwa Bilikis Aderonke, Ibrahim Ridwan Babatunde, Owoyele Victor Bamidele 
Pathophysiology 
Volume 25, Issue 1, Pages (March 2018)
DOI: /j.pathophys
Copyright © 2017 Elsevier B.V. Terms and Conditions

2. Fig. 1
The total and percentage alternations in the Y maze. Treatment with dexamethasone significantly decreased (p < 0.05) total alternation.
Pathophysiology  , 41-50DOI: ( /j.pathophys )
Copyright © 2017 Elsevier B.V. Terms and Conditions

3. Fig. 2
The effect of treatment with dexamethasone on anxiety-like behavior and rearing in the elevated plus maze and novel object recognition in the NOR test. A & B: No change was observed the percentage time spent in either the open or closed arms of the plus maze. C: treatment with dexamethasone significantly decreased (p < 0.05) rearing behavior in the plus maze. D: no significant change was observed in the time spent exploring a novel object in the NOR test, although the 8 mg/kg dexamethasone treatment markedly reduced the time spent exploring a novel object.
Pathophysiology  , 41-50DOI: ( /j.pathophys )
Copyright © 2017 Elsevier B.V. Terms and Conditions

4. Fig. 3
The effect of treatment with dexamethasone on escape latency in the Morris water maze. A: the first escape latency test (24 h after the last trial) used as a measure of long-term spatial memory shows that treatment with either 2 mg/kg or 8 mg/kg dexamethasone reduced escape latency insignificantly (P > 0.05). B: the second escape latency test (30 min after the first test) used as a measure of short-term spatial memory shows that treatment with 2 mg/kg dexamethasone had the highest effect, although insignificant (P > 0.05) in decreasing escape latency.
Pathophysiology  , 41-50DOI: ( /j.pathophys )
Copyright © 2017 Elsevier B.V. Terms and Conditions

5. Fig. 4
The effect of dexamethasone treatment on RMS and peak frequency of neural activity in the prefrontal cortex. A: the electrical wave activity/second as recorded using the Audacity software. B & C: the RMS and peak frequency of activity as analysed using the Backyard Brain spike recorder, respectively.
Pathophysiology  , 41-50DOI: ( /j.pathophys )
Copyright © 2017 Elsevier B.V. Terms and Conditions

6. Fig. 5
The effect of treatment with dexamethasone on markers of peripheral insulin resistance and central insulin level. A: no change was observed in the level of plasma insulin following treatment with dexamethasone. B: treatment with dexamethasone did not affect blood glucose levels. C: result of insulin resistance as calculated with the HOMA2 calculator shows no change in peripheral insulin resistance. D: Insignificant (P > 0.05) increases and decreases in the insulin levels of the prefrontal cortex following 2, 4, or 8 mg/kg dexamethasone treatment, respectively.
Pathophysiology  , 41-50DOI: ( /j.pathophys )
Copyright © 2017 Elsevier B.V. Terms and Conditions

7. Fig. 6
The effect of dexamethasone treatment on prefrontal cortex markers of stress. A: treatment with dexamethasone produced a mild decrease in SOD levels. B: treatment with dexamethasone produced a mild increase in LDH levels. C: treatment with 2 mg/kg dexamethasone produced a mild increase in calcium levels.
Pathophysiology  , 41-50DOI: ( /j.pathophys )
Copyright © 2017 Elsevier B.V. Terms and Conditions

8. Fig. 7
Proposed schematic; glucocorticoids induces insulin resistance (IR) and impairs insulin-dependent glucose uptake in peripheral metabolic organs; the muscle and adipose tissue and increases gluconeogenesis in the liver. The consortium of these actions induces hyperglycemia and hyperinsulinemia. We propose here in that glucocorticoids mediate its effect on memory directly or indirectly via insulin by mediating increase insulin secretion from the pancreas or endogenous insulin production in the brain.
Pathophysiology  , 41-50DOI: ( /j.pathophys )
Copyright © 2017 Elsevier B.V. Terms and Conditions