The role of CA1 α-adrenoceptor on scopolamine induced memory impairment in male rats

Introduction: Similarities in the memory impairment between Alzheimer patients and scopolamine treated animals have been reported. In the present study, the possible role of α-adrenergic receptors of the dorsal hippocampus on scopolamine state-dependent memory in adult male Wistar rats was evaluated. Methods: The animals were bilaterally implanted with chronic cannulae in the CA1 regions of the dorsal hippocampus, trained in a step-through type inhibitory avoidance task, and tested 24 h after training to measure step-through latency. Results: Post-training intra-CA1 administration of scopolamine (0.5 and 2μg/rat) dose-dependently reduced the step-through latency, showing an amnestic response. Amnesia produced by post-training scopolamine (2 μg/rat) was reversed by pre-test administration of the scopolamine (0.5 and 2 μg/rat) that is due to a state-dependent effect. Pre-test intra-CA1 injection of α1-adrenoceptor agonist, phenylephrine (0.25, 0.5 μg/rat) in the dose range that we used, could not affect memory impairment induced by post-training injection of scopolamine (2 μg/rat). However intra-CA1 pretest injection of α2-adrenoceptor agonist, clonidine (0.5 μg/rat) improved post-training scopolamine (2 μg/rat) intra-CA1 injection induced retrieval impairment. Furthermore, pre-test intra-CA1 microinjection of phenylephrine (0.25 and 0.5 μg/rat) or clonidine (0.25 and 0.5 μg/rat) with an ineffective dose of scopolamine (0.25 μg/rat), synergistically improved memory performance impaired by post-training scopolamine (2 μg/rat). Our results also showed that, pre-test injection of α1-receptor antagonist prazosin (1, 2 μg/rat) or α2-receptors antagonist yohimbine (1, 2 μg/rat) before effective dose of scopolamine (2 μg/rat) prevented the improvement of memory by pre-test scopolamine. Conclusion: These results suggest that α1- and α2-adrenergic receptors of the dorsal hippocampal CA1 region may play an important role in scopolamine-induced amnesia and scopolamine state-dependent memory

Involvement of dorsal hippocampal α-adrenergic receptors in the effect of scopolamine on memory retrieval in inhibitory avoidance task

The present study evaluated the possible role of α-adrenergic receptors of the dorsal hippocampus on scopolamine-induced amnesia and scopolamine state-dependent memory in adult male Wistar rats. The animals were bilaterally implanted with chronic cannulae in the CA1 regions of the dorsal hippocampus, trained in a step-through type inhibitory avoidance task, and tested 24. h after training to measure step-through latency. Results indicate that post-training or pre-test intra-CA1 administration of scopolamine (1 and 2μg/rat) dose-dependently reduced the step-through latency, showing an amnestic response. Amnesia produced by post-training scopolamine (2μg/rat) was reversed by pre-test administration of the scopolamine that is due to a state-dependent effect. Interestingly, pre-test intra-CA1 microinjection of α1-adrenergic agonist, phenylephrine (1 and 2μg/rat) or α2-adrenergic agonist, clonidine improved post-training scopolamine (2μg/rat)-induced retrieval impairment. Furthermore, pre-test intra-CA1 microinjection of phenylephrine (0.25, 0.5 and 1 μg/rat) or clonidine (0.25, 0.5 and 1 μg/rat) with an ineffective dose of scopolamine (0.25 μg/rat), synergistically improved memory performance impaired by post-training scopolamine. On the other hand, pre-test injection of α1-receptors antagonist prazosin (1 and 2 μg/rat) or α2-receptors antagonist yohimbine (1 and 2 μg/rat) prevented the restoration of memory by pre-test scopolamine. It is important to note that pre-test intra-CA1 administration of the same doses of prazosin or yohimbine, alone did not affect memory retrieval. These results suggest that α1- and α2-adrenergic receptors of the dorsal hippocampal CA1 regions may play an important role in scopolamine-induced amnesia and scopolamine state-dependent memory. © 2010 Elsevier Inc

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CRF1/CRF2 and MC3/MC4 Receptors Affect Glutamate- Induced Food Intake in Neonatal Meat-Type Chicken

ABSTRACT Central glutamate, melanocortin and corticotropin systems have mediatory role on several physiologic functions in the brain, but their interactions on appetite regulation are not fully elicited. So, the aim of the current study was to determine interaction of the glutamate with melanocortin and corticotropin systems on food intake in 3-h food-deprived (FD3) neonatal meat-type chicken. In experiment 1, chicken intracerebroventricular (ICV) injected (A) phosphate-buffered saline (PBS), (B) glutamate (75 nmol), (C) glutamate (150 nmol) and (D) glutamate (300 nmol). In experiment 2, (A) PBS, (B) astressin-B (CRF1/CRF2 receptors antagonist, 30 µg), (C) glutamate (300 nmol) and (D) astressin-B+glutamate were ICV injected. Experiments 3-5 were similar to experiment 2, except birds were injected with astressin2-B (CRF2 receptor antagonist, 30 µg), SHU9119 (MC3/MC4 receptor antagonist, 0.5 nmol) and MCL0020 (MC4 receptor antagonist, 0.5 nmol) instead of the astressin-B. In experiment 6, the injections were (A) PBS, (B) MTII (MC3/MC4 receptor agonist, 2.5ng), (C) glutamate (75nmol) and (D) MTII+glutamate. Then, cumulative feed intake was recorded at 30, 60 and 120 minutes after injection. According to the results, dose dependent hypophagia observed by ICV injection of the glutamate (75, 150 and 300nmol) compared to control group in neonatal broiler chicken (p<0.05). Co-injection of the astressin-B+glutamate and astressin2-B+glutamate decreased glutamate-induced hypophagia in neonatal broiler chicken (p<0.05). Co-injection of the glutamate+MC3/MC4 receptors antagonist decreased hypophagic effect of the glutamate (p<0.05). These results suggested hypophagic effect of the glutamate mediates via CRF1/CRF2 and MC3/MC4 receptors in chickens

Effects of methanol extract of soy on the apoptosis of hippocampal cells in ovariectomized rats

Background: The decline in estrogen level after menopause results in a decrease in life quality and different neurological disorders such as memory impairment. However, hormone replacement therapy remains controversial. Some studies have been investigated the effects of soy phytoestrogens (e.g. genistein) on cognitive brain functions. This study aimed to examine the effect of oral administration of soy extract on the apoptosis of hippocampus cells. Materials and Methods: In this study, 30 rats were randomly allocated into 3 equal groups: 1) Sham (surgery without ovariectomy) 2) ovariectomized (OVX) and 3) treatment (OVX+soy extract). The animals in the treatment group received soy extract (60mg/kg) daily in drinking water by gavage for six weeks. At the end of treatment, brain samples of all animals were collected for tissue sectioning. Apoptosis in hippocampal cell was studied using the TUNEL method and a light microscopy. Results: Oral administration of soy extract significantly decreased the number of apoptotic (neuronal and glial) cells (P<0.05), while ovariectomy significantly increased the number of apoptotic cells in the ovariectomized group compared to the Sham (P=0.034) and treatment groups (P=0.016). Conclusion: Results of this study indicate that the oral administration of soy extract in ovariectomized rats had neuroprotective effects by decreasing the number of apoptotic cells

Central Opioidergic System Interplay with Histamine on Food Intake in Neonatal Chicks: Role of µ-Opioid and H1/H3 Receptors

ABSTRACT The present study was designed to examine the role of Opioidergic and Histaminergic systems on feeding behavior in 3-hour food deprived neonatal meat- type chicks. In experiment 1, chicks received intracerebroventricular (ICV) injection of (A) control solution, (B) α-FMH (alpha fluoromethyl histidine; 250 nmol), (C) DAMGO (µ-opioid receptor agonist, 125 pmol) and (D) α-FMH + DAMGO. Experiments 2-4 were similar to experiment 1, except chicken ICV injected with Chlorpheniramine (histamine H1 receptors antagonist; 300 nmol), famotidine (histamine H2 receptors antagonist; 82 nmol) and Thioperamide (histamine H3 receptors antagonist; 300 nmol) instead of the α-FMH. In experiments 5-8, birds ICV injected with the same procedure as experiments 1-4, except they were injected with DPDPE (δ-opioid receptor agonist, 40 nmol) instead of DAMGO. Experiments 9-12 were similar to the experiments 1-4, except neonatal broilers ICV were injected with U-50488H (κ-opioid receptor agonist, 30 nmol) instead of DAMGO. Then the cumulative food intake was measured until 120 min post injection. According to the results, ICV injection of DAMGO, significantly decreased food intake (p0.05). Also, the hyperphagic effect of DPDPE and U-50488 had no affect by α-FMH, Chlorpheniramine, famotidine and Thioperamide (p>0.05). These results suggested that an interconnection between central opioidergic and histaminergic systems on feeding behavior is mediated via µ-opioid and H1/H3 receptors in neonatal broilers