Scopolamine Reduces the Density of M1 Muscarinic Neurons in Rats' Hippocampus

Jahanshahi, Mehrdad; Nickmahzar, E. G.; Babakordi, Fatemeh; Moharreri, Alireza

doi:10.4067/s0717-95022013000400014

Cited by 11 publications

(11 citation statements)

References 18 publications

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“…Consistently with earlier findings [44], our results revealed that treatment of Wistar rats with scopolamine led to decrease M1 muscarinic receptor-ir neuron numbers in the hippocampus. Similarly, after an injection of scopolamine to dogs, the older dogs showed a significant decrease in the density of the muscarinic receptor in some areas of cortex [4].…”

Section: Discussionsupporting

confidence: 93%

“…Furthermore, the M1 immunoreactivity was markedly decreased in AD brains [85] and also an age-related decrease in the M1 receptor has been reported [91]. Some other researches confirm a scopolamine injection, severe cell losses in hippocampal cholinergic neurons [44,57].…”

Section: Discussionmentioning

confidence: 78%

“…The post-training scopolamine dose-dependently decreased the stepthrough latency in the inhibitory avoidance task; it shows scopolamine-induced amnesia [42]. Also, scopolamine reduced dose-dependently the number of M1 muscarinic receptor-immunoreactive (ir) neurons in the male rats' hippocampus [44]. Moreover, scopolamine directly caused damage to the hippocampal circuits that might predominantly be responsible for cognitive and memory deficits [18].…”

Section: Introductionmentioning

confidence: 97%

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Vitamin E can compensate the density of M1 receptors in the hippocampus of scopolamine-treated rats

Sayyahi¹,

Jahanshahi²,

Amini³

et al. 2018

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M1 muscarinic receptor plays a fundamental role in memory and is closely associated with Alzheimer's disease (AD); it has long been assumed as a therapeutic goal. By activating of the cholinergic receptor vitamin E helps with memory retention. But effects of vitamin E on density of M1 muscarinic receptor-immunoreactive (ir) neurons remain poorly understood. The present research aimed to examine the chronic administration effect of vitamin E against scopolamine-induced memory loss and the number of M1 muscarinic receptor-ir neurons of the hippocampus in male rats. Randomly, 42 adult male Wistar rats were divided to six groups: control, Sham-saline: receiving scopolamine + saline, Sham-sesame oil: receiving scopolamine + sesame oil and three experimental groups: receiving scopolamine + vitamin E with different doses (25, 50, and 100 mg/kg/day, i.p.) for 14 days. The passive avoidance task was used for the memory test. Twenty-four hours after behavioral tests, rats' brains were taken and fixed, and after tissue processing, sections were stained using the immunohistochemical technique for M1 muscarinic receptor-ir neurons and cresyl violet for neurons. The injection of scopolamine to rats caused memory impairment and vitamin E treatment could ameliorate it. In the scopolamine-treated groups, the number of CA1 and CA3 pyramidal and dentate gyrus (DG) granular neurons was decreased significantly as compared to the control group. Vitamin E treatment significantly increased neuron numbers in the CA1 and CA3 areas of the hippocampus and DG area. Treatment with vitamin E for 14 days could compensate the loss of M1 muscarinic receptor-immunoreactive neuron numbers induced by scopolamine in the hippocampus. The most effective vitamin E dose was 50 mg/kg/day in this study. In conclusion, vitamin E can compensate the neuronal loss in the hippocampal formation and also it can raise the density of M1 receptor-ir muscarinic neurons after an injection of scopolamine.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 97%

See 1 more Smart Citation

Vitamin E can compensate the density of M1 receptors in the hippocampus of scopolamine-treated rats

Sayyahi¹,

Jahanshahi²,

Amini³

et al. 2018

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show abstract

“…A field of 30,000 µm 2 for CA1 and CA3 areas and also 4800 µm 2 in DG area was selected randomly in the all sections. To measure the area density of the androgen receptor-ir neurons, using OLYSIA Autobioreport software (Olympus, Japan), the appropriate grids were superimposed on the pictures, and the cells were counted manually [ 50 , 51 ].…”

Section: Methodsmentioning

confidence: 99%

Gonadectomy reduces the density of androgen receptor-immunoreactive neurons in male rat’s hippocampus: testosterone replacement compensates it

et al. 2016

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Background In the present study, the role of gonadectomy on memory impairment and the density of androgen receptor-immunoreactive neurons in rats’ hippocampus as well as the ability of testosterone to compensate of memory and the density of androgen receptors in the hippocampus was evaluated.MethodsAdult male rats (except intact-no testosterone group) were bilaterally castrated, and behavioral tests performed 2 weeks later. Animals bilaterally cannulated into lateral ventricles and then received testosterone (10, 40 and 120 µg/0.5 µl DMSO) or vehicle (DMSO; 0.5 µl) for gonadectomized-vehicle group, 30 min before training in water maze test. The androgen receptor-immunoreactive neurons were detected by immunohistochemical technique in the hippocampal areas.ResultsIn the gonadectomized male rats, a memory deficit was found in Morris water maze test on test day (5th day) after DMSO administration. Gonadectomy decreased density of androgen receptor-immunoreactive neurons in the rats’ hippocampus. The treatment with testosterone daily for 5 days attenuated memory deficits induced by gonadectomy. Testosterone also significantly increased the density of androgen receptor-immunoreactive neurons in the hippocampal areas. The intermediate dose of this hormone (40 µg) appeared to have a significant effect on spatial memory and the density of androgen receptor-immunoreactive neurons in gonadectomized rats’ hippocampus.ConclusionsThe present study suggests that testosterone can compensate memory failure in gonadectomized rats. Also testosterone replacement can compensate the reduction of androgen receptor-immunoreactive neurons density in the rats’ hippocampus after gonadectomy.

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“…The sections were stained with antibody against 5-HT 2A serotonergic receptor, according to our previous report [54] with slight modifications. The sections were first incubated at 37℃ for 30 minutes, then, for deparaffinization, the sections embedded in xylene and hydrated with different degrees of ethanol.…”

Section: Methodsmentioning

confidence: 99%

Hippocampal serotonin-2A receptor-immunoreactive neurons density increases after testosterone therapy in the gonadectomized male mice

et al. 2016

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The change of steroid levels may also exert different modulatory effects on the number and class of serotonin receptors present in the plasma membrane. The effects of chronic treatment of testosterone for anxiety were examined and expression of 5-HT2A serotonergic receptor, neuron, astrocyte, and dark neuron density in the hippocampus of gonadectomized male mice was determined. Thirty-six adult male NMRI mice were randomly divided into six groups: intact-no testosterone treatment (No T), gonadectomy (GDX)-No T, GDX-Vehicle, GDX-6.25 mg/kg testosterone (T), GDX-12.5 mg/kg T, and GDX-25 mg/kg T. Anxiety-related behavior was evaluated using elevated plus maze apparatus. The animals were anesthetized after 48 hours after behavioral testing, and decapitated and micron slices were prepared for immunohistochemical as well as histopathological assessment. Subcutaneous injection of testosterone (25 mg/kg) may induce anxiogenic-like behavior in male mice. In addition, immunohistochemical data reveal reduced expression of 5-HT2A serotonergic receptor after gonadectomy in all areas of the hippocampus. However, treatment with testosterone could increase the mean number of dark neurons as well as immunoreactive neurons in CA1 and CA3 area, dose dependently. The density of 5-HT2A receptor-immunoreactive neurons may play a crucial role in the induction of anxiety like behavior. As reduction in such receptor expression have shown to significantly enhance anxiety behaviors. However, replacement of testosterone dose dependently enhances the number of 5-HT2A receptor-immunoreactive neurons and interestingly also reduced anxiety like behaviors.

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Scopolamine Reduces the Density of M1 Muscarinic Neurons in Rats' Hippocampus

Cited by 11 publications

References 18 publications

Vitamin E can compensate the density of M1 receptors in the hippocampus of scopolamine-treated rats

Vitamin E can compensate the density of M1 receptors in the hippocampus of scopolamine-treated rats

Gonadectomy reduces the density of androgen receptor-immunoreactive neurons in male rat’s hippocampus: testosterone replacement compensates it

Hippocampal serotonin-2A receptor-immunoreactive neurons density increases after testosterone therapy in the gonadectomized male mice

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