The role of nitric oxide in the PKA inhibitor induced spatial memory deficits in rat: Involvement of choline acetyltransferase

ABSTRACTMethamphetamine (METH) is frequently abused drug and produces cognitive deficits. METH could induce hyper-glutamatergic state in the brain, which could partially explain METH-related cognitive deficits, but the synaptic etiology remains incompletely understood. To address this issue, we explored the role of dCA1 tripartite synapses and the potential therapeutic effects of electro-acupuncture (EA) in the development of METH withdrawal-induced spatial memory deficits in mice. We found that METH withdrawal weakened astrocytic capacity of glutamate (Glu) uptake, but failed to change Glu release from dCA3, which lead to hyper-glutamatergic excitotoxicity at dCA1 tripartite synapses. By restoring the astrocytic capacity of Glu uptake, EA treatments suppressed the hyper-glutamatergic state and normalized the excitability of postsynaptic neuron in dCA1, finally alleviated spatial memory deficits in METH withdrawal mice. These findings indicate that astrocyte at tripartite synapses might be a key target for developing therapeutic interventions against METH-associated cognitive disorders, and EA represent a promising non-invasive therapeutic strategy for the management of drugs-caused neurotoxicity.

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Attenuation by a novel synthetic analogue of ACTH4-7 of the learning and memory deficits in juvenile rats treated with amphetamine in utero: role of nitric oxide

BMC Pharmacology ◽

10.1186/1471-2210-9-s2-a26 ◽

2009 ◽

Vol 9 (Suppl 2) ◽

pp. A26

Author(s):

Valentina Bashkatova ◽

Sergey Sudakov ◽

Darya Rezvanova ◽

Helmut Prast ◽

Anatoly Vanin

Keyword(s):

Nitric Oxide ◽

Learning And Memory ◽

Memory Deficits ◽

In Utero ◽

Synthetic Analogue ◽

Juvenile Rats ◽

Learning And Memory Deficits

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Systemic administration of choline acetyltransferase decreases blood pressure in murine hypertension

Molecular Medicine ◽

10.1186/s10020-021-00380-6 ◽

2021 ◽

Vol 27 (1) ◽

Author(s):

Andrew Stiegler ◽

Jian-Hua Li ◽

Vivek Shah ◽

Tea Tsaava ◽

Aisling Tynan ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Choline Acetyltransferase ◽

Cell Subset ◽

Response Duration ◽

Reduce Blood Pressure ◽

Genetic Ablation

AbstractAcetylcholine (ACh) decreases blood pressure by stimulating endothelium nitric oxide-dependent vasodilation in resistance arterioles. Normal plasma contains choline acetyltransferase (ChAT) and its biosynthetic product ACh at appreciable concentrations to potentially act upon the endothelium to affect blood pressure. Recently we discovered a T-cell subset expressing ChAT (TChAT), whereby genetic ablation of ChAT in these cells produces hypertension, indicating that production of ACh by TChAT regulates blood pressure. Accordingly, we reasoned that increasing systemic ChAT concentrations might induce vasodilation and reduce blood pressure. To evaluate this possibility, recombinant ChAT was administered intraperitoneally to mice having angiotensin II-induced hypertension. This intervention significantly and dose-dependently decreased mean arterial pressure. ChAT-mediated attenuation of blood pressure was reversed by administration of the nitric oxide synthesis blocker l-nitro arginine methyl ester, indicating ChAT administration decreases blood pressure by stimulating nitic oxide dependent vasodilation, consistent with an effect of ACh on the endothelium. To prolong the half life of circulating ChAT, the molecule was modified by covalently attaching repeating units of polyethylene glycol (PEG), resulting in enzymatically active PEG-ChAT. Administration of PEG-ChAT to hypertensive mice decreased mean arterial pressure with a longer response duration when compared to ChAT. Together these findings suggest further studies are warranted on the role of ChAT in hypertension.

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A role of Na+, K+ -ATPase in spatial memory deficits and inflammatory/oxidative stress after recurrent concussion in adolescent rats

Brain Research Bulletin ◽

10.1016/j.brainresbull.2021.12.009 ◽

2021 ◽

Author(s):

G. Cassol ◽

R.P. Cipolat ◽

W.L. Papalia ◽

D.B. Godinho ◽

C.B. Quines ◽

...

Keyword(s):

Oxidative Stress ◽

Spatial Memory ◽

Memory Deficits ◽

Adolescent Rats

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Kainic acid lesion-induced spatial memory deficits of rats

Open Life Sciences ◽

10.2478/s11535-009-0001-9 ◽

2009 ◽

Vol 4 (2) ◽

pp. 179-185 ◽

Cited By ~ 6

Author(s):

Lucian Hritcu ◽

Toshitaka Nabeshima

Keyword(s):

Spatial Memory ◽

Kainic Acid ◽

Memory Performance ◽

Memory Deficits ◽

Reference Memory ◽

Maze Task ◽

Y Maze ◽

Processing And Storage ◽

And Storage

AbstractThe effects of lesioning the ventral tegmental area (VTA) or substantia nigra (SN) neurons by means of bilateral stereotaxic microinjections of kainic acid (KA) (0.4 mM) were investigated to clarify the role of the VTA and the SN neurons in learning and memory processes. The present study demonstrates that KA in the SN and the VTA lesioned rats significantly decreased spontaneous alternation in Y-maze task, working memory and reference memory in radial 8 arm-maze task, suggesting effects on spatial memory performance. Our findings provide further support for the role of the VTA and the SN neurons in processing and storage of information.

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