Shamseddin Ahmadi

Introduction: Vitamin D is implicated in regulation of various biological processes, including calcium homeos tasis, neurogenesis, synaptic plas ticity, the immune sys tem, and inflammation. Nowadays, mos t part of the population worldwide is affected by vitamin D deficiency. The decreases in different factors, including the cutaneous thickness, the sun exposure time, muscle mass, kidney efficiency, and sex s teroids in aged people (especially women), as well as malnutrition cause vitamin D deficiency, which in turn may act as an important risk factor for Alzheimer’s disease (AD). There is a reciprocal relationship between amyloid β (Aβ) as a core factor that initiates the onset and progression of AD and the increases in calcium (Ca2+) levels in neurons. Vitamin D via genomic functions, including either a decreasing expression of L-type Ca2+ channels or increasing expression of Ca2+ pumps, Na+/Ca2+ exchanger, as well as Ca2+ buffers, has the main role in Ca2+ homeos tasis. Therefore...

Background and Aim: Tau protein is a microtubule-associated protein that plays a critical role in microtubule dynamics and maintaining the structure of neurons. Tau isoforms with three or four repeated domains at the c-terminal are known as 3R or 4R isoforms, respectively. Hyperphosphorylation of tau impairs its original structure and function and causes accumulation of tau as tangled filaments known as neurofibrillary tangles. The aim of this study was to review the structure and physiological function of tau and also the role of accumulation and deposition of tau in induction of neurodegenerative diseases. Materials and Methods: Relevant reports about the deposition of tau protein in neurodegenerative diseases were summarized from scientific articles. Results: Deposition of the filamentous tau in neurons and glial cells causes cell damage and induces neurodegenerative diseases such as Alzheimer’s disease (AD), cortico-basal degeneration (CBD), and progressive supranuclear palsy (P...

Backgrounds: Molecular mechanisms involved in adverse effects of morphine, including tolerance and dependence, have remained elusive. We examined possible alterations in the gene expression of proenkephalin (Penk), prodynorphin (Pdyn), and mu-opioid receptor (Oprm1) in reward brain areas following frequent morphine treatment. Methods: Two groups of male Wistar rats were used. The groups received either saline (1 mL/kg) or morphine (10 mg/kg) twice daily for eight days. On day 8, rats were decapitated, brain areas involved in addiction were dissected, including the midbrain, striatum, prefrontal cortex (PFC), hippocampus, and hypothalamus, and gene expression was evaluated with real-time PCR. Results: Prolonged morphine treatment decreased Penk, Pdyn, and Oprm1 gene expressions in the midbrain but upregulated them in the striatum compared to the control group treated with saline. Significant increases in Pdyn and Oprm1 gene expressions were detected in the PFC, but there was no signi...

We have previously shown lithium-induced state-dependent learning in a step-down inhibitory avoidance task. In the present study, the effects of intracerebroventricular injections of N-methyl-D-aspartate (NMDA) receptor agents on the lithium-induced state-dependent learning have been investigated. A single-trial step-down inhibitory avoidance task was used to assess memory in male Naval Medical Research Institute (NMRI) mice. The results showed that post-training lithium (10 mg/kg) decreased the step-down latency on the test day, which was reversed by pre-test administration of the same dose of the drug; indicating state-dependent learning induced by lithium. Pre-test administration of NMDA (0.0001, 0.001 and 0.01 microg/mouse, intracerebroventricular) could also substitute for pre-test lithium to reverse the decrease of the step-down latency induced by post-training lithium. Furthermore, pre-test co-administration of an ineffective dose of NMDA (0.00001 microg/mouse, intracerebrove...