Basic and Clinical Neuroscience

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Showing 3 results for Zardooz

Influence of Nitric Oxide in the Central Amygdala on the Acquisition and Expression of Morphine-Induced Place Preference in Morphine Sensitized Rats

Sara Bijani, Sara Sadeghi-Gharachehdaghi, Homeira Zardooz, Hassan Ghoshooni, Akram Eidi, Jamal Shams, Mohammad-Reza Zarrindast, Hedayat Sahraei,
Volume 2, Issue 4 (Summer 2011 -- 2011)

Abstract

Effects of intra-central amygdala administration of L-arginine, a nitric oxide precursor, and NG-nitro-L-arginine methyl-ester (L NAME), a nitric oxide synthase inhibitor, on the morphine-induced sensitization and also on the expression of morphine-induced place conditioning in rats were studied. Subcutaneous (s.c.) administration of morphine (2.5, 5 and 7.5 mg/kg) induced place conditioning. Repeated pretreatment of morphine (5 mg/kg, i.p.) followed by 5 days no drug treatment, increased place conditioning induced by morphine (0.5 mg/kg). Repeated intra-central amygdala administration of L-arginine (0.3, 1 and 3 μg/ rat), with morphine during acquisition of sensitization, significantly increased or reduced morphine place conditioning in sensitized rats. The drug administration before testing also increased and reduced the expression of morphine place conditioning in sensitized animals. Repeated intra-central amygdala injections of L-NAME (0.3, 1 and 3 μg/rat) with morphine during acquisition of sensitization, reduced the acquisition of morphine place conditioning in the sensitized animals. The drug injection before testing also reduced morphine-induced conditioning. The results indicate that nitric oxide (NO) within the central amygdala may be involved in the acquisition and expression of morphine place conditioning in morphine-sensitized rats.

Oral Morphine Consumption Reduces Lens Development in Rat Embryos

Masoomeh Kazemi, Elaheh Tekieh, Sara Sadeghi-Gharachdaghi, Hassan Ghoshoni, Homeira Zardooz, Hedayat Sahraei, Fatemeh Rostamkhani, Hossein Bahadoran,
Volume 3, Issue 3 (Spring 2012 -- 2012)

Abstract

Introduction: Consumption of morphine, during pregnancy, in addition to inducing defects in the mother’s nervous system function, caused defects or delays in the formation and evolution of embryonic visual system. In the present study, changes in lens development were assessed in embryos exposed to morphine in utero.

Methods:

Female Wistar rats (250-300 g) were mated with male rats and pregnancy was determined by sperm observation in vaginal smear. This day was considered as embryonic day zero (E0). The females were then divided randomly into the experimental and the control groups. The control group received tap water and the experimental group received morphine (0.05 mg/ml) in their water. On embryonic day 13 ( E13), blood samples were collected from the retro-orbital sinus of all animals for plasma corticosterone detection. On embryonic day 17(E17), the animals were killed by an overdose of chloroform and the embryos were taken out surgically. The embryos were fixed in 10% formalin for 30 days. At this time, the head of the embryos were removed for tissue processing and Hematoxylin- Eosin (H&E) staining. The samples were evaluated using light microscope and MOTIC software. Results:
Our data indicated that plasma corticosterone level was dramatically increased and the lens was thinner in the experimental group. (Although the proliferation of lens cells increased in the experiment group but that lens had delay in removing the proliferated and elongation cells with abnormal density in the lateral part of the lens in comparison with the control group). Moreover, the opening of the eyelids was delayed in the off springs of the mothers who received morphine. Discussion:
This study showed that morphine consumption during pregnancy leads to defects in fetal visual system development, particularly in the lens, and eyelids.

Effects of Memantine, an NMDA Antagonist, on Metabolic Syndromes in Female NMRI Mice

Naser Osanloo, Nahid Sarahian, Homeira Zardooz, Hedayat Sahraei, Mohammad Sahraei, Bahareh Sadeghi,
Volume 6, Issue 4 (Automn 2015 -- 2015)

Abstract

Introduction: The brain glutamate neurotransmitter system and its NMDA receptors in the nucleus accumbens play an important role in the incidence of the phenomena of sensitivity and addiction. The present study examined the inhibitory effect of glutamate NMDA receptors in the nucleus accumbens in response to chronic stress.

Methods: After the unilateral and bilateral cannula placement in the nucleus accumbens, one group of the animals received different intra-accumbens doses of memantine (0.1, 0.5 and 1 µg/mouse) 5 minutes before receiving the electric shock stress at their soles (using a Communication Box) and the other group received intraperitoneal doses of memantine (0.1, 0.5 and 1mg/kg) 30 minutes before receiving the same shock. Chronic stress increased the animals' plasma corticosterone, food and water intake and weight and reduced their defecation rates and eating latency.

Results: The intraperitoneal administration of memantine increased plasma corticosterone, water intake, fecal weight and eating latency, but had no effect on food intake or weight. The dose and site-dependent intra-accumbens administration of memantine either exacerbated the effects of stress on plasma corticosterone levels and water and food intake, or else had no effect on these parameters. Furthermore, the administration of memantine had no effect on animal’s weight and inhibited the effects of stress on fecal weight and eating latency.

Discussion: The inhibition of glutamate NMDA receptors in the nucleus accumbens can inhibit and/or exacerbate the dose and site-dependent effects of chronic stress, with gender playing a significant role in producing this effect.

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