Biomedical subjects

Azita Khalilzadeh

Publications and source records attributed to Azita Khalilzadeh.

9 recordsLinked to original sources

PubMed2006

Influence of ATP-sensitive potassium channels on lithium state-dependent memory of passive avoidance in mice.

The effects of ATP-sensitive potassium channels on lithium induced state-dependent memory of passive avoidance task were examined in mice. The pre-training (5 mg/kg) and pre-test (5 mg/kg) injection of lithium impaired memory retrieval on the test day. Impairment of pre-training lithium was restored by pre-test administration of lithium (5 mg/kg), diazoxide, an ATP-sensitive potassium channel opener, (15, 30 and 60 mg/kg) or glibenclamide, an ATP-sensitive potassium channel blocker, (6 and 18 mg/kg). Pre-test administration of inactive doses of lithium (2.5 and 10 mg/kg) plus lower and inactive dose of glibenclamide (2 mg/kg) or diazoxide (1.5 mg/kg) also reversed the amnesia induced by pre-training lithium (5 mg/kg). In conclusion, the ATP-sensitive potassium channel opener or blocker not only mimicked the effect of lithium in state-dependent learning in the absence of lithium on the test day, but also potentiated the effect of low dose of lithium in restoration of memory. Therefore, ATP-sensitive potassium channels may have a modulatory influence on lithium response.

Animals↗

PubMed2006

Morphine state-dependent learning sensitization and interaction with nitric oxide.

In the present study, the effects of nitric oxide (NO) precursor L-arginine and L-NAME, a potent inhibitor of NO synthase (NOS), on the expression of sensitization of morphine were investigated. Pre-training administration of morphine (5 mg/kg) impaired memory retrieval compared to pre-training saline-treated animals. Amnesia due to pre-training morphine (5 mg/kg) was restored by pre-test morphine (5 mg/kg). The retrieval impairment was also inhibited in mice which had received once-daily injections of morphine (20 and 30 mg/kg, s.c.) for 3 days, followed by 5 days of no drug treatment before training (in order to induce morphine sensitization). Administration of L-arginine (60 mg/kg/day - 3 days) or L-NAME (20 mg/kg/day - 3 days) before training did not alter morphine state dependency. During acquisition of sensitization, administration of L-arginine (60 mg/kg) 20 min before morphine (10 mg/kg/day, for 3 days) increased, while injection of L-NAME (20 mg/kg) 20 min before morphine (30 mg/kg/day, for 3 days) decreased morphine state dependency. It is concluded that NO is involved in the morphine-induced sensitization.

Animals↗

PubMed2006

Influence of intracerebroventricular administration of dopaminergic drugs on morphine state-dependent memory in the step-down passive avoidance test.

The effects of dopaminergic drugs on morphine state-dependent memory of passive avoidance task were examined in mice. Pre-training administration of morphine (5mg/kg) led to state-dependent learning with impaired memory retrieval on the test day which was reversed by pre-test administration of the same dose of the opiate. The pre-test intracerebroventricular (i.c.v.) administration of the dopamine D1 receptor agonist (SKF38393), dopamine D2 receptor agonist (quinpirole) and dopamine D2 receptor antagonist (sulpiride) not only reversed the effect of pre-training morphine treatment, but also increased this action of the drug. Furthermore, the pre-test i.c.v. administration of dopamine D1 receptor antagonist (SCH23390) prevented the restoration of memory by morphine. In conclusion, the morphine-induced recovery of memory, on the test day, seems to be induced, at least in part, through dopamine receptors.

Analysis of Variance↗

PubMed2006

Influence of morphine- or apomorphine-induced sensitization on histamine state-dependent learning in the step-down passive avoidance test.

Effects of morphine- or apomorphine-induced sensitization on histamine state-dependent memory of passive avoidance task were examined in mice. Pre-training intracerebroventricular (i.c.v.) administration of histamine (20 microg/mouse) decreased the learning of a one-trial passive avoidance task. Pre-test administration of histamine (10 and 20 microg/mouse) reversed amnesia induced by pre-training of histamine, with maximum response at 20 microg/mouse. Pre-training histamine-induced amnesia was also reversed in morphine- or apomorphine-sensitized mice that had previously received once daily injections of morphine (20 and 30 mg/kg) or apomorphine (0.5 and 1 mg/kg) for 3 days. The reversion of histamine-induced amnesia in morphine-sensitized mice was decreased by once daily administration of naloxone (0.5 and 1 mg/kg), SCH 23390 (0.05 and 0.1 mg/kg) or sulpiride (25, 50 and 100 mg/kg) prior to injection of morphine (30 mg/kg/day, 3 days). Furthermore, once daily administration of sulpiride (50 and 100 mg/kg) but not SCH 23390 (0.01, 0.05 and 0.1 mg/kg) prior to apomorphine (1 mg/kg, for 3 days) decreased the reversion of pre-training histamine-induced amnesia by apomorphine. The results suggest that apomorphine or morphine sensitization affects the impairment of memory induced by histamine and thus it is postulated that opioid and dopamine receptors may play an important role in this effect.

Animals↗

PubMed2006

Influence of intracerebroventricular administration of cannabinergic drugs on morphine state-dependent memory in the step-down passive avoidance test.

The effects of cannabinergic drugs on morphine state-dependent memory of passive avoidance task were examined in mice. Pre-training (0.25, 0.5 and 5 mg/kg) and post-training (5 mg/kg) administration of morphine impaired memory retrieval on the test day. Impairment of memory retrieval by morphine (5 mg/kg) on the test day was reversed by pre-test administration of the same dose of the opioid. The pre-test intracerebroventricular administration of the cannabinoid CB1/CB2 receptor agonist (WIN55,212-2) (0.75 and 1 microg/mouse) not only mimicked the effect of pre-test morphine treatment, but also increased this action of the opioid. Furthermore, the pre-test intracerebroventricular administration of CB1 receptor antagonist (AM251) (20 and 100 ng/mouse) prevented the restoration of memory by morphine. Pre-training administration of WIN55,212-2 (1 microg/mouse) led to state-dependent learning with impaired memory retrieval on the test day as well, which was reversed by pre-test administration of the drug (0.5, 0.75 and 1 microg/mouse) or morphine (1 and 5 mg/kg). Restoration of impairment induced by WIN55,212-2 was decreased by both the opioid receptor antagonists, naloxone (0.01 microg/mouse) and AM251 (20 and 100 ng/mouse). In conclusion, the improvement of memory retrieval by morphine treatment on the test day seems to be induced, at least in part, by the cannabinoid CB1 receptors.

Analgesics, Opioid↗

PubMed2005

Effects of intracerebroventricular administration of ultra low doses of histaminergic drugs on morphine state-dependent memory of passive avoidance in mice.

The effects of intracerebroventricular (i.c.v.) administration of ultra low doses (ULDs) of histamine, clobenpropit and pyrilamine are studied on morphine state-dependent (STD) memory in mice. Although pre-test administration of different doses of histamine and clobenpropit showed no effect on impairment of memory induced by pre-training morphine, when the above drugs were co-administered with morphine, they inhibited the restoration of memory by morphine. These effects were opposite to microgram doses of the same drugs.

Analgesics, Opioid↗

PubMed2005

Cross state-dependent retrieval between histamine and lithium.

Histamine and lithium state-dependent (StD) retrieval of passive avoidance task and their interactions was examined in mice. The pre-training or pre-test intracerebroventricular (i.c.v.) injection of histamine (20 microg/mouse) impaired retrieval when it was tested 24 h later. In the animals, in which retrieval was impaired due to histamine pre-training administration, pre-test administration of histamine, with the same dose, restored retrieval. The H1 blocker, pyrilamine (20 microg/mouse, i.c.v.), but not the H(2) blocker; ranitidine prevented the restoration of retrieval by pre-test histamine. The pre-training (5 and 10 mg/kg) or pre-test (5 mg/kg) injection of lithium also impaired retrieval, when it was tested 24 h later. In the animals that received lithium (5 mg/kg) or histamine (20 microg/mouse) as pre-training treatment, administration of histamine, clobenpropit or lithium, respectively, resulted in restoration of memory retrieval. Neither pyrilamine nor ranitidine prevented the restoration of retrieval by pre-test lithium. In conclusion, histamine or lithium can induce state-dependent retrieval and a cross-StD exists between these drugs, which may be mediated through the inositol pathway.

Analysis of Variance↗

PubMed2005

Influence of intracerebroventricular administration of histaminergic drugs on morphine state-dependent memory in the step-down passive avoidance test.

The effects of histaminergic drugs on morphine state-dependent memory of a passive avoidance task were examined in mice. Pre-training administration of morphine (5 mg/kg) led to state-dependent learning with impaired memory recall on the test day which was reversed by pre-test administration of the same dose of the opioid. The pre-test intracerebroventricular (i.c.v.) administration of the H(1) blocker (pyrilamine) prevented the restoration of memory by morphine. The H(2) blocker (ranitidine) was ineffective in this regard and the H(3) blocker (clobenpropit) potentiated the effect of morphine on memory recall. The pre-test i.c.v. administration of histamine alone (5, 10, and 20 microg/mouse) not only mimicked the effect of pre-test morphine treatment, but also increased this action of the opioid. The effect of histamine on memory recall was not changed by the pre-test administration of mu-opioid receptor antagonist, naloxone. In conclusion, the improvement of memory recall by morphine treatment, on the test day, seems to be, at least in part, through the release of histamine followed by the stimulation of H(1) receptors. Histamine by itself, when administered on the test day, mimicked morphine-induced memory improvement by a mechanism independent of the mu-opioid receptors.

Animals↗

PubMedDate not supplied

The effect of furosemide infusion on serum epidermal growth factor concentration after acute lung injury.

Acute lung injury and its more severe form, acute respiratory distress syndrome, are clinical syndromes of progressive hypoxemia and ventilation-perfusion mismatch with decreasing pulmonary compliance in the absence of congestive heart failure. Epidermal growth factor is involved in the pathogenesis of airway inflammation as well as a proinflammatory effect in other tissues. Furosemide has been shown to improve pulmonary gas exchange and intrapulmonary shunt by a nondiuretic mechanism in animal models of acute respiratory distress syndrome. The current study was undertaken to clarify whether furosemide attenuates the inflammatory response by changing the epidermal growth factor level in patients with acute lung injury. A prospective, randomized clinical trial involving 30 patients with acute lung injury was designed and conducted over 7 days. The measured outcomes included hemodynamics, acute physiology and chronic health evaluation (APACHE II) scores, and oxygenation. The serum specimens were analyzed with enzyme-linked immunoassay (ELISA) for epidermal growth factor at baseline, then 3 and 7 days after acute lung injury. The ratio of partial pressure of arterial oxygen (PaO2) to fraction of inspired oxygen (FIO2) improved in the furosemide-treated group within 24 hours (from 180 to 264; P = .01). The mean arterial pressure and heart rate was greater in this group than in the control group (that received no furosemide) on day 7 (P = .027). The mean arterial pressure increased and the heart rate decreased over time in the treatment group, but not significantly. Serum epidermal growth factor levels also were not significantly different between the furosemide treatment group and the control group (P > .05). Continuous furosemide infusion improves oxygenation and hemodynamics in patients with acute lung injury, but not through a change in the serum epidermal growth factor level. Further study is needed to determine the exact mechanism of furosemide action in patients with acute lung injury and acute respiratory distress syndrome.

APACHE↗