جستجوی مقالات مرتبط با کلیدواژه « nbm » در نشریات گروه « پزشکی »

Alzheimer’s Disease (AD) is a chronic neurological disorder characterized by memory impairment, cognitive dysfunction, behavioral disturbances, and deficits in activities of daily living. AD has been found to be associated with a cholinergic deficit in the post-mortem brain characterized by a significant decrease in acetylcholine amount and loss of cholinergic neurons of the nucleus basalis of Meynert (NBM). This study investigated the effect of Zizyphus jujuba (ZJ) extract on motor activity in NBM-lesioned rat model of AD and intact rats. In this study, 49 wistar rats were divided into 7 groups. Rats received bilateral electrolytic lesions of the NBM. The control and sham group received distilled water while NBM-lesioned groups received ZJ extract via gastric gavage for 20 days. Intact rats received ZJ extract for 20 days without any surgery. The motor activity assessed with rota-rod apparatus. Data were compared using one way ANOVA followed by LSD post test. ZJ extract for 20 days improved motor activity in NBM-lesioned rats and intact rats that received extract at the dose of 1000 mg/kg. Results suggest that ZJ extract can improve the motor coordination both in NBM-lesioned rats and in intact rats.

Cholinergic neurons of nucleus basalis magnocellularis (NBM) have a key role in learning and memory process. It has been shown that these neurons are degenerated in patients with Alzheimer disease (AD). On the other hand, using the cholinomimetic agents and acetylcholinesterase inhibitors improve cognition in these patients. Some studies have shown that the frontal cortex receives some cholinergic projections from NBM. In the present study, the effect of intrafrontal cortex administration of physostigmine (acetylcholinesterase inhibitor) was investigated on active avoidance learning on the animal model of AD. In this experimental study, NBM was lesioned electricaly in Wistar male rats, (250-300g body weight) for making the animal model of AD. Because the frontal cortex receives cholinergic projections from NBM, different doses of physostigmine (2.5, 5, 7.5 µg/µl) were injected bilaterally into the frontal cortex of lesioned rats 20 minutes before active avoidance learning (8 sessions, 30 steps in each session) in Y-maze. The results showned that active avoidance learning was decreased significantly in NBM-lesioned group. Also intrafrontal cortex injection of phsostigmine (2.5, 5, and 7.5 µg/µl) significantly severed NBM lesion-induced learning deficiency. The findings of this study suggest that the cholinergic projection of NBM to frontal cortex in lesioned animals has a negative role on this type of learning. It seems that other neurotransmitter systems such as glutamate and other afferent projections from different brain areas to frontal cortex probably are involved in this phenomenon.

Cholinergic neurons of nucleus basalis magnocellularis (NBM) have a key role in learning and memory process. It has been shown that these neurons are degenerated in patients with Alzheimer disease (AD). On the other hand, using the cholinomimetic agents and acetylcholinesterase inhibitors improve cognition in these patients. Some studies have shown that the frontal cortex receives some cholinergic projections from NBM. In the present study, the effect of intrafrontal cortex administration of physostigmine (acetylcholinesterase inhibitor) was investigated on active avoidance learning on the animal model of AD. In this experimental study, NBM was lesioned electricaly in Wistar male rats, (250-300g body weight) for making the animal model of AD. Because the frontal cortex receives cholinergic projections from NBM, different doses of physostigmine (2.5, 5, 7.5 µg/µl) were injected bilaterally into the frontal cortex of lesioned rats 20 minutes before active avoidance learning (8 sessions, 30 steps in each session) in Y-maze. The results showned that active avoidance learning was decreased significantly in NBM-lesioned group. Also intrafrontal cortex injection of phsostigmine (2.5, 5, and 7.5 µg/µl) significantly severed NBM lesion-induced learning deficiency. The findings of this study suggest that the cholinergic projection of NBM to frontal cortex in lesioned animals has a negative role on this type of learning. It seems that other neurotransmitter systems such as glutamate and other afferent projections from different brain areas to frontal cortex probably are involved in this phenomenon.