1. Neurogenesis and memory
1.1. Neurogenesis in the hippocampus
The hippocampus is a brain region that responsible for learning, memory and mood. One of the important reasons for memory and mood dysfunction is the dentate gyrus (DG) reduction [12, 13]. The subventricular zone (SVZ) and the subgranular zone (SGZ) of neural progenitor cells generated neurons and glia in adulthood and during adulthood [14]. Neurogenesis also have a role in mood regulation; the dorsal hippocampus is an important region in memory formation and retrieval, whereas ventral hippocampus is an important region in emotions [15] .
The spatial learning and memory retrieval in the MWM (Morris Water Maze) associated with neurogenesis Levels in MWM test of rats and …show more content…
Then, Colchicine recognized as prophylaxis of Mediterranean fever attacks, after decades that its use for amyloidosis preventing [29,30]. The distribution of colchicine in the brain is unequal and in the hippocampus (the area that most affected in AD) is three times higher than in other brain regions [31]. The drug selectively blocks acetylcholine transferase in the basal forebrain and hippocampus, which these regions are responsible for memory [32]. When colchicine penetrates to subarachnoid space showed symptoms, including jumpy and irritable behavior, become aggressive and loss in body …show more content…
Trimethyltin (TMT)
Trimethyltin chloride (C3H9ClSn) (TMT) has neurotoxicant effects which used in neuronal degeneration researches. Studies showed that TMT treatment caused to loss of pyramidal neurons in hippocampus of rats [75-77]. When TMT drug injection in animal appeared some behavioral changes such as seizure, aggressive behavior, self-biting, impairment of working memory, and hyperactivity [78-80]. Studies showed that TMT intoxication caused to cognitive and behavioral dysfunction in experimental animals and humans [79].
Studies showed that TMT drug used in researches of Alzheimer-like diseases in experimental model [81, 82]. The first target of TMT is the hippocampus, where make toxic effects on pyramidal neurons. Structural damage begin 2–3 days after TMT injection (that appeared within 21 days), and continues during several weeks [83]. Although the time of onset and prolonged duration in consequence of relationship with the hemoglobin of rat for TMT. The Hemoglobin associated with slowly and continuously releasing TMT into the plasma, and subsequently into brain [84].
The TMT caused to the cytotoxic effect on glial cells; studies showed that follow TMT administration, increased glial fibrilary acidic protein levels [85] and Na+-K+-ATPase activity changes that due to swelling of primary cultures of astrocytes
1.1. Neurogenesis in the hippocampus
The hippocampus is a brain region that responsible for learning, memory and mood. One of the important reasons for memory and mood dysfunction is the dentate gyrus (DG) reduction [12, 13]. The subventricular zone (SVZ) and the subgranular zone (SGZ) of neural progenitor cells generated neurons and glia in adulthood and during adulthood [14]. Neurogenesis also have a role in mood regulation; the dorsal hippocampus is an important region in memory formation and retrieval, whereas ventral hippocampus is an important region in emotions [15] .
The spatial learning and memory retrieval in the MWM (Morris Water Maze) associated with neurogenesis Levels in MWM test of rats and …show more content…
Then, Colchicine recognized as prophylaxis of Mediterranean fever attacks, after decades that its use for amyloidosis preventing [29,30]. The distribution of colchicine in the brain is unequal and in the hippocampus (the area that most affected in AD) is three times higher than in other brain regions [31]. The drug selectively blocks acetylcholine transferase in the basal forebrain and hippocampus, which these regions are responsible for memory [32]. When colchicine penetrates to subarachnoid space showed symptoms, including jumpy and irritable behavior, become aggressive and loss in body …show more content…
Trimethyltin (TMT)
Trimethyltin chloride (C3H9ClSn) (TMT) has neurotoxicant effects which used in neuronal degeneration researches. Studies showed that TMT treatment caused to loss of pyramidal neurons in hippocampus of rats [75-77]. When TMT drug injection in animal appeared some behavioral changes such as seizure, aggressive behavior, self-biting, impairment of working memory, and hyperactivity [78-80]. Studies showed that TMT intoxication caused to cognitive and behavioral dysfunction in experimental animals and humans [79].
Studies showed that TMT drug used in researches of Alzheimer-like diseases in experimental model [81, 82]. The first target of TMT is the hippocampus, where make toxic effects on pyramidal neurons. Structural damage begin 2–3 days after TMT injection (that appeared within 21 days), and continues during several weeks [83]. Although the time of onset and prolonged duration in consequence of relationship with the hemoglobin of rat for TMT. The Hemoglobin associated with slowly and continuously releasing TMT into the plasma, and subsequently into brain [84].
The TMT caused to the cytotoxic effect on glial cells; studies showed that follow TMT administration, increased glial fibrilary acidic protein levels [85] and Na+-K+-ATPase activity changes that due to swelling of primary cultures of astrocytes