1. Home
  2. Knowledge Base
  3. References
  4. Decrease of Arc protein expression and delay of memory acquisition by immunolesion

Decrease of Arc protein expression and delay of memory acquisition by immunolesion

Jeong D, Lee D, Chang J (2010) Decrease of Arc protein expression and delay of memory acquisition by immunolesion. Neuroscience 2010 Abstracts 145.5/H6. Society for Neuroscience, San Diego, CA.

Summary: Cholinergic neuronal deficit is one of the common characteristics in both Alzheimer’s disease dementia (AD) and vascular dementia (VaD). Forebrain Cholinergic neurons in the basal forebrain project to the neocortex and the hippocampus which make an important role in memory function. We used 192 IgG-saporin to produce selective lesion of cholinergic basal forebrain neurons including the medial septum (MS) and the nucleus basalis magnocellularis (NBM). We intracerebroventricularly injected 192 IgG-saporin (0.63 µg/µl dose, 6 µl, 8 µl and 10 µl) or phosphate buffered saline (8 µl). Morris water maze and tissue perforation for immunohistochemistry and western blotting were sequentially performed 2 weeks after injection of 192 IgG-saporin. In the acquisition phase of Morris water maze, latency of 6ul group (2nd day), 8 µl group (2nd day) and 10 µl group (3rd day) was significantly delayed but it was recovered within 1week. Time in platform and the number of crossing were significantly different between 8 µl LV injection group and sham group in probe test. In immunohistological study, the extent of the cholinergic lesion was showed in the basal forebrain complex region of all 192 IgG-saporin injected rats. Expression of Arc protein is significantly decreased in the frontal cortex (8 µl and 10 µl groups) but hippocampus. Decrease of parvalbumin in the frontal cortex (8ul and 10 ul groups) and the hippocampus (10 µl) means nonselective lesion because of high dose of immunotoxin. We observed recovery after memory acquisition delay and decrease of synaptic activity in the frontal cortex except in the hippocampus. High dose of immunotoxin injured not only cholinergic neuron but also GABAergic neuron in the frontal cortex and the hippocampus. Hippocampal GABAergic cell synapse on to glutamatergic pyramidal cells. Deficit of the hippocampal inhibitory cell may facilitate hippocampal synaptic plasticity and the recovery.

Related Products: 192-IgG-SAP (Cat. #IT-01)