Neuroscience 2004 Abstract
| Presentation Number: | 675.5 |
|---|---|
| Abstract Title: | VDM-11, an endocannabinoid reuptake inhibitor, improves amnesia induced by â-amyloid fragment 1-42. |
| Authors: |
Micale, V.*1
; Mazzola, C.1
; Consoli, D.1
; Incognito, T.1
; Leggio, G. M.1
; Di Marzo, V.2
; Drago, F.1
1Dept Exp & Clin Pharmacol, Univ Catania, Catania, Italy 2Italy, Viale Andrea Doria 6, 95125, |
| Primary Theme and Topics |
Cognition and Behavior - Human Cognition, Behavior, and Anatomy -- Working memory |
| Session: |
675. Anti-Ab Treatments: Animal Models II Poster |
| Presentation Time: | Tuesday, October 26, 2004 8:00 AM-9:00 AM |
| Location: | San Diego Convention Center - Hall A-H, Board # TT16 |
| Keywords: | PASSIVE AVOIDANCE, BEHAVIOR, COGNITION, CANNABINOIDS |
There is evidence that i.c.v. infusion of the â-amyloid (Aâ) 1-42 peptide fragment (BAP 1-42) may cause brain dysfunction as evidenced by neurodegeneration and impairment of learning and memory, typical symptoms of Alzheimer’s disease. Neurodegeneration affects subcortical nuclei involved in cognitive behavior and disrupt cholinergic neurotransmission in these nuclei.
Endogenous cannabinoids decrease brain ACh levels and may induce a deficit of memory capacity. These effects are mediated by the activation of CB1 cannabinoid receptors. In fact, administration of the selective CB1 cannabinoid receptor antagonist, SR141716A, reversed in mice the cognitive impairment induced by cannabinoids, such as marijuana and its active ingredient Ä9 – tetrahydrocannabinol, or endogenous cannabinoids, such as anandamide. SR141716A also counteracted the amnesia induced by BAP 1-42 in the passive avoidance paradigm.
It is likely that a direct correlation exists between the amnesic effect induced by Aâ and cerebral CB1 action. Administration of the endocannabinoid reuptake inhibitor, VDM-11 (5 mg/kg, for 2 weeks) improved memory capacity of mice pretreated with BAP 1-42 (400 pmol/mouse). Cognitive impairment was evaluated 14 and 21 days after treatment with Aâ fragment. Pre-training administration of Aâ fragment induced a decrease of latency in step-through type passive avoidance task. VDM-11 when injected intraperitoneally 3 days after BAP 1-42, improved behavioral performance of animals but did not modify Aâ effects when administered 7 days after the i.c.v. of BAP 1-42.
These data suggest that cannabinoids can modulate learning and memory processes affected by Aâ peptide in mice tested in passive avoidance paradigm in a time-dependent manner.
Endogenous cannabinoids decrease brain ACh levels and may induce a deficit of memory capacity. These effects are mediated by the activation of CB1 cannabinoid receptors. In fact, administration of the selective CB1 cannabinoid receptor antagonist, SR141716A, reversed in mice the cognitive impairment induced by cannabinoids, such as marijuana and its active ingredient Ä9 – tetrahydrocannabinol, or endogenous cannabinoids, such as anandamide. SR141716A also counteracted the amnesia induced by BAP 1-42 in the passive avoidance paradigm.
It is likely that a direct correlation exists between the amnesic effect induced by Aâ and cerebral CB1 action. Administration of the endocannabinoid reuptake inhibitor, VDM-11 (5 mg/kg, for 2 weeks) improved memory capacity of mice pretreated with BAP 1-42 (400 pmol/mouse). Cognitive impairment was evaluated 14 and 21 days after treatment with Aâ fragment. Pre-training administration of Aâ fragment induced a decrease of latency in step-through type passive avoidance task. VDM-11 when injected intraperitoneally 3 days after BAP 1-42, improved behavioral performance of animals but did not modify Aâ effects when administered 7 days after the i.c.v. of BAP 1-42.
These data suggest that cannabinoids can modulate learning and memory processes affected by Aâ peptide in mice tested in passive avoidance paradigm in a time-dependent manner.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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