Prolonged cannabinoid treatment results in spatial working memory deficits and impaired long-term potentiation in the CA1 region of the hippocampus in vivo.
Matthew N Hill, David J Froc, Christopher J Fox, Boris B Gorzalka, Brian R Christie
The European journal of neuroscience August 2004 DOI: 10.1111/j.1460-9568.2004.03522.x (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Adult male Long-Evans rats |
| Intervention | HU-210 |
| Dose | 100 microg/kg, i.p., daily for 15 days |
| Duration | 15 days of administration, followed by behavioral testing over 5 days |
| Measures | Morris water maze (matching-to-place version), long-term potentiation (electrophysiology) |
| Key findings | Rats given HU-210 for 15 days showed initial reference memory deficits that resolved over five days, working memory impairments only at longer intertrial delays, and significantly impaired hippocampal long-term potentiation. |
Abstract
Adult male Long-Evans rats were administered the potent cannabinoid 1 receptor agonist HU-210 (100 microg/kg, i.p.) for 15 days continuously and their performance on a matching-to-place version of the Morris water maze was subsequently evaluated. Overall, experimental animals performed significantly worse initially on the reference memory component of this task, but their performance improved over 5 days until it was indistinguishable from that of control animals. Animals given HU-210 did not exhibit working memory impairments at short intertrial delays (30 s); however, significant impairments were observed in learning performance with longer intertrial delays (300 s). In vivo electrophysiological analyses revealed that long-term potentiation in the CA1 region of the hippocampus was significantly impaired following the administration of HU-210 for 15 days. These results indicate that long-term cannabinoid exposure can produce marked deficits in reference and working memory performance, and also impair hippocampal synaptic plasticity in vivo.