Cannabinoid Receptor Involved in Cognitive Effects: ECS Study From China
Out on PubMed, in Psychiatry Research, from researchers in Chongqing, China is this study:
Inhibition of CB1 receptor alleviates electroconvulsive shock-induced memory impairment by regulating hippocampal synaptic plasticity in depressive rats.
Psychiatry Res. 2021 Apr 3;300:113917. doi: 10.1016/j.psychres.2021.113917. Online ahead of print.PMID: 33848965
The abstract is copied below:
Electroconvulsive therapy (ECT) is one of the most effective treatments for depression, but it can cause cognitive deficit. Unfortunately, effective preventive measures are still lacking. The endocannabinoid system is thought to play a key role in regulation of cognitive process. Whether the endocannabinoid system is involved in the learning and memory impairment caused by ECS remain unclear. In this work, we first found that cannabinoid receptor type 1 (CB1R) and 2-arachidonoylglycerol (2-AG) were strongly expressed in hippocampus by electroconvulsive shock (ECS) in a rat depression model established by chronic mild stress (CMS). Pharmacological inhibition of CB1R using AM251 in vivo resulted in a pronounced relief in ECS-induced spatial learning and memory impairment as well as in a marked reversal of impaired hippocampal long-term potentiation (LTP), and reduced synapse-related proteins expression. Furthermore, results of sucrose preference test (SPT) and open-field test (OFT) showed that AM251 had no significant impact on the therapeutic effects of ECS on pleasure and psychomotor activity. Taken together, we identified that CB1R is involved in the ECS-induced spatial learning and memory impairment and Inhibition of CB1R facilitates the recovery of memory impairment and hippocampal synaptic plasticity, without interfering with the therapeutic effects of ECS in depressed rats.Keywords: 2-arachidonoylglycerol; Am251; Endocannabinoid system; Learning.
And from the text:
On the
whole, these evidences described previously endorse the hypothesis that
the memory impairments are closely related to activation of hippocampal CB1R. Interestingly, several recent studies have shown that the
level of CB1R ligands increased significantly in cerebrospinal fluid and
hippocampal tissue after ECT/ECS(Hill et al., 2007; Kranaster et al.,
2017, 2019).
Hence, based on all these mentioned above, we hypothesized that the
endocannabinoid system could be involved in ECS-induced cognitive
impairment and might be associated with synaptic plasticity. In this
present work, our data showed that ECS activates the endocannabinoid
system in the hippocampus of depressed rat model. Inhibition of CB1R
can alleviate ECS-induced cognitive damage and synaptic plasticity
impairment without affecting the therapeutic effects of ECS.
Conclusion:
This work provides the first evidence that inhibition of CB1R alleviates ECS-induced memory impairment, possibly by reversing the
dysfunction of hippocampal synaptic plasticity and the down-regulation
of synapse-related proteins, without interfering with the therapeutic
effects of ECS in a rat depression model. CB1R may be a novel target for
preventing cognitive side effects of ECS.
This is a well-presented basic science ECS study investigating potential mechanisms of the cognitive effects of ECS and therefore, potentially, ECT. I feature it today to show 1) (generically) that ECS research into mechanisms of action of ECT continues to be robust and 2) (specifically) the endocannabinoid system may be involved in cognitive effects of seizures and subject to manipulation. Despite all the limitations of translating animal models to psychiatric illness in humans, the conclusion here is interesting.
For neurochemistry buffs, this paper is worth a full read, ~25 minutes; for the rest of us, the above synopsis of the information should suffice.
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