Plotting the I/O as fEPSP vs FV gives an interesting result, I have some ideas but would be curious how the more experienced would interpret this
Beautiful registration of focal evoked responses in the CA1 region of the hippocampus with cannabidiol application. You know well that cannabinoids are retrograde transmitters, they are released from the postsynaptic cell and act on receptors of the presynaptic cell (mainly, CB1 receptors). Activation of cannabinoid receptors temporarily reduces the release of conventional neurotransmitters. In your experiments, the input-output curve is shifted to the left and this confuses you. Let's take into account that cannabinoid receptors are located on the terminals of GABAergic and glutamatergic neurons. Therefore, it is possible to influence the activity of neurons in several ways (changing the balance and effects of exciting and inhibitory mediators, controlling the release of mediators), although presynaptic mechanisms are the most universal. And now we must take into account that cannabidiol affects the release of many other neurotransmitters (acetylcholine, norepinephrine, serotonin ...). Recall the "noncanonical" effects of cannabinoids, which are capable of directly affecting various ion channels and receptors. For example, even in physiological concentrations, they are capable of inhibiting potential-dependent Ca ++ channels, and at extremely low concentrations they act on sodium and potassium channels. Take into account the variety of possible effects and boldly put forth your alternative hypothesis.
We have similar results in CA1, CA3 and amygdala though I only did IO in CA1. Thanks for reminding me about the complexity of these studies. Interesting thought, in my opinion the main effect here is a local anesthetic like pre-synaptic effect that inhibits the fiber volleys, increases the lag time of the response and reduces the postsynaptic response, the legend below summarizes my findings:
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