I've been looking at some sources, but I have not been able to find a different mechanisms of action/effects for the two drugs. Yet, it is said that Lyrica is more physically addictive, in the sense that it is harder to withdraw from. From a practical point of view, the longer duration of action would be welcome. Do both drugs affect the brain in the same manner ?
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N&PD Moderators: Skorpio | thegreenhand
Different effects/mechanism of action of Lyrica vs gabapentin ?
- Thread starter Kdem
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Cotcha Yankinov
Bluelight Crew
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I think they are essentially the same but Lyrica is more potent and may be better as far as PK factors
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I've used them both extensively. I would ultimately consider their differences in terms of effects to be like the difference between Hydrocodone and Morphine. It's really not major. The major drawback about Gabapentin is its wildly varying bioavailability and the chore of properly staggering doses to get the most out of the medication. Pregabalin (Lyrica) can just be taken, with or without food. It's so much better and simpler for this reason, but in my opinion, they're practically interchangeable.
I just found this:
'Gabapentin interacts with cortical neurons at auxillary subunits of voltage-sensitive calcium channels. Gabapentin increases the synaptic concentration of GABA, enhances GABA responses at non-synaptic sites in neuronal tissues, and reduces the release of mono-amine neurotransmitters. One of the mechanisms implicated in this effect of gabapentin is the reduction of the axon excitability measured as an amplitude change of the presynaptic fibre volley (FV) in the CA1 area of the hippocampus. This is mediated through its binding to presynaptic NMDA receptors. Other studies have shown that the antihyperalgesic and antiallodynic effects of gabapentin are mediated by the descending noradrenergic system, resulting in the activation of spinal alpha2-adrenergic receptors. Gabapentin has also been shown to bind and activate the adenosine A1 receptor.'
https://www.drugbank.ca/drugs/DB00996
'Gabapentin interacts with cortical neurons at auxillary subunits of voltage-sensitive calcium channels. Gabapentin increases the synaptic concentration of GABA, enhances GABA responses at non-synaptic sites in neuronal tissues, and reduces the release of mono-amine neurotransmitters. One of the mechanisms implicated in this effect of gabapentin is the reduction of the axon excitability measured as an amplitude change of the presynaptic fibre volley (FV) in the CA1 area of the hippocampus. This is mediated through its binding to presynaptic NMDA receptors. Other studies have shown that the antihyperalgesic and antiallodynic effects of gabapentin are mediated by the descending noradrenergic system, resulting in the activation of spinal alpha2-adrenergic receptors. Gabapentin has also been shown to bind and activate the adenosine A1 receptor.'
https://www.drugbank.ca/drugs/DB00996