Kava fact of the day: Kavalactone effects at noradrenaline (norepinephrine).
Continuing our trip around the wheel of neurotransmitter effects, we now arrive at noradrenaline, also known as norepinephrine NE, or NA.
What is norepinephrine?
Norepinephrine or NE is a substance that is released from the ends of specific nerve fibres that mobilize our brain and body for action. It’s lowest during sleep, and reaches much higher levels during stress or danger [1].
How does it work?
NE functions by binding to α- and β-adrenergic receptors throughout the body which exerts effects such as dilating pupils, opening airways, increasing heart rate, and constricting blood vessels. It plays an essential role in the regulation of arousal, attention, cognitive function, and stress reactions [2].
What is “reuptake?”
Reuptake is defined as the reabsorption of a neurotransmitter by a neurotransmitter transporter after it has performed its function transmitting a neural impulse. This will look familiar to those who have ever taken an SSRI as this function is precisely what they target and block. When reuptake is blocked, more of the neurotransmitter is allowed to exist in the synapse, giving it a greater chance to bind and cause a neuronal action [3].
How does kava interact with this neurotransmitter?
In 1997 researchers took a close look at the NE reuptake inhibition properties of a few kavalactones. They studied kavain, it’s artificial racemate ±-Kavain, and methysticin when applied to slices of rat brain. Significant uptake inhibition began to be shown at concentrations above 10um with kavain. Little was observed with methysticin. Concentrations of 400um kavain blocked 70-80% of NE seen in controls. Both kavain and artificial kavain were seen to have the same values for inhibition [4].
What does this mean to the kava experience?
This is likely where we see cognitive increases and increases of alertness as well as better object recognition with kava. The stimulatory properties of kava may owe their existence to this effect. What’s becoming abundantly clear is that kavain is the heaviest of players in terms of the psychological effects kava can give. This actually correlates to our understanding of kava at a commercial level, as those kavas with 4 towards the beginning of the chemotype will be ones that are more euphoric and stimulatory.
Summary:
Natural kavain, and methysticin as well as artificial kavain were studied for their ability to inhibit the reabsorption of the neurotransmitter, noradrenaline (norepinephrine). This is the neurotransmitter responsible for our level of alertness. It was found that kavain, artificial kavain, and to a lesser extent methysticin inhibited the reuptake of this chemical in a dose dependent manner. This research may speak to the stimulatory effects seen with kava consumption.
[1] Wikimedia Foundation. (2021, April 30). Norepinephrine. Wikipedia.
(https://en.wikipedia.org/wiki/Norepinephrine)
[2] Hussain, Laila S., Vamsi Reddy, and Christopher V. Maani. 2021. “Physiology, Noradrenergic Synapse.” In StatPearls. Treasure Island (FL): StatPearls Publishing.
(https://www.ncbi.nlm.nih.gov/pubmed/31082021)
[3] Iversen, L. 2000. “Neurotransmitter Transporters: Fruitful Targets for CNS Drug Discovery.” Molecular Psychiatry 5 (4): 357–62.
(https://doi.org/10.1038/sj.mp.4000728)
[4] Seitz, U., A. Schüle, and J. Gleitz. 1997. “[3H]-Monoamine Uptake Inhibition Properties of Kava Pyrones.” Planta Medica 63 (6): 548–49.
(https://doi.org/10.1055/s-2006-957761)
Continuing our trip around the wheel of neurotransmitter effects, we now arrive at noradrenaline, also known as norepinephrine NE, or NA.
What is norepinephrine?
Norepinephrine or NE is a substance that is released from the ends of specific nerve fibres that mobilize our brain and body for action. It’s lowest during sleep, and reaches much higher levels during stress or danger [1].
How does it work?
NE functions by binding to α- and β-adrenergic receptors throughout the body which exerts effects such as dilating pupils, opening airways, increasing heart rate, and constricting blood vessels. It plays an essential role in the regulation of arousal, attention, cognitive function, and stress reactions [2].
What is “reuptake?”
Reuptake is defined as the reabsorption of a neurotransmitter by a neurotransmitter transporter after it has performed its function transmitting a neural impulse. This will look familiar to those who have ever taken an SSRI as this function is precisely what they target and block. When reuptake is blocked, more of the neurotransmitter is allowed to exist in the synapse, giving it a greater chance to bind and cause a neuronal action [3].
How does kava interact with this neurotransmitter?
In 1997 researchers took a close look at the NE reuptake inhibition properties of a few kavalactones. They studied kavain, it’s artificial racemate ±-Kavain, and methysticin when applied to slices of rat brain. Significant uptake inhibition began to be shown at concentrations above 10um with kavain. Little was observed with methysticin. Concentrations of 400um kavain blocked 70-80% of NE seen in controls. Both kavain and artificial kavain were seen to have the same values for inhibition [4].
What does this mean to the kava experience?
This is likely where we see cognitive increases and increases of alertness as well as better object recognition with kava. The stimulatory properties of kava may owe their existence to this effect. What’s becoming abundantly clear is that kavain is the heaviest of players in terms of the psychological effects kava can give. This actually correlates to our understanding of kava at a commercial level, as those kavas with 4 towards the beginning of the chemotype will be ones that are more euphoric and stimulatory.
Summary:
Natural kavain, and methysticin as well as artificial kavain were studied for their ability to inhibit the reabsorption of the neurotransmitter, noradrenaline (norepinephrine). This is the neurotransmitter responsible for our level of alertness. It was found that kavain, artificial kavain, and to a lesser extent methysticin inhibited the reuptake of this chemical in a dose dependent manner. This research may speak to the stimulatory effects seen with kava consumption.
[1] Wikimedia Foundation. (2021, April 30). Norepinephrine. Wikipedia.
(https://en.wikipedia.org/wiki/Norepinephrine)
[2] Hussain, Laila S., Vamsi Reddy, and Christopher V. Maani. 2021. “Physiology, Noradrenergic Synapse.” In StatPearls. Treasure Island (FL): StatPearls Publishing.
(https://www.ncbi.nlm.nih.gov/pubmed/31082021)
[3] Iversen, L. 2000. “Neurotransmitter Transporters: Fruitful Targets for CNS Drug Discovery.” Molecular Psychiatry 5 (4): 357–62.
(https://doi.org/10.1038/sj.mp.4000728)
[4] Seitz, U., A. Schüle, and J. Gleitz. 1997. “[3H]-Monoamine Uptake Inhibition Properties of Kava Pyrones.” Planta Medica 63 (6): 548–49.
(https://doi.org/10.1055/s-2006-957761)
