Bees Benefit From Caffeine

Caffeinated plants provide an unforgettable experience.

Honeybees rewarded with caffeine remember the smell of specific flowers longer than bees given only sucrose, according to a study published in Science. “By using a drug to enhance memories of reward,” the study says, “plants secure pollinator fidelity and improve reproductive success.”

Many drugs used by humans come from plants. But what role do the drugs play for the plants themselves? Frequently, they play the role of toxic avenger, providing a chemical defense against attacks by herbivores. But in smaller doses, they often have pharmacological effects on mammals. The researchers looked at two genera of caffeine-producing plants—Coffea and Citrus. “If caffeine confers a selective advantage when these pants interact with pollinators,” the investigators reasoned, “we might expect it to be commonly encountered in nectar.” And it was. Caffeine at very low doses was measured in the nectar of several of the caffeine-producing plant species, including several Coffea species, as well as some citrus nectars—grapefruit, lemons, and oranges among them.

Next, the researchers wanted to find out if the caffeine-laced nectar could affect learning and memory in pollinating bees. They trained individual honeybees to associate various floral scents with sucrose containing various concentrations of caffeine. This pairing of odor and reward, with high-concentration sucrose as the control, demonstrated that low doses of caffeine had almost no effect on the rate of honeybee learning—but a profound effect on long-term memory. Three times as many caffeinated bees remembered the conditioned floral scent 24 hours later, “and responded as if it predicted reward.” Twice as many bees remembered the scent at the 72-hour mark.

What’s the trick? Caffeine’s ability to influence mammalian behavior is due to its action as an adenosine receptor antagonist. “In the hippocampal region,” the authors write, “inhibition of adenosine receptors by caffeine induces long-term potentiation, a key mechanism of memory formation." The Kenyon cells in mushroom bodies of the insect brain, which showed “increased excitability” under the influence of caffeine, are similar in function to hippocampal neurons, they write. “Remembering floral traits is difficult for bees to perform at a fast pace as they fly from flower to flower and we have found that caffeine helps the bee remember where the flowers are,” said Geraldine Wright of the UK’s Newcastle University, who was lead author on the study. “So, caffeine in nectar is likely to improve the bee’s foraging prowess while providing the plant with a more faithful pollinator.”

It is an interesting balancing act by nature: Too much caffeine makes the nectar toxic and repellent to honeybees. Too little, and there is no behavioral effect on bee memory. “This implies that pollinators drive selection toward concentrations of caffeine that are not repellent but still pharmacologically active,” says the report.  Humans have selected for a not-too-much, not-too-little dose of caffeine in the form of soda drinks and coffee. Is it possible that the humble coffee bean is pharmacologically manipulating us into taking good care of it? And do we drink it when we read or study because, for one thing, it enhances long-term memory? And speaking of memory, people often forget where they tucked the oregano, but they usually have little difficulty remembering where they stashed the coffee.

More pragmatically, honeybees on caffeine may lead researchers toward a better understanding of the foraging strategies of pollinator insects, and allow for improved management of crops and landscapes.

Wright G.A., Baker D.D., Palmer M.J., Stabler D., Mustard J.A., Power E.F., Borland A.M. & Stevenson P.C. (2013). Caffeine in Floral Nectar Enhances a Pollinator's Memory of Reward, Science, 339 (6124) 1202-1204. DOI: 10.1126/science.1228806

Photo credit: http://www.coorgblog.orangecounty.in

What is Drug Craving?

Exploring the engine of drug relapse.


“In terms of treatment, you can’t just attack the rewarding features of the drug. In the case of alcohol, we already have a perfect drug to make alcohol aversive--and that’s Antabuse. But people don’t take it. Why don’t they take it? Because they still crave. And so they stop taking it. You have to attack the other side, and hit the craving.”
--Dr. Ting-Kai Li, 1990 interview

It causes relapses and treatment failure. It leads good people to break good promises and do harm to themselves and others. What is this thing called craving? Isn’t it just another word for lack of will power?

Scientists have gained a much deeper understanding of how and why addicts crave. For years, craving was represented by the tortured tremors and sweaty nightmares of extreme heroin and alcohol withdrawal. Significantly, however, the symptom common to all forms of withdrawal and craving is anxiety. This prominent manifestation of craving plays out along a common set of axes: depression/dysphoria, anger/irritability, and anxiety/panic. These biochemical states are the result of the “spiraling distress” (George Koob’s term) and “incomprehensible demoralization” (AA’s term) produced by the addictive cycle. The mechanism driving this distress and demoralization is the progressive dysregulation of brain reward systems, leading to biologically based craving. The chemistry of excess drives the engine of addiction, which in turn drives the body and the brain to seek more of the drug.

Whatever the neuroscientists wanted to call it, addicts knew it as “jonesing,” from the verb “to jones,” meaning to go without, to crave, to suffer the rigors of withdrawal. Most doctors don’t get it, and neither did many of the therapists, and least of all the public policy makers. Drug craving is ineffable to the outsider.

Drug craving itself is mediated by glutamate receptor activity in the hippocampus—the seat of learning and memory. A fundamental branch of what we might dub the “relapse pathway” runs through the glutamate-rich areas of the hippocampus. The puzzling matter of craving and relapse began to come into focus only when certain researchers began to rethink the matter of memory and learning as it applies to the addictive process. This led back to the role of glutamate, and it gradually became clear that the drug high and the drug craving were, in a manner of speaking, stored in separate places in the brain. Research at the National Institute for Drug Abuse (NIDA) strongly supports the hypothesis that drug memories induced by environmental triggers originate primarily in the hippocampus. And glutamate may be the substance out of which the brain fashions “trigger” memories that lead certain addicts down the road to relapse.

Glutamate is the most common neurotransmitter in the brain. (In sodium salt form, as monosodium glutamate, it is a potent food additive.) About half of the brain’s neurons are glutamate-generating neurons. Glutamate receptors are dense in the prefrontal cortex, indicating an involvement with higher thought processes like reasoning and risk assessment. The receptor for glutamate is called the N-methyl-D-aspartate (NMDA) receptor. And unfortunately, as the gifted science writer Constance Holden related in Science 292, NMDA antagonists, which might have proven to be potent anti-craving drugs, cannot be used because they induce psychosis. Dissociative drugs like PCP and ketamine are glutamate antagonists.

However, drugs that play off receptors for glutamate are already available, and more are in the pipeline. As a precursor for the synthesis of GABA, glutamate has lately become a tempting new target for drug research. Ely Lilly and others have been looking into glutamate-modulating antianxiety drugs, which might also serve as effective anti-craving medications for abstinent drug and alcohol addicts.

Photo credit: Changing Lives Foundation