Feelin’ good today
Are your animals happy? Do you ever wonder what neurological magic accomplishes this? Become involved in training or behavior and you’re bound to hear someone describe dopamine as the brain’s pleasure transmitter. Alas, like everything associated with the brain and behavior, dopamine is more complex than that. Its story currently unfolds like a drama of discovery. In it, dopamine plays the part of a talented child actor who became so typecast by a sugary role in a media hit 40 years ago, she’s had to struggle to get others to recognize how much more talented she is.
Dopamine’s media hit was a paper published in 1978 that positioned dopamine as a feel-good neurotransmitter. Researcher Roy Wise discovered that dopamine-depleted rats would stop working to get treats or drugs they should have craved. Because they were physically capable of doing what was necessary to get these substances, he concluded that dopamine was necessary to make doing so worth the effort. Over the next decade, other research supported this role and dopamine became synonymous with pleasure. Because of its feel-good potential, the media soon embraced this limited explanation and the dopamine-pleasure link became a done deal.
But then neuroscientists Kent Berridge and Terry Robinson at the University of Michigan conducted a series of experiments that provided more insight into dopamine’s function. Berridge studied facial expressions associated with pleasure (which are surprisingly similar in animals and humans), and Robinson’s population of dopamine-deprived rats (used to study Parkinson’s disease) seemed like an ideal population to further reinforce the dopamine-pleasure connection. But when Berridge fed the dopamine-deprived rats a sweet substance, their facial expressions were the same as those seen in animals with normal dopamine levels.
However, when the researchers increased the dopamine levels of another group of rats to above normal levels, the rats ate as much as they could get, but they didn’t act more pleased. Even more intriguing, some of the rats looked less pleased when eating the treats even as they continued ravenously eating them.This led the researchers to conclude that instead of producing pleasure, dopamine was related to a desire for pleasure that they labeled wanting. They referred to pleasure associated with feeling satiated—which did not seem to be related to dopamine—as liking. Anyone who’s engaged in comfort eating, drinking, exercise, or sex when stressed vs. relaxed engagement in those same activities knows the difference between those two.
Since then other studies involving animals and humans have linked dopamine to multiple behavioral phenomena. The lineup currently includes:
Attention and vigilance
Compulsion
Drug Misuse and Addiction
Hallucinations and Paranoia
Inhibition of Breast Milk Production
Learning
Mood
Pain Perception
Reward and Motivation
Repetitive Behavior
Sleep/Wake Cycle
Working Memory
A little frazzled.
That’s a lot of different roles! And no doubt surveys of the scientific literature for studies of each neurotransmitter’s functions would result in equally diverse and constantly changing lists as more research occurs. ( See Frazer and Hensler’s article for a mind-numbing description of what was known about serotonin’s effects in the late 1990s. This almost certainly is only a fraction of what’s known now or will be known in the future.) I tried to find a nice graphic that summed all this up, but the lack of agreement among them ruled that out.
What does this have to do with the interaction of companion animal health, behavior, and the bond? When their animals experience behavioral problems such as aggression or those related to separation anxiety, it’s understandable that some people would want medication that would cure the problem. However, many pet owners don’t appreciate the number of unknowns involved in this process.
For starters, the bulk of the drugs currently being used in animals were developed to treat human depression, not animal aggression or separation anxiety. And even the human depression and antidepressant experts acknowledge that they don’t know what causes depression or how these drugs work. Bizarre as that may sound, that’s not surprising because we know precious little about how the brain works. Currently we don’t even know how many neurotransmitters there are, let alone all the functions of each one. Scientists estimate that, of a total of 30-100, 10 of them do 99% of the work. But because so little is known about neurotransmitters and their functions, those estimates don’t mean a lot. Suffice it to say, defining the cause of a behavioral problem as a “chemical imbalance” in the brain or attributing it to some malfunction related to a specific neurotransmitter doesn’t mean a lot either.
In addition to neurotransmitters being multi-functional, receptors for them may be located all over the body. To get a very general idea of where these other receptors might be, read the itty-bitty print that describes the side-effects of drugs developed to effect neurotransmitter levels in some way. Ideally any medication only would target those receptors in those parts of the brain that would decrease or eliminate the problem behavior. But because of the previously mentioned lack of knowledge regarding these substances and how they work, there’s no guarantee that this will be the case.
This is where pre-medication screening comes in. It involves basic blood work, plus tests to determine the fitness of the animal’s organs–liver, kidneys, heart, etc.—that may be affected by the chosen drug. If the tests indicate a potential problem, another drug may be chosen. If the test results are within normal limits, this becomes the baseline to which future tests will be compared when the animal is on the medication to detect any potentially harmful side-effects.
Additionally, it can take weeks or months for some of these medications to work and then only when accompanied by a program of committed owner and animal change. Problem behaviors aren’t like some bacteria that can be killed in 7-10 days by drugs specifically developed to do that. Any seemingly miraculous behavioral improvement perceived with drugs more likely results from the placebo or caregiver placebo effect. I’m a big fan of the brain’s ability to generate such effects. Add its effects to the efforts of a committed owner willing to change who has a strong bond with the animal and it doesn’t get much better than that.
But it’s different when people choose to give such power to drugs about which so little is known that possess the potential to create harmful side-effects. It’s different when people want to do it to avoid mustering the commitment to make the necessary changes in themselves and their households to reduce or eliminate the stressors fueling their animals’ negative behaviors. It’s different when animals must accept the responsibility for choices people make for their own convenience.
Feelin’ good today
Are your animals happy? Do you ever wonder what neurological magic accomplishes this? Become involved in training or behavior and you’re bound to hear someone describe dopamine as the brain’s pleasure transmitter. Alas, like everything associated with the brain and behavior, dopamine is more complex than that. Its story currently unfolds like a drama of discovery. In it, dopamine plays the part of a talented child actor who became so typecast by a sugary role in a media hit 40 years ago, she’s had to struggle to get others to recognize how much more talented she is.
Dopamine’s media hit was a paper published in 1978 that positioned dopamine as a feel-good neurotransmitter. Researcher Roy Wise discovered that dopamine-depleted rats would stop working to get treats or drugs they should have craved. Because they were physically capable of doing what was necessary to get these substances, he concluded that dopamine was necessary to make doing so worth the effort. Over the next decade, other research supported this role and dopamine became synonymous with pleasure. Because of its feel-good potential, the media soon embraced this limited explanation and the dopamine-pleasure link became a done deal.
But then neuroscientists Kent Berridge and Terry Robinson at the University of Michigan conducted a series of experiments that provided more insight into dopamine’s function. Berridge studied facial expressions associated with pleasure (which are surprisingly similar in animals and humans), and Robinson’s population of dopamine-deprived rats (used to study Parkinson’s disease) seemed like an ideal population to further reinforce the dopamine-pleasure connection. But when Berridge fed the dopamine-deprived rats a sweet substance, their facial expressions were the same as those seen in animals with normal dopamine levels.
However, when the researchers increased the dopamine levels of another group of rats to above normal levels, the rats ate as much as they could get, but they didn’t act more pleased. Even more intriguing, some of the rats looked less pleased when eating the treats even as they continued ravenously eating them.This led the researchers to conclude that instead of producing pleasure, dopamine was related to a desire for pleasure that they labeled wanting. They referred to pleasure associated with feeling satiated—which did not seem to be related to dopamine—as liking. Anyone who’s engaged in comfort eating, drinking, exercise, or sex when stressed vs. relaxed engagement in those same activities knows the difference between those two.
Since then other studies involving animals and humans have linked dopamine to multiple behavioral phenomena. The lineup currently includes:
Attention and vigilance
Compulsion
Drug Misuse and Addiction
Hallucinations and Paranoia
Inhibition of Breast Milk Production
Learning
Mood
Pain Perception
Reward and Motivation
Repetitive Behavior
Sleep/Wake Cycle
Working Memory
A little frazzled.
That’s a lot of different roles! And no doubt surveys of the scientific literature for studies of each neurotransmitter’s functions would result in equally diverse and constantly changing lists as more research occurs. ( See Frazer and Hensler’s article for a mind-numbing description of what was known about serotonin’s effects in the late 1990s. This almost certainly is only a fraction of what’s known now or will be known in the future.) I tried to find a nice graphic that summed all this up, but the lack of agreement among them ruled that out.
What does this have to do with the interaction of companion animal health, behavior, and the bond? When their animals experience behavioral problems such as aggression or those related to separation anxiety, it’s understandable that some people would want medication that would cure the problem. However, many pet owners don’t appreciate the number of unknowns involved in this process.
For starters, the bulk of the drugs currently being used in animals were developed to treat human depression, not animal aggression or separation anxiety. And even the human depression and antidepressant experts acknowledge that they don’t know what causes depression or how these drugs work. Bizarre as that may sound, that’s not surprising because we know precious little about how the brain works. Currently we don’t even know how many neurotransmitters there are, let alone all the functions of each one. Scientists estimate that, of a total of 30-100, 10 of them do 99% of the work. But because so little is known about neurotransmitters and their functions, those estimates don’t mean a lot. Suffice it to say, defining the cause of a behavioral problem as a “chemical imbalance” in the brain or attributing it to some malfunction related to a specific neurotransmitter doesn’t mean a lot either.
In addition to neurotransmitters being multi-functional, receptors for them may be located all over the body. To get a very general idea of where these other receptors might be, read the itty-bitty print that describes the side-effects of drugs developed to effect neurotransmitter levels in some way. Ideally any medication only would target those receptors in those parts of the brain that would decrease or eliminate the problem behavior. But because of the previously mentioned lack of knowledge regarding these substances and how they work, there’s no guarantee that this will be the case.
This is where pre-medication screening comes in. It involves basic blood work, plus tests to determine the fitness of the animal’s organs–liver, kidneys, heart, etc.—that may be affected by the chosen drug. If the tests indicate a potential problem, another drug may be chosen. If the test results are within normal limits, this becomes the baseline to which future tests will be compared when the animal is on the medication to detect any potentially harmful side-effects.
Additionally, it can take weeks or months for some of these medications to work and then only when accompanied by a program of committed owner and animal change. Problem behaviors aren’t like some bacteria that can be killed in 7-10 days by drugs specifically developed to do that. Any seemingly miraculous behavioral improvement perceived with drugs more likely results from the placebo or caregiver placebo effect. I’m a big fan of the brain’s ability to generate such effects. Add its effects to the efforts of a committed owner willing to change who has a strong bond with the animal and it doesn’t get much better than that.
But it’s different when people choose to give such power to drugs about which so little is known that possess the potential to create harmful side-effects. It’s different when people want to do it to avoid mustering the commitment to make the necessary changes in themselves and their households to reduce or eliminate the stressors fueling their animals’ negative behaviors. It’s different when animals must accept the responsibility for choices people make for their own convenience.