Oxytocin as an Anxiolytic

Did anyone try using probiotics to reduce stress? Did it work? Yes? No? Well, I have another suggestion.

Try having sex.

Now, I know some of you will probably think this seems obvious. Don’t we usually feel really good after sex? I am going to ask, however, that we ignore the notion of the post-coital glow, runner’s high, or whatever it is you get after copulation. Let’s cool those jets and look at two studies involving the anxiolytic effects of oxytocin in rat mating.

First, let’s give a preface that is kind of given by both of these studies. Oxytocin is involved in a lot of good stuff psychologically. Oxytocin has been shown to reduce stressful behavior in animals, and medical researchers are even working on using it to treat anxiety in humans. It is also involved in prosocial behaviors. Basically, this is a peptide involved in being trusting, friendly, cuddly and calm or open.

Now, let’s look at how the males do with sex. Waldherr and Neumann demonstrated that mating with a receptive female led male mice to exhibit less stress behavior and more risk-taking associated behavior (2007). They ran a number of different tests. They found that males who were mated to females explored with open arms and exhibited more risk taking behaviors even 6 hours later. They also monitored the periventricular nucleus of conscious rats exposed to receptive (primed) and non-receptive (non-primed) females. They were able to set up a partition allowing visual, auditory and olfactory, but not physical contact between the male and female. What they found was elevated oxytocin release in males presented with receptive females. When the researchers injected the males with an oxytocin receptor antagonist (a chemical that blocks oxytocin) the rats ceased to exhibit the open behavior, demonstrating that it was, in fact, the oxytocin that had had the anxiolytic effect.

Nyuyki and colleagues looked at oxytocin and mating in female mice (2011). What they found was that females needed to control or pace the situation in order to have positive effects (the major one being oxytocin release) from sexual encounters. What they did was place primed or unprimed females in one of two situations with a male. There was a non-paced arena and a paced one in which a partition allowed the smaller female to hide from the male. The behavioral tests they ran were quite similar to the previous test. The results indicated that steroidally primed females, in a paced sexual environment were able to achieve the anxiolytic release of oxytocin. However, those placed in non-paced situations quickly lost the effect of priming, and did not achieve the oxytocin levels the paced females did. Basically, the female mouse needed to be ready to get the beneficial effects of sex.

These studies suggest that, at least in rats, sex leads to a stress-relieving rush of oxytocin from the periventricular nucleus in both sexes. However, for the female to get the proper effect, the copulation must be done on her terms, at her pace.

Now I’m wondering if this may be related to that feeling of ennui some guys get post-climax. Perhaps I’ll look into that for next week…

… either that or chocolate.

Nyuyki KD, Waldherr M, Baeuml S, Neumann ID (2011) Yes, I Am Ready Now: Differential Effects of Paced versus Unpaced Mating on Anxiety and Central Oxytocin Release in Female Rats. PLoS ONE 6(8): e23599. doi:10.1371/journal.pone.0023599

Waldherr M, Neumann ID (2007) Centrally released oxytocin mediates mating-induced anxiolysis in male rats. PNAS 104(42): 16681-16684.

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Artificial Hippocampus? Immortality? Plausible?

MythBusting time!

I am definitely expecting a classmate to blog about this also. Did anyone catch Curioity: Can You Live Forever with Adam Savage the other night? Pretty cool as far as speculative science goes, right? My answer to that is yes. Now, can we make the MythBuster immortal? Maybe we can, but there is one part of this that aroused my desire to go MythBusting.

The hypothetical future Adam says at one point that at 500 years, the hippocampus, a large mass in the brain involved in memory, ran out of space. His solution: Build an artificial hippocampus. Also, multiple bodies. Way far out, right?

Wait! Let’s put the Kurzweil-esque thinking aside. What was this about the hippocampus (which literally means “seahorse”)? I remember hearing in psychology courses that the hippocampus was involved in memory, but that it probably was not the location of memory storage.

Myth: (1) The Hippocampus is the brain’s natural storage center, and (2) it is possible to increase memory storage capacity by making an artificial extension of the brain.

Let’s first take a look at this myth via Wikipedia.

Role in memory

See also: Amnesia

Psychologists and neuroscientists generally agree that the hippocampus has an important role in the formation of new memories about experienced events (episodic or autobiographical memory).[16][20] Part of this role is hippocampal involvement in the detection of novel events, places and stimuli.[21] Some researchers view the hippocampus as part of a larger medial temporal lobe memory system responsible for general declarative memory (memories that can be explicitly verbalized—these would include, for example, memory forfacts in addition to episodic memory).[15]

Due to bilateral symmetry the brain has a hippocampus in both cerebral hemispheres, so every normal brain has two of them. If damage to the hippocampus occurs in only one hemisphere, leaving the structure intact in the other hemisphere, the brain can retain near-normal memory functioning.[22] Severe damage to the hippocampus in both hemispheres results in profound difficulties in forming new memories (anterograde amnesia), and often also affects memories formed before the damage (retrograde amnesia). Although the retrograde effect normally extends some years before the brain damage, in some cases older memories remain—this sparing of older memories leads to the idea that consolidation over time involves the transfer of memories out of the hippocampus to other parts of the brain.

Interesting. So far, it seems that the hippocampus is more of an encoding structure. But, a good MythBuster does not stop at Wikipedia. So let’s look at some recent primary research!

In 2009, Leonardo Restivo and colleagues wanted to see what structural changes happened in the hippocampus and anterior cingulate cortex. What they did was condition contextual fear in mice, except that they also had a control group of non-conditioned or pseudoconditioned mice. Next, they tested some of the mice 24 hours later (recent memory recall), tested some mice 36 days later (remote memory recall), and left some mice untested (another control measure). After this, they put the mice to sleep, cut out their brains and put the brains in a Golgi-Cox staining solution to look at neural growth.

Now that the scientists had these beautifully stained mouse brains, it was time to look at the structure. They made slides and checked for dendritic spine growth, a sign of neural plasticity. What they found was that in mice tested for recent memory recall there was more structural change going on in the CA1 region of the hippocampus, but in mice tested for remote memory, there was a high dendritic spine density in the anterior cingulate cortex (aCC) (Restivo et al., 2009, Fig 2).

In both recent and remote tested mice, as well as untested, there was a higher density of dendritic spines than in pseudoconditioned and naive mice. (Plasticity in behaviorally untested mice means that this stuff is going on without needing recall.) Pseudoconditioned mice also had higher spine density than naive mice.

They also tested what would happen when they formed hippocampal lesions. It turned out that lesions formed soon after conditioning hindered recall, and when slides were made of the brain, but significantly more spines were seen than in control mice on dendrites of aCC cells. However, when lesions were caused later (day 24) recall was not as severely hindered, and more spines were seen on aCC pyramidal cells than in the mice who had early lesions. (Restivo et al., 2009, Fig 5).

What does this all mean? Well, it suggests that the hippocampus has an important but limited role in memory formation and storage. We can see things going on (spines being formed) in the hippocampus when memory is being formed, and those spines are still somewhat present in tests for remote memory. However, when testing later after conditioning, more new connections are seen in the anterior cingulate cortex. We also have the evidence from lesions, showing that damage to the hippocampus does not much of an effect on remote memory. Therefore, we can probably conclude that the hippocampus is not a storage center, but rather a memory processing center.

Myth: “Hippocampus specifically a Memory Storage Center”: This part is BUSTED.

Myth: “Creating an External Hard Drive for your Brain”: This part is PLAUSIBLE and is also a whole other subject.

Cited

Restivo L, Vetere G, Bontempi B, Ammassari-Teule M. The formation of recent and remote memory is associated with time-dependent formation of dendritic spines in the hippocampus and anterior cingulate cortex. J. Neurosci. 29(25): 8206-8214.

Also thanks to wikipedia, youtube and Discovery: Curiosity.

Sorry for the Lack of a Post Last Week…

… Ooh! Lolcats! … Wait, I’m sorry, what was I talking about?

Ah, yes, the class-required blog. I must apologize. Things have been busy, and that brings me into conflict with my scatterbrain. And it almost literally is a scatterbrain. You see: I have ADHD.

“ADHD?! What a load of crap. That’s some bogus stuff made up by doctors and pharmaceutical companies.”

Quite wrong you are, awkward strawman argument. ADHD is real and well documented and researched. Here, for example, is a link to a recent article (or its abstract if you don’t have a subscription) that supports my use of the word “scatterbrain”. This shows evidence that there is some interference coming from altered patterns of very low frequency (VLF) activity in the ADHD brain (as measured in wave functions on an EEG). Basically, my resting-state brain functions don’t attenuate, or decrease power, when I go into a goal-oriented mode, and this is what is thought to lead to the interference.

I suppose this is just one way in which my brain is different from others. It’s a complex organ, each of ours is unique, and it tends to do things we don’t want it to do sometimes, or it doesn’t do them how we want them to. Imagine you are a computer yelling at yourself “Dammit, Windows! Where did you put that file? Open task manager. No, not Firefox.” That is how it is some days. We all have issues with our internal processor, and this is just a little glitch with which I have to deal.

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Literature

Helps SK, Broyd JB, James CJ, Karl A, Chen W, Sonuga-Barke EJS. Altered spontaneous low frequency brain activity in Attention Deficit/Hyperactivity Disorder. Brain Research. 2010, 1322: 134-143.