Advice vs Victim-blaming: a proposed study on #safetytipsforladies

So there has been a lot of noise about whether giving women 'safety tips' to avoid being raped is a form of 'victim blaming'.

Don't get Raped (source)

This culminated in a great hashtag (as many things do). Follow #safetytipsforladies to see some lovely tips for avoiding rape.

For example:

Don't be anywhere. 100% of rapes happen in places and locations. #safetytipsforladies
— Conna Stevenson (@1000DaysOfRain) March 25, 2013

Others suggest simply not being a woman, not ever drinking anything, not ever wearing anything (but not being naked either), not ever leaving the house (or since many rapes happen inside the house, not ever being home). And so forth.

The main point is that it's absurd to tell women to not get raped. Rape by definition is NOT under the victim's control.

Yet people still tend to blame the victim in rape cases. An interesting study was published in 2011 showing that people were more likely to blame the victim in a rape case than in a robbery case. The authors gave people short vignettes describing either a rape or a robbery, and had these participants fill out a perpetrator blame scale and a victim blame scale.

Bienek and Krahe 2011 Figure 4

Interestingly, but maybe not surprisingly, rape always had more victim blame and less perpetrator blame than robbery and this difference increased with how close the victim and perpetrator were to each other (stranger, acquaintance, ex-partner). 

Now some people say 'hey, I'm just trying to keep women safe by telling them to avoid dark places, and not take drinks from strangers.' But here's the thing, maybe the mere suggestion that women can do something to avoid being raped is enough to subtly nudge one's opinion toward thinking that if a woman got raped, she should have done something to avoid it and is therefore somewhat to blame.

So I propose the following study:

Have one group of people read a short article on tips for women to avoid being raped (a serious and well meaning one), and one group of people read some unrelated article. Then have both groups read rape vignettes similar to the ones described in the Bienek and Krahe study and fill out the victim and perpetrator blame scales. They would also fill out a scale for how much punishment the perpetrator should get in a court of law.

I hypothesize that simply reading a list of well meant tips for how women can avoid being raped would increase victim blame and would make people more lenient in their prescribed punishment for the perpetrator.

Somebody please do this experiment!

© TheCellularScale


Bieneck S, & Krahé B (2011). Blaming the victim and exonerating the perpetrator in cases of rape and robbery: is there a double standard? Journal of interpersonal violence, 26 (9), 1785-97 PMID: 20587449

Guest Post: AMPA Receptors are not Necessary for long term potentiation

Today's post is brought to you by @BabyAttachMode, who is an electrophysiologist and blogger. Today we are blog swapping! I have a post over at her blog and her post about AMPA receptors and LTP is here. So enjoy, and when you're done reading about the newest advances in synaptic plasticity here, you can head over to InBabyAttachMode and read about my personal life.
 
AMPA Receptors are not Necessary for long term potentiation

Science is most interesting to me when you’re testing a hypothesis, and not only do you prove the hypothesis to be false, but you discover something unexpected. I think that happened to Granger et al. They were trying to find which part of the AMPA receptor is necessary for long-term potentiation (LTP), the process that strengthens the connection between two brain cells when that connection is used often. Indeed they find that AMPA receptors are not necessary at all for LTP, which is very surprising given the large body of literature describing how the GluA1 subunits of the AMPA receptor, through interactions with other synaptic molecules that bind to the intracellular C-tail (the end of the receptor that is located inside the cell), are inserted into the synapse to induce LTP.

LTP (source)

The authors made an inducible triple knock-out, which means that they could switch off the genes for the three different AMPA receptor subunits GluA1, GluA2 and GluA3. This way, they ended up with mice that had no AMPA receptors at all. The authors were then able to selectively put back one of the AMPA receptors, either the entire receptor or a mutated receptor. By inserting mutated receptors, for example a receptor that lacks its intracellular C-tail that was thought to be important for insertion of the AMPA receptor into the synapse, they could then study whether this mutated receptor was still sufficient for induction of LTP.

Surprisingly, they found that deleting the C-tail of the GluA1 subunit does not change the cell’s ability to induce LTP. Even more so, they showed that you don’t even need any AMPA receptor to still be able to induce LTP; the kainate receptor (another type of glutamate receptor that has never been implicated in LTP) can take over its job too.

Figure 6C from Granger et al. (2013). Kainate receptor overexpression can lead to LTP expression, without the presence of AMPA receptors.

About this surprising discovery the authors say the following:

"These results demonstrate the synapse's remarkable flexibility to potentiate with a variety of glutamate receptor subtypes, requiring a fundamental change in our thinking with regard to the core molecular events underlying synaptic plasticity."

Of course if you say something like that, the main players in the LTP field will have something to say about it, and they did. Three giants in the field of synaptic physiology commented in the journal Nature, but their opinions differed. Morgan Shang called it "a step forward", whereas Roberto Malinow and Richard Huganir called it "two steps back", saying that LTP without AMPA receptors can only happen in the artificial system that the authors of the paper use to study this. They expect that cells lacking all three AMPA receptors will look so different from the normal cells that the results are difficult to interpret.

Either way, this paper opens new views and questions to how LTP works, and whether AMPA receptors are as important as we thought.


Granger AJ, Shi Y, Lu W, Cerpas M, & Nicoll RA (2013). LTP requires a reserve pool of glutamate receptors independent of subunit type. Nature, 493 (7433), 495-500 PMID: 23235828
 
Sheng M, Malinow R, & Huganir R (2013). Neuroscience: Strength in numbers. Nature, 493 (7433), 482-3 PMID: 23344353

What is up with the "Dopamine Project"?

Someone is trying to make me eat my words.

yum. (source)

That someone is the Dopamine Project. I am on record as saying "It is better for the public to learn simplified bite-size science morsels than to learn nothing at all." And my specific example was that it's better for people to know that 'dopamine is a reward molecule' than to not even know the term dopamine.

But sometimes things just go too far. The "Dopamine Project" is a website run by Charles Lyell with a stated 'self-help' purpose:

"The Dopamine Project was founded to foster positive change by encouraging open-minded individuals to share readily available research into the connections between dopamine and a growing list of addictive behaviors." -About Tab

Doesn't sound too terrible, right? Share research about dopamine? sign me up! .... However, I don't see ANY research, or even references to research, on this website. In fact it's quite wootastic. Going through the posts, you get some gems like

"A Message from you Dopamine Angel"

and

"Keeping a Dopamine Diary: Wrestling with Dopamine-Induced Ignorance"

It's all about how 'good dopamine' makes you want things you should want (food) and 'bad dopamine' makes you want things that will hurt you later (addictive drugs for example). Basically the website's message is a self-help, self-control one with the word dopamine sprinkled all over it.

The worst part is that not only does the website not include a single citation to a research paper, it actively rails against science.

"The future depends on how long it takes scientists to discover what they haven’t been interested in discovering so far. Rather than wait for the mainstream scientists and media to get started, we’re reaching out to anyone interested in fostering positive change by raising dopamine awareness." -Welcome to the Dopamine Project

Trust me, scientists want to understand dopamine. At the IBAGS conference half the talks related to dopamine, and there is a conference completely devoted to dopamine coming up in May. The specific action of dopamine is really really complex, and scientists are working really really hard to unravel its intricacies. This Charles Lyell guy is pulling out a typical woo card, implying that he knows what scientists don't want you to know.

"If the thought of fostering positive change through dopamine awareness triggers a shot of dopamine that brings a smile to your face, this might be your chance to be among the top .001% who go on record as the first to understand and apply what we know about dopamine to make a difference."  -Welcome to the Dopamine Project

 He also seems to feel personally attacked by Steven Poole's New Statesman article on Neurobollocks.

Is the 'Dopamine Project' ridiculous and unscientific? Absolutely.

Is it harmful and dangerous to people? ... Honestly, I'm not sure. Reading it certainly makes me want to throw up, but there are worse things for pseudoscience to encourage than self-control. I'm not sure if I should devour my earlier words quite yet.

© TheCellularScale

To read more on the confusing line between science and pseudoscience, see Michael Shermer's Scientific American article:



Shermer M (2011). What is pseudoscience? Scientific American, 305 (3) PMID: 21870452

Is it 'Important' or is it 'valuable'?

We've recently discussed dopamine as a reward prediction signal. But that is really just the start of the complicated dopamine story.

Dopamine's role in reward and punishment (by the hiking artist)

Some research groups have also found that dopamine neurons respond to aversive stimuli, like an air puff to the face or an electric shock. This finding seems to be be completely incompatible with the idea that dopamine is a signal for reward.

Luckily some scientists took the time to try to resolve this discrepancy. Bromberg-Martin, Matsumoto, and Hikosaka (2010) have written an excellent review paper explaining that some dopamine neurons do code for value (reward), but other dopamine neurons code for salience (importance).

Differential Dopamine Coding (Bromberg-Martin et al., 2010 Fig 4)

When researchers are recording from a value coding dopamine neuron, it looks like the neuron responds to reward and actually reduces its response to the air puff. This makes sense as a 'dopamine = good' signal.

However, when a researcher is recording from a salience coding dopamine neuron, it looks like the neuron is responding equally to the good thing (reward) and the bad thing (air puff). This is confusing if you think 'dopamine = good', but makes sense if you think 'dopamine = important'. When the cue comes on (a light or a tone that signifies a reward is coming next or an air puff is coming next), these dopamine neurons fire if that cue means something.


Instead of just being confused about why sometimes dopamine would code for value and sometimes it would code for salience, Hikosaka's group showed that these two types of neurons are actually separate populations, and even seem separated in space.

(Bromberg-Martin et al., 2010 Fig 7B)

The value dopamine neurons are more ventral in the (monkey) brain, while the salience dopamine neurons are more dorsal-lateral. Importantly these two populations of neurons go to slightly different parts of the striatum and receive signals from different parts of the brain. The review paper suggests that the salience coding neurons receive their input from the central nucleus of the amygdala, while the value coding neurons receive their input from the lateral habenula-RMTg pathway.

The important thing here is that dopamine does not do just one thing to the brain. It doesn't just tell the rest of the brain 'yay, you won!' or 'you want that' etc... It says different things depending on different specific conditions. 

Dopamine doesn't 'mean' anything, the cell it comes from and the cell it goes to are what determine what it does. It certainly can't be classified as the 'love molecule'

 © TheCellularScale



Bromberg-Martin ES, Matsumoto M, & Hikosaka O (2010). Dopamine in motivational control: rewarding, aversive, and alerting. Neuron, 68 (5), 815-34 PMID: 21144997

Should reviewers be required to cite their sources?

When I got back from the IBAGS conference, I was greeted by an 'paper rejection email'.

Failure with a capital F (source)

I was disappointed of course, but I slept off my jetlag and then built my self-confidence back up by saving the universe. I will retool the paper and submit it somewhere else.

However, the reviews for this paper were particularly infuriating (aren't they always?). Here's a summary:

I say: "Thing X is true (citation, citation), so we did thing Y which uses thing X."

Reviewer says: "You act like thing X is true, but it's not (no citations)."

The reviewer did this for two specific aspects of the paper, saying that the basis for our model and our ideas just aren't true, but giving no citations. In both case, I have citations in the paper to back up my claim that these things ARE true.  

This particular form of irritating review has not happened to me before. I've always had well-cited responses to my claims. It's common courtesy to cite some papers when you say that someone is completely wrong about something, but I guess it's not required.

Anyone have any thoughts on this? Has it happened to you? Am I just having the normal 'grrr' response to a negative review?

© TheCellularScale
 

Dopamine and Reward Prediction Error

I am back from the IBAGS conference and full of new information! I plan to blog about tons of amazing things over the next month or so, but today we'll start with some foundation building.

Dopamine nails (source)

The IBAGS (international basal ganglia society) meeting is all about the basal ganglia (which includes the striatum), and as you may know, dopamine is a super important molecule for the proper function of the striatum (it is the dopamine cells that die in Parkinson's Disease).

There were many fantastic talks during the IBAGS meeting and almost a third of them showed the exact same figure on one of their slides. So much so that everyone would start to laugh when someone showed it. And as you may have guessed, it is about dopamine. Here it is:

Schultz 1998 Figure 2

This figure is the basis for the belief that dopamine represents a 'reward prediction error'.  Let me explain. The scattered dots on the lower half of each panel represent action potentials from individual dopaminergic neurons. The x axis it time in seconds. The black columns above them are a histogram showing how much firing is going on at each point in time. When the black columns are tall, there was more dopamine neuron firing. You can see that the height of the black columns matches up with the density of the scattered dots below them.

During 'reward learning', an animal is trained to associate a stimulus (like a tone or a flash of light) with getting a reward (like a drop of water or juice). These three panels show how dopamine responds to this whole process. The first panel shows that when there is no stimulus (CS) and the reward is a surprise, the dopamine neurons respond very strongly to it. The second panel shows that when there is a stimulus that tells the animal that a reward is soon to come, the dopamine neurons respond to the stimulus, but not to the reward. Finally the third panel shows that when there is a stimulus the dopamine neurons respond to it, but if the reward (R) never comes, the dopamine neurons actually stop firing when the reward should have happened.

What is so fascinating about this is that it shows dopamine neurons do not just fire in response to reward, they encode the actual reward with respect to the expected reward. In the author's words:

"Dopamine neurons report rewards relative to their prediction rather than signaling primary rewards unconditionally (Fig. 2). The dopamine response is positive (activation) when primary rewards occur without being predicted. The response is nil when rewards occur as predicted. The response is negative (depression) when predicted rewards are omitted. Thus dopamine neurons report primary rewards according to the difference between the occurrence and the prediction of reward, which can be termed an error in the prediction of reward..." Schultz 1998

This finding is so important to researchers now because it shows that dopamine neurons can encode learning rules. Dopamine neurons constantly and dynamically tell the rest of the brain which stimuli lead to reward, and which stimuli don't. The implications here for pathological learning are huge as well. Mis-signalling in dopamine neurons could lead to an inability to tell what is rewarding and what is not.

© TheCellularScale



Schultz W (1998). Predictive reward signal of dopamine neurons. Journal of neurophysiology, 80 (1), 1-27 PMID: 9658025

Honoring a Legend

The Cellular Scale is at the International Basal Ganglia Society meeting this week (#IBAGS2013), and finally has internet!

Sunrise over the Gulf of Aqaba (I took this picture)

It's already been two days of conferencing, and I plan to mainly write some follow up posts when I get back. But I will just briefly mention the "Lifetime Member" lecture that was given on the first evening of the conference.

Mahlon Delong (source)

This year's lifetime member is Mahlon DeLong.
I've written before about deep brain stimulation (DBS) as a treatment for Parkinson's Disease, and DeLong has done some fascinating work that has lead up to DBS in the  subthalamic nucleus (STN).

One particular treat was to see a video during the talk of the very first attempt at alleviating Parkinson's symptoms through a subthalamotomy, the lesion of the subthalamic nucleus.

A Parkinson's Disease monkey was given the subthalamotomy on only one side of the brain and the video shows Mahlon DeLong interacting with the monkey and noting that it's treated side is less stiff than the untreated side. A second video shows the monkey later able to move its arm with no problems.

It was exciting to see this sort of 'moment of discovery' from 1989. There were no cries of "Eureka!" or anything it was more of a 'hm, interesting' tone. You actually hear his post-doc on the video saying
(paraphrasing from memory) "the right side has better tone, at least Mahlon thinks so" and then start laughing.

(source)

One other cool thing about Dr. DeLong is that he is Muhammad Ali's physician.

© TheCellularScale

Conference Time

I am at the international Basal Ganglia society meeting this week. I will probably blog about some of the great new research that I learn about, but not for a week. The internet here is pay-for and buggy, and all my blogger information is all suddenly in Hebrew (I am actually typing this right to left for some reason). So I'll be away from twitter and blogger for about a week. But I'll have tons of cool stuff to write about after that .

The Cellular Scale