Monday, November 11, 2019

Olfactory Attraction and Smell Dating


Smell Dating, an interactive exhibit by Tega Brain and Sam Lavigne


A conceptual art installation, an extended olfactory performance piece, an elaborate participatory project, or an actual smell-based dating service? Smell Dating is all of these and more!




How it works
  1. We send you a t-shirt
  2. You wear the shirt for three days and three nights without deodorant.
  3. You return the shirt to us in a prepaid envelope.
  4. We send you swatches of t-shirts worn by a selection of other individuals.
  5. You smell the samples and tell us who you like.
  6. If someone whose smell you like likes the smell of you too, we'll facilitate an exchange of contact information.
  7. The rest is up to you.

My initial view of the project was based a recent showing of the interactive exhibit, where the participants could sniff small swatches of cloth, rate the unknown wearer's attractiveness (UNATTRACTIVE — NEUTRAL — ATTRACTIVE), learn how others voted, and see basic background information about the wearer (e.g., 30 year old female bisexual pescatarian). The first two I sniffed were odorless, but then there was #8...

The art installation is part of Useless Press, “a publishing collective that creates eclectic Internet things.” I assumed it was an elaborate joke, not an actual matchmaking service, but the artists must have had a grant to implement the idea in real life.





In Shanghai, people signed up over a two week period and paid ¥100 to become a “member.”
Smell Dating @ Shanghai [culminated] in the Sweat Lab, a participatory installation event... Visitors are invited to volunteer in the Smell Dating Sweat Lab and intimately experience the smells of strangers. During this event we will prepare the smell samples from our members t-shirts. Shirts will be meticulously cut up and batched to be sent back to Smell Dating members.

Smell Dating premiered in New York in March 2016 and received extensive press coverage, most of which took it seriously. Young female writers at The Guardian, Business Insider, Time, Racked, and a gay man at HuffPo tried out the service. The Buzzfeed reporter realized, “Yes, this is mostly a stunt-y gag” but also touched on the science behind smell and attraction. The health reporter at Time wrote about the underlying science in detail (e.g., major histocompatibility complex) and interviewed smell scientists, including Dr. Noam Sobel (founder of SmellSpace.com), Dr. Richard Doty (author of The Great Pheromone Myth), and Dr. Gary Beauchamp (Emeritus Director of the Monell Chemical Senses Center).

The creators of Smell Dating (Tega Brain and Sam Levine) consulted with olfactory scientists and provided an extensive reading list on the web site.

Most everyone agrees that odors evoke emotion, and the sense of smell has a unique relationship to autobiographical memory. But, as Richard Doty asks, do human pheromones exist?
While it is apparent that, like music and lighting, odors and fragrances can alter mood states and physiological arousal, is there evidence that unique agents exist, namely pheromones, which specifically alter such states?

It turns out that scientific opinion on this matter is decidedly mixed, even polarizing, as I'll discuss in the next post.


Reference

Doty RL. (2014). Human Pheromones: Do They Exist? In: Mucignat-Caretta C, editor. Neurobiology of Chemical Communication. Boca Raton (FL): CRC Press/Taylor & Francis; Chapter 19.




Smell Dating from Tega Brain.

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Saturday, November 02, 2019

The Neural Correlates of Channeling the Dead



November 2nd is the Day of the Dead, a Mexican holiday to honor the memory of lost loved ones. If you subscribe to certain paranormal belief systems, the ability to communicate with the dearly departed is possible via séance, which is conducted by a Medium who channels the spirit of the dead.

Since I do not subscribe to a paranormal belief system, I do not think it's possible to communicate with my dead wife. Nor am I especially knowledgeable about the differences between mediumship vs. channeling:
Mediumship is mostly about receiving and interpreting messages from other worlds.

Mediums often deliver messages from loved ones and spirit guides during readings.
. . .

...channeling is often about receiving messages from other types of entities, such as nature spirits, spirit guides, or even angels.

In short, Channels can communicate with a broader class of non-corporeal entities, for instance Mahatma Ghandi or Cleopatra (not only the dead relatives of paying clients).

What seems to be uncontroversial, however, is that Channels who enter into a trance state to convey the wisdom of Gandhi may experience an altered or “expanded” state of consciousness (regardless of the veracity of their communications). This permuted state of arousal should be manifest in the electroencephalogram (EEG) as an alteration in spectral power across the range of frequency bands (e.g., theta, alpha, beta etc.) that have been associated with different states of consciousness.

A group of researchers at the Institute of Noetic Sciences adopted this view in a study of persons who claimed the ability to channel (Wahbeh et al., 2019). The participants (n=13; 11 ♀, 2 ) were on average 57 year old white women of upper middle class socioeconomic status, representative of the study site in Marin County, California. The authors screened 155 individuals to arrive at their final sample size.1 Among the stringent inclusion criteria was the designation of being a Channel who directly and actively conveys the communications of a discarnate entity or spirit (rather than being a passive relay).2 The participants were free of major psychiatric disorders, including psychosis and dissociation (according to self-report). Oh, and they had the ability to remain still during the channeling episodes, which was advantageous for the physiological measurements.

The participants alternated between channeling and no-channeling in 5 minute blocks while EEG and peripheral physiological signals (skin conductance, heart rate, respiration, temperature) were recorded. At the end of each counterbalanced session (run on separate days), voice recordings were obtained while the participants read stories.




Contrary to the authors' predictions, they found no significant differences between the channeling and no-channeling conditions for any of the physiological measures, nor for the EEG analyzed in standard frequency bands (theta 3–7 Hz; alpha 8–12 Hz; beta 13–20 Hz and low gamma 21–40 Hz) across 64 electrodes. I'll note here that the data acquisition and analysis methods were top-notch. The senior author (Arnaud Delorme) developed the widely used EEGLAB toolbox for data analysis, which was described in one of the most highly cited articles in neuroscience.3

Modest differences in voice parameters were observed: the channeled readings were softer in volume and slower in pace. The authors acknowledged that the participants could have impersonated an alternate voice during the channeling segments, whether consciously or unconsciously.

So does this mean that channeling is a sham? The authors don't think so. Instead, they recommended further investigation: “future studies should include other measures such as EEG connectivity analyses, fMRI and biomarkers.”


Footnotes

1 This is a rather esoteric population, so I won't fault the researchers for having a small sample size.

2 “The channeler goes into a trance state at will (the depth of the trance may vary) and the disincarnate entity/spirit uses the channeler’s body with permission to communicate directly through the channeler's voice, body movements, etc. (rather than the channeler receiving information mentally or otherwise and then relaying what is being received).”

3 I was rather critical of a previous study by this research group, which was ultimately retracted from Frontiers in Neuroscience. See Scientific Study Shows Mediums Are Wrong 46.2% of the Time.


Reference

Wahbeh H, Cannard C, Okonsky J, Delorme A. (2019). A physiological examination of perceived incorporation during trance. F1000Research 8:67.



Bev Tull, the fake medium on Bad Girls.

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Sunday, October 06, 2019

Is Mourning Rewarding? (revisited)



Can we reduce the persistent, unbearable pain of losing a loved one to 15-20 voxels of brain activity in the nucleus accumbens (O'Connor et al., 2008)? No? Then what if I told you that unrelenting grief — and associated feelings of sheer panic, fear, terminal aloneness, and existential crisis — isn't “suffering”. It's actually rewarding!

Well I'm here to tell you that it isn't.

Looking back on a post from 2011, you never realize it's going to be you.1


The top figure shows that activity in the nucleus accumbens was greater in response to grief-related words vs. neutral words in a group of 11 women with “Complicated” Grief (who lost a mother or sister to breast cancer in the last 5 years), compared to a group of 10 women with garden-variety Non-complicated Grief (O'Connor et al., 2008). Since the paper was published in 2008, and the standards for conducting fMRI studies have changed (larger sample sizes are necessary, no more “voodoo correlations”), I won't go on about that here.


When Grief Gets Complicated?

Grief is never simple, it's always complicated. The death of a cherished loved one can create a situation that seems totally intolerable. Almost everyone agrees that navigating such loss doesn't rely on one acceptable road map. Yet here it is. Normal people are supposed to move through a one year mourning period of “sorrow, numbness, and even guilt and anger. Gradually these feelings ease, and it's possible to accept loss and move forward.” If you don't, well then it's Complicated. This is a stigmatizing and limiting view of what it means to grieve the loss of a loved one.2

But is there really such there a thing as Complicated Grief? Simply put, it's “a chronic impairing form of grief brought about by interference with the healing process.” There are “maladaptive thoughts and dysfunctional behaviors” according to The Center for Complicated Grief. However, it's not named as an actual disorder in either of the major psychiatric manuals. In ICD-11, preoccupation with and longing for the deceased, accompanied by significant emotional distress and functional impairment beyond six months, is called Prolonged Grief Disorder. In DSM-5, Complicated Grief has morphed into Persistent Complex Bereavement Disorder, a not-exactly-reified condition subject to further study.


Dopamine Reward

Dopamine and its putative reward circuitry are way more complex than a simple one-to-one mapping. Studies in rodents have demonstrated that the nucleus accumbens (NA) can code for negative states, as well as positive ones, as shown by the existence of “hedonic coldspots” that generate aversive reactions, in addition to the usual hotspots (Berridge & Kringelbach, 2015). These studies involved microinjections of opioids into tiny regions of the NA.




If a chronically anguished state is portrayed as rewarding, it's time to recalibrate these terms. As I said in 2011:

If tremendous psychological suffering and loss are associated with activity in brain regions such as the ventral tegmental area and nucleus accumbens, isn't it time to abandon the simplistic notion of dopamine as the feel-good neurotransmitter? To quote the authors of Mesolimbic Dopamine in Desire and Dread (Faure et al., 2008):
It is important to understand how mesocorticolimbic mechanisms generate positive versus negative motivations. Dopamine (DA) in the nucleus accumbens is well known as a mechanism of appetitive motivation for reward. However, aversive motivations such as pain, stress, and fear also may involve dopamine in nucleus accumbens (at least tonic dopamine signals).

Grief-Related Words Are Rewarding

So what happens when you take a disputed diagnostic label and combine it with reverse inference in a neuroimaging study? (when you operate under the assumption that activity in a particular brain region must mean that a specific cognitive process or psychological state was present).

The NA activity was observed while the participants viewed grief words vs. neutral words that were superimposed over a photograph: a photo of the participant's deceased mother or a photo of someone else's mother. And it didn't matter whose mother was pictured, the difference was due to the words, not the images.3



Sample stimulus provides an [unintentional?] example of the emotional Stroop effect.


That's pretty hard to explain by saying that “the pangs of grief would continue to occur with NA activity, with reward activity in response to the cues motivating reunion with the deceased” if the effect is not specific to an image of the deceased.


Yearning and the Subgenual Cingulate

Why beat a dead horse, you ask? Because a recent study (McConnell et al., 2018) did not heed the advice above (sample size should be increased, beware reverse inference). The participants were 9 women with Complicated Grief (CG), 7 women with Non-complicated Grief (NG), and 9 Non-Bereaved (NB). The NA finding did not replicate, nor were there any differences between CG and NG and NB (over the entire brain). A post-hoc analysis then extracted a single question from a 19-item inventory and found that yearning for the dead spouse in all 16 Bereaved participants was correlated with activity in the subgenual cingulate (“depression-land” or perhaps “rumination-land”), for the comparison of an anticipation period vs. presentation of spouse photo. There were 5 spouse photos and 5 photos of strangers (note that it was not possible to predict which would be presented). The authors recognized the limitations of the study, yet pathologized yearning in Complicated and Non-complicated Grief alike.

I realize that the general motivation behind these experiments might be admirable, but you really can't come to any conclusions about how grief — a highly complex emotional response unique to each individual — might be represented in the brain.


Footnotes

1 See There Is a Giant Hole Where My Heart Used To Be from October 2, 2018.

The posts on illness and death that I never wrote:
(yes, I was really serious about these)

2 I was skeptical when someone sent me this book, It's OK That You're Not OK: Meeting Grief and Loss in a Culture That Doesn't Understand (by Megan Devine). I thought it was going to be overly 'self-helpy'. But it's actually been immensely helpful.

3 The idea of creating a self-relevant stimulus set was utterly horrifying to me.


References

Berridge KC, Kringelbach ML. (2015). Pleasure systems in the brain. Neuron 86(3):646-64.

Faure A, Reynolds SM, Richard JM, Berridge KC. (2008). Mesolimbic dopamine in desire and dread: enabling motivation to be generated by localized glutamate disruptions in nucleus accumbens. J Neurosci. 28:7184-92.

McConnell MH, Killgore WD, O'Connor MF. (2018). Yearning predicts subgenual anterior cingulate activity in bereaved individuals. Heliyon 4(10):e00852.

O'Connor MF, Wellisch DK, Stanton AL, Eisenberger NI, Irwin MR, Lieberman MD. (2008). Craving love? Enduring grief activates brain's reward center. Neuroimage 42:969-72.


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Sunday, September 22, 2019

Are there evil people or only evil acts?


“I can guarantee that someone in the world thinks you are evil. Do you eat meat? Do you work in banking? Do you have a child out of wedlock? You will find that things that seem normal to you don't seem normal to others, and might even be utterly reprehensible. Perhaps we are all evil. Or, perhaps none of us are.”

– Julia Shaw, Evil: The Science Behind Humanity's Dark Side

Earlier this month, Science magazine and Fondation Ipsen co-sponsored a webinar on Impulses, intent, and the science of evil. “Can research into humankind’s most destructive inclinations help us become better people?”

It's freely available on demand. Let the controversy commence...


Are There Evil People or Only Evil Acts?

Moderator (Sean Sanders, Ph.D. Science/AAAS):  “... How do we define evil? ... Are there evil people or only evil acts?”

In brief, Dr. Abigail Marsh said no, there are absolutely not evil people; Dr. David Brucato mostly agreed with that; and Dr. Michael Stone gave an elaborate example using an offensive term ("gay pedophile" – as if anyone would refer to a male pedophile who targets little girls as a "straight pedophile").



Dr. Marsh was not amused...

More detail below.

Read more »

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Saturday, August 24, 2019

Ivanka Trump to Head New Agency of Precrime


A Precog capable of predicting future crimes in the film version of Minority Report.


In a strange twist suitable for the dystopian reality show broadcast from the West Wing dining room, a charity formed to fight pancreatic cancer has morphed into project SAFE HOME — “Stopping Aberrant Fatal Events by Helping Overcome Mental Extremes”.



After three highly publicized mass shootings killed 34 people in the US, a variation on the “guns don't kill people...” trope was issued by President Trump: “mental illness and hatred pulls [sic] the trigger, not the gun.” He was right about hatred: two of the shooters espoused white supremacist views, the other was a misogynist. But rather than anger the NRA with tiny incremental changes to control access to firearms, a better approach is to develop a national plan to stigmatize people with mental illnesses, who are more likely to be the victims of violent crime than the perpetrators:
White House considers new project seeking links between mental health and violent behavior

Bob Wright, the former NBC chair and a Trump friend, is one of the proposal’s supporters.

The White House has been briefed on a proposal to develop a way to identify early signs of changes in people with mental illness that could lead to violent behavior.

Supporters see the plan as a way President Trump could move the ball forward on gun control following recent mass shootings as efforts seem to be flagging to impose harsher restrictions such as background checks on gun purchases.

The proposal is part of a larger initiative to establish a new agency called the Health Advanced Research Projects Agency or HARPA, which would sit inside the Health and Human Services Department. Its director would be appointed by the president, and the agency would have a separate budget, according to three people with knowledge of conversations around the plan.

The Suzanne Wright Foundation, started by Bob Wright to fight pancreatic cancer after his wife died from the disease, has advocated for the formation of a DARPA-like federal agency called HARPA. The original vision for HARPA was to “leverage federal research assets and private sector tools to develop capabilities for diseases, like pancreatic cancer, that have not benefited from the current system.”



91% of pancreatic cancer patients die within 5 years– often because the cancer is too advanced to treat by the time of diagnosis. An early detection test for pancreatic cancer would be the most effective weapon to save lives from this disease. ... CodePurple advocates for HARPA ... as the most promising vehicle to develop a pancreatic cancer detection test.



According to the Washington Post:
The HARPA proposal was initially pitched as a project to improve the mortality rate of pancreatic cancer through innovative research to better detect and cure diseases. Despite internal support over the past two years, the model ran into what was described as “institutional barriers to progress,” according to a person familiar with the conversations. 

So why not flip your game by seizing a tragic moment in time to transform yourself into legacy-making material?
“[Trump is] very achievement oriented and I think all presidents have difficulties with science,” Wright said in an interview. “I think their political advisers say, ‘No that’s not a game for you,’ so they sort of back off a bit.”

He added: “But the president has a real opportunity here to leave a legacy in health care.”

The newly-realized HARPA would use artificial intelligence, machine learning, commercial surveillance technology (e.g., Apple Watches, Fitbits, Amazon Echo, Google Home), and “powerful tools [NOT] collected by health-care provides like fMRIs, tractography and image analysis.”
HARPA would develop “breakthrough technologies with high specificity and sensitivity for early diagnosis of neuropsychiatric violence,” says a copy of the proposal. “A multi-modality solution, along with real-time data analytics, is needed to achieve such an accurate diagnosis.”

And because of her vast experience in these technologies and her theoretical contributions to the neuroethics of predicting violent behavior, Ivanka Trump is the best person to lead such an effort:
“It would be perfect for her to do it — we need someone with some horsepower — someone like her driving it. ... It could get done,” said one official familiar with the conversations.

Further Reading

Oh Good, White House Reportedly Considering Dystopian Plan to Try to Detect the Next Mass Shooter

The Minority Report, by Philip K. Dick


Further Watching

Person of Interest, created by Jonathan Nolan (Memento)

   ( How Person of Interest Became Essential Science Fiction Television )

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Sunday, August 11, 2019

Manipulating Visual Cortex to Induce Hallucinations




What is a hallucination? The question seems simple enough. “A hallucination is a perception in the absence of external stimulus that has qualities of real perception. Hallucinations are vivid, substantial, and are perceived to be located in external objective space.” When we think of visual hallucinations, we often think of trippy colorful images induced by psychedelic drugs (hallucinogens).

Are dreams hallucinations? How about visual imagery? Optical illusions of motion from viewing a non-moving pattern? No, no, and no (according to this narrow definition). Hallucinations are subjective and inaccessible to others, much as my recent posts discussed the presence or absence of visual imagery in individual humans. However, people can tell us what they're seeing (unlike animals).

Visual hallucinations can occur in psychotic disorders such as schizophrenia and schizoaffective disorder, although auditory hallucinations are more common in those conditions. Visual hallucinations are more often associated with neurodegenerative disorders. Among patients with Parkinson's Disease, 33% to 75% experience visual hallucinations, usually related to dopaminergic or anticholinergic drug therapy.

In contrast, hallucinations in dementia with Lewy Bodies (DLB) are diagnostic of the disease, and not related to pharmacological treatment. “Recurrent complex visual hallucinations ... are typically well-formed, often consisting of figures, such as people or animals.” The cause may be related to pathology in subcortical visual structures such as the superior colliculus and the pulvinar, rather than the visual cortex itself. A more specific hypothesis is that loss of α7 nicotinic receptors in the thalamic reticular nucleus could lead to hallucinations in DLB.


Charles Bonnet Syndrome (CBS)

Visual hallucinations are also caused by certain types of visual impairment, e.g. age-related macular degeneration, which leads to the loss of central vision. Damage to the macular portion of the retina can cause people to “see” simple patterns of colors or shapes that aren't there, or even images of people, animals, flowers, planets, and scary figures. Individuals with CBS know that the hallucinations aren't real, but they're distressing nonetheless.


image from the Macular Society 1


“Why are you discussing DLB and CBS here,” you might ask, “because these conditions don't involve abnormal stimulation of the visual cortex.” I brought them up because visual hallucinations in humans can occur for any number of reasons, not just from manipulation of highly specific cell types in primary visual cortex (which only occurs in optogenetic experiments with animals).



Electrical Stimulation Studies in Humans

A typical starting point here would be Wilder Penfield and the history of surgical epileptology, but I'll skip ahead to the modern day. Patients with intractable epilepsy present teams of neurosurgeons, neurologists, neurophysiologists, and neuroscience researchers with a unique opportunity to probe the inner workings of the human brain. Stimulating and recording from regions thought to be the seizure focus (or origin) guide neurosurgeons to the precise tissue to remove, and data acquired from neighboring brain bits is used to make inferences about neural function and electrophysiological mechanisms.




An exciting study by Dr. Joseph Parzivi and colleagues (2012) stimulated regions of the fusiform face area (FFA) in the inferior temporal cortex while a patient was undergoing surgical monitoring. Two FFA subregions were identified using both fMRI and electrocorticography (ECoG).



The location of the face-selective regions converged across ECoG and fMRI studies that presented various stimuli and recorded brain responses in the FFA and nearby regions (1 = posterior fusiform; 2 = medial fusiform). Then the investigators stimulated these two focal points while the patient viewed faces, objects, and photos of famous faces and places. Electrical brain stimulation (EBS) of the FFA produced visual distortions while the patient viewed real faces. Sham stimulation, and EBS of nearby regions, did not produce these perceptual distortions. The article included a video of the experiment, which is worth watching.




Another patient viewed pictures of faces during FFA stimulation and reported the persistence of facial images once they were gone, and the mixing of facial features, but no distortions (this is known as palinopsia). A third study induced the scary phenomenon of seeing yourself (self-face hallucination, or autoscopic hallucination), upon EBS of a non-FFA region (right medial occipitoparietal cortex). A video of this experiment is on YouTube.

“But wait,” you say, “you've been describing complex visual hallucinations and distortions of the face because the EBS was in higher-order visual areas that are specialized for faces. What happens when you stimulate primary visual cortex?” The answer is less exciting (but not unexpected): phosphenes, those non-specific images of light that appear when you close your eyes and press on your eyeballs (Winawer & Parvizi, 2016). These can be mapped retinotopically according to their location in the visual field. {also see this 1930 article by Foerster & Penfield: 2
"Stimulation of the occipital pole in area 17 produces an attack which is ushered in by an optic aura such as light, flames, stars, usually in the opposite visual field."}

But EBS of primary visual cortex is a coarse instrument. Here's where the latest refinements in optogenetics finally enter the picture (Marshel et al., 2019).



I won't attempt to cover the complex and novel techniques in Panel 1 and Panel 2 above. So I'll quote others who rave about what a breakthrough they are (and they are): amazing work, incredible breakthrough, Key advances in current paper include multiSLM to stimulate neurons based on function, and a red-shifted opsin allowing simultaneous 2p. And one day (hypothetically speaking), I'd like to present more than direct quotes and my cartoonish version of the optogenetic ensemble and behavioral training methods. But today isn't that day.
Using ChRmine [a fancy new opsin] together with custom holographic devices to create arbitrarily specified light patterns [horizontally or vertically drifting gratings], we were able to measure naturally occurring large-scale 3D ensemble activity patterns during visual experience and then replay these natural patterns at the level of many individually specified cells. We found that driving specific ensembles of cells on the basis of natural stimulus-selectivity resulted in recruitment of a broad network with dynamical patterns corresponding to those elicited by real visual stimuli and also gave rise to the correctly selective behaviors even in the absence of visual input.

Briefly, the investigators captured patterns of activity in V1 layer 2/3 neurons and layer 5 neurons that responded to horizontal or vertical gratings, and then played back the same patterns to those neurons in the absence of a visual stimulus. There goes the coarseness of EBS-induced phosphenes in humans... But obviously, the one great advantage of human studies is that your subjects can tell you what they see. Nonetheless, everyone wants to say that laser-activated nerve cells cause the mice to hallucinate vertical bars.

What really happened is that mice were trained to discriminate between horizontal and vertical gratings. The task required them to respond to the vertical, but not the horizontal. After training, visual stimulation with gratings was compared to optogenetic stimulation of classifier-identified neural ensembles in the absence of gratings. How well did the mice perform with optogenetic-only stimulation?

Modified from Fig. 5 (Marshel et al., 2019). (A) Discrimination performance during visual-only stimulation (black) and tuned-ensemble stimulation (red) over several weeks. (B) Discrimination performance for tuned-ensemble stimulation versus visual trials (P > 0.1 paired t test, two-tailed, n = 112 sessions across five mice).


Eventually the mice did just about as well on the discrimination task with optogenetic stimulation of the horizontally or vertically-tuned neurons, compared to when the horizontal or vertical stimuli were actually presented. Were these mice “hallucinating” vertical gratings?  Or did they merely learn to respond when a specific neural ensemble was activated? Isn't this somewhat like neurofeedback? During training, the mice were rewarded or punished based on their correct or incorrect response to the “vertical” ensemble stimulation. They can't tell us what, if anything, they saw under those conditions.

And the authors themselves noted the following limitation, that “mice initially required some training involving paired optogenetic and visual stimuli before optogenetic activation alone sufficed to drive behavioral discrimination.” Marshel et al. correctly invoked the “it takes a village” explanation that many other cortical and subcortical regions are required to generate a full natural visual percept.

My frustration with the press coverage stems from inaccurate language and overblown interpretations.3  [So what else is new?]  From the New York Times:

Why Are These Mice Hallucinating? Scientists Are in Their Heads
In a laboratory at the Stanford University School of Medicine, the mice are seeing things. And it’s not because they’ve been given drugs.

With new laser technology, scientists have triggered specific hallucinations in mice by switching on a few neurons with beams of light. The researchers reported the results on Thursday in the journal Science.

The technique promises to provide clues to how the billions of neurons in the brain make sense of the environment. Eventually the research also may lead to new treatments for psychological disorders, including uncontrollable hallucinations.

The Stanford press release doesn't use “hallucination” in the title, but a few are sprinkled throughout the text for dramatic effect: “Hallucinations are spooky” and “Hallucinating mice.”

Should we classify the following as a spooky hallucination: Optical stimulation of 20 vertical bar neurons in behaviorally trained mice who then perform the task as if the drifting vertical gratings were present in their visual field. I would say no. To be fair, in the Science paper the authors used the word “hallucinations” only once, and it wasn't to describe mouse percepts.
Studying specific sensory experiences with ensemble stimulation under different conditions may help advance development of therapeutic strategies . . . for neuropsychiatric symptoms such as hallucinations or delusions. More broadly, the ability to track and control large cellular-resolution ensembles over time during learning, and to selectively link cells and ensembles together into behaviorally relevant circuitry, may have important implications for studying and leveraging plasticity underlying learning and memory in health and disease.

I'm focusing on only one small aspect of the study, albeit the one that grabs media attention. The results were highly informative in many other ways, and I do not want to detract from the monumental technical achievements of the research team.


Footnotes

1 This is a terrific resource, with loads of information, additional artistic renderings, an eBook, and a must-see video.

2 There's no escaping Penfield...

3 See Appendix for expert opinion, since I am not an expert...


References

Foerster O, Penfield W. (1930). The structural basis of traumatic epilepsy and results of radical operation. Brain 53:99-119.

Marshel JH, Kim YS, Machado TA, Quirin S, Benson B, Kadmon J, Raja C, Chibukhchyan A, Ramakrishnan C, Inoue M, Shane JC, McKnight DJ, Yoshizawa S, Kato HE, Ganguli S, Deisseroth K. (2019). Cortical layer-specific critical dynamics triggering perception. Science Jul 18.

Parvizi J, Jacques C, Foster BL, Witthoft N, Rangarajan V, Weiner KS, Grill-Spector K. (2012). Electrical stimulation of human fusiform face-selective regions distorts face perception. J Neurosci. 32(43):14915-20.

Winawer J, Parvizi J. (2016). Linking Electrical Stimulation of Human Primary Visual Cortex, Size of Affected Cortical Area, Neuronal Responses, and Subjective Experience. Neuron 92(6): 1213-1219.


Appendix

Before lodging this critique, I consulted select experts on Twitter...






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Monday, August 05, 2019

Brain Awareness Video Contest 2019



What Color is Monday? This video on synesthesia is one of the Top Ten videos in the Society for Neuroscience Brain Awareness Video Contest.  

Voting for the 2019 People's Choice Award closes 12 p.m. Eastern time on August 30, 2019.

However, it wasn't immediately apparent to me how you're supposed to cast your vote...


UPDATE (Aug 6 2019): vote for your favorite for the People's Choice award by liking it on YouTube.


The entire playlist is on YouTube.  


2


How Ketamine Treats Depression


3


Procrastination: I'll Think of a Title Later


4


Seeing Culture in Our Brain


5
6


How Neuroscience Informs Behavioural Economics


7


What Color is Monday


8


Why do adolescents go to sleep late?


9


An Inside Look: Alzheimer's Disease

10
 

Technology Makes Us Bigger

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