Get those auditory neurons firing! This blogpost is an update to my post from 3 years ago on neuroscience podcasts. I’m a complete podcast addict and really believe that podcasts are the way of the future–they’re a great way to learn on the go, while you do chores, or exercise. Also, you can control the speed of what you’re listening to and pause to take notes. Neuroscience podcasts can be a great way to hear how scientists talk and think, to get exposed to a variety of topics, and to keep up-to-date with this quickly moving field.

Top 8 Neuroscience and Behavior Podcasts:

In no particular order. They’re really apples and oranges (and in one case an apple-orange). Why top 8 and not top 10?Because these are the podcasts I listen to personally and can recommend. Read the descriptions and decide what’s right for you.

1. Naked Neuroscience Podcast – A podcast recorded out of Cambridge University, this podcast has been around since 2001, but it’s new to me! This podcast includes news from European conferences and interviews with scientists from around the world. It has high production values, good stories, rigorous science, but as you can see from the picture a sense of humor as well. Monthly episodes, ~30 mins.


2. NPR’s Invisibilia – Think Radiolab focused on “the invisible forces that control human behavior – ideas, beliefs, assumptions and emotions.” Each episode, hosted by rising stars Lulu Miller and Alix Spiegel, interviews scientists and crafts small narratives around themes. For example, this season featured episodes on interactions with technology, blindness, and fear. The first season is 6 episodes, ~1 hr, more to come (and hopefully soon!)


3. High Proof Podcast – Another podcast with a sense of humor, their tagline reads: “We demand high proof for our science and our spirits.” I really enjoy this podcast. Ryan and Joel think they pick interesting topics and I especially like the philosophical slant, though I wish they spent more time explain the background of the philosophy they cover. Maybe I’m doing something wrong, but I can’t find their earliest episodes. I wish I knew a little bit more about their backgrounds and sometimes I wish they planned and researched their topics a little better, but I also don’t want them to sacrifice the conversational tone. Regardless, highly recommend it. ~1/wk 12 episodes total as I write this

3. Brain Science Podcast – “The show for everyone who has a brain.” Hosted by an ER doctor, Ginger Campbell, does a great job of getting big name neuroscientists to talk in depth on a topic while keeping things accessible. I think Dr. Cambell is doing a huge service to the world by making this podcast. Its great for getting introduced to perspectives of psychology out neuroscience outside of your own field. I also love that Dr. Campbell repeats and clarifies important points in the middle and end of episodes and always asks the guests to give advice to students interest in neuroscience. The website also features annotated transcripts of the episodes. Monthly episodes ~1 hr.

4. Neuropod – Nature’s official neuroscience podcast hosted by neuroscience journalist Kerri Smith (though I believe the host is changing soon). Each episode is around a half hour and usually features 3-4 pieces interviewing authors of recent papers and reviews. (The website also has links to the papers if they peak your interest.) The podcast has high production value on  par with public radio. Monthly episodes ~30 min.

5. UTSA’s Neuroscientist’s Talk Shop – As the name implies, NTS is hardcore neuroscience. Each episode has an invited guest who takes part in a discussion and answers questions posed by other neuroscientists. Generally, the topics covered focus on computational neuroscience and electrophysiology. Often speakers assume listeners are well versed in the field, but I think even if you aren’t, you can still get a lot out of it by hearing the way scientists think and talk informally about research and speculate on the gray areas of neuroscience (though like any good scientists, they make it more than clear when they are speculating). Frequency varies 1-3 weeks during the school year ~45 min.

Probably the best podcast logo

6. Freakonomics – “The hidden side of everything.” Hosted by the authors of the best-selling book of the same name, Freakanomics Radio podcast has released over 200 episodes since 2010. The show uses a narrative style and interviews to explain studies of behavioral economics–a field that uses economic statistical techniques and theory to determine what factors like incentives drive the behavior of people and systems. This podcast is incredibly interesting and accessible. Though it doesn’t touch strictly on neuroscience, I really would recommend it to any human being, but especially so anyone interested in behavior and decision-making. 1/wk 30-60 mins

7. The Laughter Research Podcast – This podcast is really cool in that its guests include not just professors, but comedians and entrepreneurs. I think this broader perspective is in part due to the fact that This Laughter Research Podcast is hosted by Glen Duggan, a non-traditional psychology PhD candidate in Trinity College, Dublin, with a lot of real world experience. I briefly chatted to on twitter and seems like a genuinely great guy. I’m of the opinion that positive emotions like happiness and behaviors like laughter are far understudied compared to negative emotions, so I think the work he’s doing to promote this work is very important. ~ 2 episodes / Month

8. All about Autism Podcast – This podcast is a little more niche, but it’s a fascinating and easy listen, and I would recommend it to anyone interested in autism, psychiatry, especially those who are curious about a patient’s or parents perspective. The All about Autism Podcast is hosted by Heather and Dave Eaton. (Dave is the co-owner and co-founder of Eaton Alliance Inc., which supports individuals with disabilities, specializing in autism.) It’s really interesting to hear people’s perspectives on autism from a less academic, but extremely well informed perspective (in fact far more informed than most academics as to the everyday lives of patients with autism). I think this podcast is a powerful force for good in the world right now, especially as it educates and rebuffs the misconception that vaccines cause autism. (To repeat the obvious, there is no scientific evidence showing vaccines cause autism and many have looked. The one original study that did show this has been shown to be a fraud propagated by a scientist with a conflict of interest.) Used to be once a week, but now closer to once a month.


I’m sure I’m missing some podcasts from this list, and, as I mentioned above, I’m a podcast addict. So I’d love to hear what you’re listening to and what you’d recommend, even podcasts that aren’t directly related to neuroscience and behavior. Also, if you liked this post and want to see more like it please share it and if you want updates on what I’m thinking and listening to please follow me on twitter, or like the Neuroamer page on facebook.


Ben Kuebrich

I’m trying to collect all of the lectures relevant to songbirds into one place. I’m going to start by combing  through some sources I’m already familiar with like podcasts. If I leave any out, please post them in the comments and I’ll try to update the main post. Thanks!

Songbird lectures sorted by date:

Sam Sober, UTSA Neuroscientists Talk Shop Oct 2014

Todd Roberts, UTSA Neuroscientists Talk Shop Mar 2014

Eric Fortune, UTSA Neuroscientists Talk Shop Sep 2013

Annemie Van der Linden, “Functional Magnetic Resonance Imaging (fMRI) with Auditory Stimulation in Songbirds,” Jove Jun 2013

Mimi Kao, “What songbirds can teach us about learning and the brain,” TEDxCaltech Feb 2013

Sam Sober, “A Lightweight, Headphones-based System for Manipulating Auditory Feedback in Songbirds” Jove Nov 2012

Erich Jarvis, “Brain Evolution: How Birds and Humans Learn to Sing and Talk” Georgia Tech Honors Program Oct 2012

Alan Kamail, “Bird Brain! Compliment or Insult,” Nebraska Lecture  Sep 2012

Erich Jarvis, UTSA Neuroscientists Talk Shop Apr 2012

Michale Fee, “The Role of Basal Ganglia Circuits in Vocal Learning in the Songbird: A Hypothesis” NIH Videocasts Jan 2012

Allison Doupe, 15th Annual Swartz Foundation MIND/BRAIN Lecture Apr 2011

William Grisham, UCLA Modular Digital Course in Undergraduate Neuroscience Education – Lecture 1Lecture 2, Lecture 3, Lecture 4 Oct 2011

Ila Fiete, UTSA Neuroscientists Talk Shop Nov 2009

Harvey Karten, “Bird Brains,” UCTV Grey Matters Jan 2008


Also possibly of interest:

Dopamine Symposium w/ Bruce Bean, Jim Surmeier, Carlos Paladini, Jochen Roper, John Williams, and Charles Wilson, UTSA Neuroscientists Talk Shop.


Differences between direct an indirect MSNs are not obvious from morphology or electrophysiology. However, the two cell types and pathways can be separated and selectively manipulated using genetic tools, such as lines of reporter mice that express GFP in either D1 or D2 expressing MSNs, so many recent studies have tried to sort apart the pathways. This paper is a review of more classic studies on DA’s differential effects through D1 versus D2 signalling on glutamatergic signaling, intrinsic activity, and plasticity.

Continue reading ‘Summary of D1 and D2 DA-Receptor Modulation of Striatal Glutamatergic Signaling in MSNs – Surmeier 2007.’


People and animals do not always make ‘rational’ choices that maximize the amount of reward they receive. For example, deviations from ‘rational’ economic decision making include risk aversion and decreasing marginal utility of a given reward. But what determines this utility? Continue reading ‘Is human irrationality due to irregularities in dopaminergic neuron firing? Notes from Stauffer, Lak, and Schultz 2014 – Dopamine Reward Prediction Error Responses Reflect Marginal Utility’

Try and cross your eyes to make the top gridded circles overlap. Give up? Try doing it on the bottom ones that are surrounded by the border.

A lot easier, right? The square surrounding the circles helps your eyes stabilize as you cross them.

Free fusion optical illlusion vergent eye movements

From Blake 1989

Also notice how your eyes process the diagonal lines themselves. Your brain is receiving drastically different signals from each eye creating a state of binocular rivalry, where your perception often alternates between the signals received from one eye and the other.

If you’re interested in this phenomena and learning a theory about it’s neural underpinnings check out the paper where I came across it.


Blake, R. A neural theory of binocular rivalry. Psychol. Rev. 96, 145-167 (1989).

Found this book at a bookstore and was hooked after reading the first few pages, based on it’s topic and clear and well-written prose.

James Davies

James Davies

Chapter 1

James Davies, with a PhD in social and medical anthropology from Oxford, begins with a history of psychiatry starting in the 1970s and a crisis of confidence it faced. A series of experiments questioned the validity and reliability of psychiatric diagnosis.

The 1973 Rosenhan experiments on “Being Sane in Insane Places” questioned the validity of psychiatric diagnoses. Neurotypical confederates checked themselves into asylums claiming to have heard a voice once, but then once admitted acted normal and saw what they were diagnosed with and saw the great lengths it took to be deemed healthy again and get discharged from the institutions. After publishing the results, they were challenged by a hospital to send pseudopatient imposters back in. Rosenhan agreed to the challenge but did not send any patients. A month later the hospital reported they suspected 41 imposters.

Another experiment showed that diagnoses were not consistent between psychiatrists. It sent the same patients to different psychiatrists and showed that they got different diagnoses from psychiatrists around a third of the time. Additionally, the prevalence of different diagnoses seemed to be regional, with some diagnoses being more prevalent in certain countries.


These criticisms of psychiatry lead to a drastic rewrite of the 3rd edition of psychiatrists diagnostic manual, the DSM III, headed by Robert Spitzer, who attempted to increase diagnostic reliability by making the definitions of disorders more precise and adding an explicit checklist to each disorder. These checklists created thresholds between psychiatric disease and “normal” human experience that, while decided by expert consensus, were ultimately arbitrary.

Additionally, the DSM III removed many disorders, especially those that had been introduced by psychoanalysts, as that discipline was falling out of favor. He brings up an interesting story about the removal of homosexuality as a “sexual deviation,” which he says was largely due to pressure from the Gay Rights movement and came down to a vote at an American Psychiatric Association meeting in the 70s, with 5,854 psychiatrists voting to remove homosexuality as a disease and 3,810 voting to keep it in. Davies makes the point that many of these decisions were political and not directly based on any changes in scientific research.

Despite the reforms made in the DSM III and subsequent manuals, diagnostic reliability remains a difficulty. Interestingly, I looked up a citation Davies makes to Aboraya, 2006, which he says “showed that reliability actually has not improved in thirty years.”I’m uncertain about how Davies reached that conclusion from this paper, as it clearly states:

  • that while diagnostic reliability remains a problem, the third generation of psychiatric diagnoses “from 1980 to present… more reliability papers were published and the reliability of psychiatric diagnosis has improved,” and
  • “The development of the DSM-III and its subsequent versions has been a major accomplishment in the history of psychiatric nomenclature. Clinicians use the DSM criteria in clinical practice as an effective way to communicate the clinical picture, the course of illness, and efficacy of treatment.”

This citation seems academically sloppy and perhaps shows that Davies seeks to oversimplify a complex and murky issue into a one-sided story (though this also might reflect my innate bias against pop-science books).

Chapter 1 ends questioning the validity of psychiatric diagnoses even if we fix the reliability problem. Even if we could get every psychiatrist to agree on the diagnoses, does that mean it’s a real disease entity, or that we’ve just made a reliable but arbitrary construct? He argues that we need biomarkers to prove it’s a “discrete, identifiable biological disease.” While I agree, I think that psychiatric definitions do a good job of separating normal but different from disease, by often requiring that the disease is disruptive to the patients social relationships or occupational function. What makes psychiatric illnesses, diseases is that they are problematic for people’s lives, and people, whether the patient themselves or their friends and family, want something done about it. I’m unsure if we will be able to find or need to find biomarkers for every disease. While some diagnoses may ultimately be arbitrary, if they are clinically helpful and can show statistical and long-term improvements in patients quality of life, then they are valuable.

Let me know if you have any comments on this blog post. I hope to continue blogging my thoughts on this book as I read through it.

SFN logo 2014 #SFN14 Society For Neuroscience Blog

Joe Paton from the Saltzman lab – Time encoding cells in the rodent striatum.

You can use an operant conditioning train animals to press a lever and get a reward. Using a fixed interval paradigm, you then do not reward the animal for lever presses until a certain time interval is passed. Animals will learn roughly learn this time association, and pause from lever presses until a point some intermediate time before the interval will expire, and then they begin pressing the lever again.

If you record in the striatum of rodents that have learned this task, you see neurons that fire at every point in the fixed interval and rescale with the fixed interval, if the interval changes. They saw that the rescaling was always slightly subproportional, and also that striatal cells multiplex information about action and time.

I think this is a really great clear electrophysiological link between striatal activity and the task being performed. I wonder if labs have tested mutant mice such as FOXP2 KOs or Shank3B knockouts with proposed striatal defects in tasks like this.

Also, it’s harder to learn the association between a Conditioned Stimulus (CS) and Unconditioned Stimulus (US), if you stretch out the time delay between the CS and US, while keeping the inter-trial interval the same. However, for some reason if you increase the inter-trial interval proportionally with the delay between CS and US, then that increased difficulty of learning the CS/US association doesn’t occur.

Maybe, it’s more difficult to make the association between CS/US with a longer delay, and therefore it takes the brain longer to process the association. But, if you leave the brain to process the old trial offline without interference from new tasks, then it can form the association. To restate that, when the trials happen too quickly, processing the subsequent trial interferes with the ongoing processing of the previous trial and interferes with learning.

Carlos Lois – Transgenic Songbirds – Genetic tools to investigate brain circuit assembly and cellular basis of behavior.

Lois mentioned that HVCà RA neurogenesis occurs during song learning. Neurons migrate into the HVC after making soma-soma contact with resident neurons. A thought I had never really had was how much is going on during windows of time when fetuses are learning about speech. A lot of developmental psychology work has shown that babies learn to identify prosaic cues of language, their mother’s voice, etc. while in the womb. I wonder to what extent these process are concurrent with and depend on neurogenesis. More generally, do we have a good sense from autopsy studies and/or radiation exposure studies when neurogenesis ends in normal human development for cortical areas, the striatum, etc.

Collaborating with the Gardner lab, Lois designed an adeno-associated virus (AAV) to express GCAMP6 in a small population of neurons in the HVC. (For some reason with the current viruses and promoters they’re getting much smaller yields of infected cells than people normally do with mice. ~2,000 neurons in birds compared to ~20 million in mice. Of course this isn’t always bad–sparse labeling can be good for measuring morphology or separating cell-autonomous effects from emergent effects). By mounting a low weight CMOS camera on top of the birds head, they could record activation of many cells simultaneously in a singing behaving bird (and know where these cells lay relative to each other in the rostro-caudal and medial-lateral axes).

Lois’s group also infected HVC with a virus driving expression of a bacterial Na+ channel ‘NaChBaC.’ Neurons in this channel went from firing single discrete spikes to prolonged depolarizations. As the channel starts being expressed, song gets completely distorted, but remarkably a few days later the bird has found a way to compensate and get song back to normal. They said that they did histology to confirm the infected neurons were still alive and expressing the channel. However, maybe the bird simply down-regulated all of the synaptic strengths of the infected neurons, and there is enough redundancy to produce the song with the remaining neurons.

Finally, Lois showed data from transgenic zebra finches that have been germline transfected with RNAi to knock down CNTNAP2 expression, which is associated with developmental language disorders and autism. They showed that the CNTNAP2 knockdown birds showed normal learning of simple syllables, but impaired learning of complex syllables. He also mentioned that they had developed a line of GCAMP6 transgenic animals which is pretty exciting. I believe viral infection of germline cells cann be combined with the CRISPR-CAS system to cause deletions and premature stops at target genes, and theoretically even induce homologous recombination (by also providing a template strand complementary to the region where the DNAase has cut the DNA.

Someone asked a question about CRE lines in birds, and Lois said that economically it probably wasn’t viable. Not enough people do research on birds to justify that kind of investment, and making such animals would be a largely thankless job. However, there are still a ton of experiments that could be done on simpler transgenics such as: plain KOs, KDs, transgenics that express fluorescent proteins and optogenetic channels. I think just having that level of genetic tools combined with the song system’s anatomical modularity, the strength of song as a behavior, and the strong phenotypes seen in FOXP2 KDs and CNTNAP2 KDs show that genetic songbirds could be an extremely powerful models for diseases of speech, social behavior, and motor learning. Further, birds have similar reproductive cycle lengths as mice and live longer, so stocks of transgenics can be bred in reasonable amounts of time. I wanted to ask Lois what he thought about creating inbred strains of zebra finches, but I didn’t have the chance. (I’m almost tempted to start this as a side project in my apartment, but I’m afraid of then bringing an infection into the lab.)

Lois had the impression that the NIH was not interested in funding zebra finch transgenics. His grants came from mouse projects and work he did on zebra finches were side projects.

A member of the Simons Foundation “SFARI program” said that they have wide agreement that rodents aren’t “sophisticated.” However, the program is most concerned with investigating the rare genetic causes of autism and generating high-throughput screening models for autism. Personally, I think this is short sighted and the basic science just isn’t there yet. We really need to investigate the basic mechanisms of communication, imitative learning, etc., and I think songbirds are one of the best model organisms for these behaviors—and without a doubt better than rodents. So, while using genetics we’ve done amazing work on specific etiologies like Rhett syndrome, as someone in the audience rightly pointed out there are still almost no examples of rational drug design in neuroscience and neurology, except for the new example of orexin antagonists for insomnia and how good of a drug they’ll be in the long term is unclear.

Dennis Drayna – genetics of stuttering and mouse models

Stuttering affects 4% of the population at some point in their life, but only .5-1% of adults are persistently affected and at that point there is a 4:1 ratio of males to females.

Most human genetics has focused on this persistent stuttering population. They’ve shown that it’s about 85% Continue reading ‘Striatal time cells, transgenic birdsongs, stuttering mice and more – Birdsong4 Sattelite and #SFN14 Notes’


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