Better Know A Brain Region: Insula

The insula (aka insular cortex, “Island of Reil”) is the cerebral cortex’s lonely island. Pushed deep into the lateral Sylvian fissure by the  expansion of parietal and temporal lobes in human brain, the insula can not be observed from the brain surface and it’s separated from the neighboring claustrum by white matter (extreme capsule). It is relatively long rostrocaudally and recent studies have suggested the possibility of as many as 13 distinct functional subdivisions (Uddin et al, 2017).

Insula

Horizontal section of human brain. Red arrow points to insular cortex. Image from http://www.thehumanbrain.info 

In rodents, the insular cortex is in generally the same anatomical location, but exposed on the lateral brain surface. The insula lies at the transition between isocortex (6 layers) and allocortex (3 layers): bracketed ventrally by the piriform (olfactory) cortex and secondary somatosensory cortex dorsally. Traditionally, insula subregions in rodent were defined based on the gradual presence of layer 4 (granule layer): granular insula (has layer 4), dysgranular insula (kinda has layer 4), and agranular insula (no layer 4). Over decades, investigations in rodents would identify the insula as a major site for higher-order visceral and gustatory signal processing, particularly within the granular and dysgranular cortex. In the mouse Allen Reference Atlas, the granular and dysgranular insular cortex were renamed as ‘visceral cortex’ (VISC) and ‘gustatory cortex’ (GU), with only the agranular insula (AI; itself having anterior dorsal/ventral vs. posterior subdivisions) retaining the insula name.

InsulaCyto-01

Coronal mouse ARA section 53 (left) with corresponding Neurotrace Blue tissue section (right). The insula includes agranular, dygranular, and granular subregions distinguished by layer 4 (the granule cell layer). The posterior agranular insula (AIp), adjacent to 3-layered piriform cortex (PIR), lacks a clear layer 4. The dysgranular insula (aka gustatory cortex (GU)) has a layer 4 but its granule cells are not quite fully laminar compared to granular insula (aka visceral cortex (VISC)). Other structures noted are SSs (secondary somatosensory cortex), claustrum (CLA), dorsal endopiriform nucleus (EPd).

The functional role of the insula is still a bit mysterious, despite the growing amount of research on this structure. In the human imaging field, the insula is a structure that wears many hats: it is implicated in a variety of roles including addiction, multimodal sensory processing, motor control, homeostasis, emotions (i.e. disgust, pain, anger, fear), empathy, saliency, and interoceptive awareness. With an involvement in so many different brain functions, it is difficult to understand exactly how the insula fits in to the function of the brain as a whole system.

The idea that the insula is involved in interoception — the conscious feeling of your internal state — has been particularly popular because it combines the insula’s role within gustatory and visceral circuits with the general perception of the cortex’s role in consciousness. Multisynaptic viral tract-tracing has shown the insula is positioned at the top of the pre-autonomic nervous system network –brain circuits which produce top-down control on autonomic neurons in the spinal cord/brainstem. In addition, the insula is densely connected to other parts of cortex, providing a gateway through which many cortical regions could alter homeostasis in the body. As is often the case, understanding the neural connectivity of a region gives you a pretty good of what it is doing functionally.

However, the insula is a prime example of where better anatomical understanding is needed if we are to take things further. In both human and rodent research, the insula is a large structure with multiple uncharacterized subdivisions. As you can see from the picture above in the mouse, the VISC, GU, and AI subregions are particularly thin and difficult to target selectively via injection. Many behavioral lesion studies often destroy the entire insula (and more), leaving the resulting interpretation ambiguous as to which subregion is really involved. In the human imaging field, there is an effort to define subdivisions, but MRI is limited in resolution and often cannot localize effects to small areas. As tools become more specific and we can obtain higher resolution, the need for anatomy will become more important than ever. Those who are willing to appreciate the details of the anatomy will be those who make the next big break-through.

-M

Hitchhiker’s Guide to Neuroanatomy: Tract-Tracing Part 1

NTT3

This book is a classic guide to tract-tracing methods. You can get a free PDF here: https://link.springer.com/book/10.1007/0-387-28942-9 

Sensory information comes in and motor behavior comes out. Along the way, information has to flow through neural circuits in a specific way so that the correct behavior is produced in response to the environment. Tracing neural circuits across the brain has been a goal of neuroscience since Cajal put arrows on his drawings.

The problem in neuroscience has always been a problem of too much. Nissl staining shows every cell. A Golgi stain labels ~10% of all neurons, but even this produces a tangles web of axons and dendrites. The major white matter tracts are known to contain axons, but it is impossible to follow a single axon amidst a bundle of thousands. What if we want to know how one group of neurons is connected to another group of neurons without all the other neurons getting in the way?

A great number of careers were built upon this one question. The earliest method of tract tracing was founded upon the concept of Wallerian degeneration: severing an axon from its cell body causes the axon to degenerate in an anterograde fashion (anterograde = away from the cell body). These degenerating axons could be visualized if the tissue was impregenated with silver. Decades of research went into improving the silver degeneration staining methods, as the background was quite high in the tissue. Ultimately, the solution arrived in the Nauta-Gygax method and later Fink-Heimer method.

Nauta1993

Nauta-Gygax fiber staining (from Nauta, 1993)

Shortly after the Fink-Heimer method was developed, a very different approach to tract tracing was being adapted by Maxwell Cowan: autoradiography of transported radioactively-labeled amino acids. Neurons will generally take up molecules within the extracellular environment during their constant process of endo- and exo-cytosis. Injections of radioactively-labeled amino acids into a brain region would ultimately be taken up by the neurons and transported anterogradely. The result could be visualized by placing film over the tissue sections where the radioactivity could be visualized. The use of radioactively-labeled amino acids flourished in the 1970’s, although it has now been shown that tritiated amino acids diffuse trans-neuronally across connections, confounding the interpretations of direct connections within these studies. In the 1980’s, other molecules, particularly horse-radish peroxidase (HRP) and plant lectins, were found to be taken up and transported either retrogradely (retrograde = toward the cell body) or anterogradely and visualized using peroxidase reactions or immunohistochemistry.

ILA_SW120404-03A

PHA-L (green) is considered the ‘gold standard’ for anterograde tract tracing

Varicosities

PHA-L stained axons with varicosities (small swellings along the axon) that are indicative of presynaptic terminal sites (known as boutons en passant).

These tracer molecules (which I now consider ‘classic’ tracer molecules) were highly sensitive and had greater validity over previous methods:

TracingValidity

Table from Bota, Dong, and Swanson, 2003

Although I consider these tracer molecules to be ‘classic’, they are still widely used today and are a major component of our lab’s Mouse Connectome Project (www.MouseConnectome.org). They have been substantiated by decades of work and proof-of-principle studies. However, there are still some limitations and known confounds which must be considered when using them (I will discuss these later).

In Tract-tracing Part 2, I will discuss the history and development of ‘modern’ tracing methods: neurotropic viruses.

 

-M

Under the Microscope #2

UndertheMicroscope2

And we’re back! Under the Microscope #2 image is from one of our Mouse Connectome Project anterograde/retrograde coinjections (both tracers are coinjected into a single brain region). The green axons are labeled anterogradely by the tracer PHA-L and the magenta neuron cell bodies retrogradely-labeled by Cholera Toxin Subunit B (CTB). The strong overlap in the distribution of the green axons with the magenta neurons suggests that the area in the image is reciprocally connected with the injection site!

  1. Can you name the area of the brain where the anterograde/retrograde labeling is located?
  2. Can you guess where the coinjection site is located?

 

I’ll update this post on Monday (7/23/18) with the answer!

-M

 

 

Under the Microscope Answer:

 

UndertheMicroscope2-02

This data is from case SW121221-01A and all sections can be viewed using the iConnectome viewer at http://www.MouseConnectome.org. Tracer labeling is located in the caudal part of the thalamus that contains the auditory nuclei (which I’ve always thought look like ear lobes in coronal sections). I’ve outlined the cytoarchitecture on the tissue section (left) which is roughly similar to ARA level 85 (right). We can see now that the labeling is distinctly distributed within the medial geniculate nucleus of the thalamus (MG), particularly the ventral (MGv) and medial (MGm) subnuclei.

The MG is the primary sensory thalamic nucleus for auditory information. MGv, in particular, is the subdivision most connected with primary auditory cortex (AUDp, aka A1). As it turns out, that’s where our coinjection site is located (ARA level 77 bottom).

UndertheMicroscope2-01

-M

 

Art and History of Neuroscience #1 The Brain Hieroglyph

Over the course of millenia, our understanding of the brain has evolved with the artistic depictions of its structure. Visualization is key to understanding and artists have had a great impact on how scientists and philosophers thought about how the brain might work.

 

The Brain Hieroglyph

The earliest known reference to the brain comes from the Edwin Smith Surgical Papyrus, believed to be written in 1700 BC, but copied from a much older text (~3000 BC). The Papyrus contains descriptions of 48 injury cases and relays an impressive amount of early Egyptian medical knowledge (https://ceb.nlm.nih.gov/proj/ttp/flash/smith/smith.html). The brain hieroglyph is first used to in case 6: “Instructions concerning a gaping wound in his head, penetrating to
the bone, smashing his skull, and rending open the brain of his
skull.”

brain_hieroglyph

The hieroglyph for brain (outlined by red box) has four characters and is written from right to left. From https://ceb.nlm.nih.gov/proj/ttp/flash/smith/smith.html

A translation of this case can be found in Feldman and Goodrich, 1999:

“Examination
If thou examinest a man having a gaping wound in his head, penetrating
to the bone, smashing his skull, and rending open the brain
of his skull, thou shouldst palpate his wound. Shouldst thou find
that smash which is in his skull like those corrugations which form
in molten copper, and something therein throbbing and fluttering
under thy fingers, like the weak place of an infant’s crown before
it becomes whole – when it has happened there is no throbbing
and fluttering under thy fingers until the brain of his the patient’s
skull is rent open – and he discharges blood from both his nostrils,
and he suffers with stiffness in his neck…

Diagnosis
Thou shouldst say concerning him: “An ailment not to be treated.”

Treatment
Thou shouldst anoint that wound with grease. Thou shalt not bind
it; thou shalt not apply two strips upon it: until thou knowest that
he has reached a decisive point.”

The description of the brain surface with its sulci and gyri as looking like corrugations of molten copper is pretty interesting. I found this youtube video showing traditional copper smelting technique and I guess it does look somewhat similar:

copper_smelting.jpg

Traditional copper smelting was performed in a pit. From https://www.youtube.com/watch?v=FEQaEgkxqUk

So the first description of the brain, is something of a corrugated blob. Not much to go on if you’re a scientist trying to figure things out, but it is a start. The next known description of the brain wouldn’t arise until the ancient Greeks over 1000 years later.

-M

Where have all the neuroanatomists gone?

I mentioned this briefly in the blog introduction, but neuroanatomists are few and far between these days. In the hey day of Cajal, neuroanatomy was probably the biggest field in neuroscience. This decline in neuroanatomy expertise was brought up again in a tweet in response to my last blog post:

So what happened to neuroanatomy over the last few decades that brought us to this underrepresented state? There are likely multiple reasons that created a snowballing effect.

In some sense, all scientific fields follow cycles of boom and bust. The advent of new technologies leads to ‘booms’ in research as new investigations are possible. These cycles of boom and bust are fed by young graduate students and postdocs and their pursuit of making ‘the next step’. Those graduate students and postdocs go on to become professors and pass on their training to the next generation. But what happens when the professors are no longer there to pass on their expertise and training? What happens when NIH and other funding agencies devalue your whole field of research?

For neuroanatomy, this is essentially what happened in the 1990’s. At this point, the best anterograde tracer, PHAL, had been injected almost everywhere in the brain. At the same time, MRI and the human imaging field were taking off. Then, major advances and powerful techniques in genetics started happening which have continued on to today. Particularly, these fields became good choices for graduate students as these skills could more easily transition into industry jobs. Neuroanatomy attracted less and less young students.

Funding agencies notice these trends. They pay attention to what’s hot and exciting and they pay for those kinds of studies. As a result, neuroanatomy research funding became very difficult to come by. With fewer and fewer graduate students entering the field and less money available, many neuroanatomist PI’s had to transition by learning complementary functional techniques. Even today, there are very few labs that get by on studying neuroanatomy alone.

The result is that today the field of neuroscience is dominated by physiologists and behavioral neuroscientists who study brain function and a minority of people who study brain structure (neuroanatomy isn’t even an option for expertise on the SFN website). I’ve had more than a few of them tell me that brain function is somehow greater than or more important than brain structure and if we understand function we don’t need anatomy. Neither one is more important, they are two sides of the same coin and we need both. I think that the function > structure thinking was partly influenced by early electrophysiologists and behavioral neuroscientists who were limited by their technology and couldn’t really incorporate neuroanatomy with their techniques. Essentially, if a field of study has no impact on your own work, why should it matter to you? Ironically, perhaps the savior of neuroanatomy was the development of optogenetics in the mid 2000’s. Optogenetics, unlike electrophysiology, is capable of studying the function of neurons in anatomically-specific ways. The advances in genetic fields started to impact other areas of neuroscience and the ability to manipulate viruses as vectors for tracing anatomically-specific circuits opened up a whole new world. In addition, new fields like network neuroscience developed which rely heavily on accurate wiring diagram data. Suddenly, neuroanatomy became very important again. The NIH and NSF launched the BRAIN Initiative and the idea of identifying cell types and circuit diagrams has come back to equal footing, but the field of neuroanatomy had already been depleted and the events of the 1990’s have created a generation gap. Many of the neuroanatomists who were around during the boom of the 1980’s are approaching retirement and we must make sure their knowledge and training are not lost!

This generation gap in the field of neuroanatomy has me very concerned for the outcome of the BRAIN Initiative. First, I don’t think that current graduate students are getting the systems neuroanatomy training that they need to understand the circuit diagrams that will be generated by the BRAIN Initiative. As a graduate student in the late 2000’s, I certainly don’t remember learning about anatomical tracer data in graduate courses. Second, the devaluation of neuroanatomy has led to a very low standard of evidence in journals. This has become very obvious to me in reading the reviews of my own papers that many neuroscientists don’t know how to interpret anatomical tracer data (and it’s not like they learned in grad school).

I believe that these low neuroanatomy publishing standards are a major contributor to the reproducibility crisis (this might have to be a whole different blog post). There are a lot of papers being published showing optogenetic effects on behaviors for pathways that don’t physically exist and could easily be confirmed in less than 5 minutes by looking for that data via several online databases (http://www.mouseconnectome.org/ or http://connectivity.brain-map.org/). Essentially, it’s become more important in neuroscience to manipulate function or get a behavioral effect that is p <0.05 than to understand where in the brain that effect is happening.

Ultimately, the system will correct itself, but the lack of neuroscientists with neuroanatomy expertise means it will be slow and likely will depend on the next generation of scientists (looking at you grad students). There are a lot of opportunities for those willing to learn. Hopefully, keep reading this blog and I will share all I know!

-M

 

 

 

Hitchhiker’s Guide to Neuroanatomy: Cytoarchitecture

The Brain is complicated. Really Complicated. You just won’t believe how vastly hugely, mind-bogglingly complicated it is. I mean, you may think the universe is complex, but that’s just peanuts to the Brain…

Don’t Panic!

Cytoarchitectonics

Cytoarchitectonics (cyto = cell; cytoarchitecture = cell architecture) is the study of the size, shape, orientation, and staining intensity of cells within brain tissue. It’s one of the oldest ways to understand the brain and identify brain regions so it’s pretty fundamental to almost all neuroscience. Before cytoarchitectonics, scientists looked at the brain and saw two flavors: gray and white matter. That’s it! Once people figured out how to slice and stain brain sections (histology) it opened a whole new world. And like the explorers who sailed to the New World, they put their names on everything! Meynert, Brodmann, Wernicke, von Economo, Nissl, Forel are just a few of the early anatomists who got their names immortalized for discovering new brain areas by looking at cytoarchitecture.

So what does the size, shape, orientation and staining intensity of cells tell us about the brain. Well, first off, it tells us that neurons and other cells can look very different from one another. We now know that these differences in the way they look seems to relate to differences in how they work. The question why neurons are different is a bit tricky to answer, but I’ve always believed that neurons are shaped by what is around them. Outside of neurons lies a rich plexus of fibers, blood vessels, and other cells. In this way, neurons are probably shaped by their local environment rather than anything inherent to the neuron itself. In addition, the size of the cell body may be related to the overall cell size (big cell bodies needed to support long axons and processes).

The best way to stain cells within brain tissue is using a Nissl stain like Crestyl Violet (NeuN immunohistochemisty is also useful but does not stain the glia (neurons only)). Crestyl Violet stains the ‘Nissl substance’ (RNA) blue. Rough endoplasmic reticulum is stained particularly dark because of dense ribosomal RNA (see below).

Image result for nissl stain

Crestly Violet staining of the ventral horn of the spinal cord. Credit FD Neurotechnologies.

Within the last 20 years, fluorescent Nissl-like stains have become the most common cytoarchitecture stain in neuroscience (Neurotrace, DAPI, Hoechst, etc.). These stains are really easy to use (only 2 hours in solution) and come in a variety of fluorescent colors (blue fluorescence is most common because blue is usually the weakest fluorescent signal to image and these stains are bright). You almost always see this stain as the background in fluorescent images, because it helps validate where you are in the brain.

HitchhikerGuideNissl-01

(left) Coronal section with Neurotrace Blue (435/455) staining in the mouse primary somatosensory cortex (SSp). (right) Delineation of the cortical layers in SSp (1-6) based on cytoarchetectural differences of the cells. Note the size and shape of the layers changes as well! The large bumps in layer 4 are the famous ‘barrels’ that define the SSp barrel field (SSp-bfd, SSp trunk region (SSp-tr) adjacent). Each ‘barrel’ corresponds to input from a specific whisker on the mouse’s face.

As you can see from the example above, we can use cytoarchitecture staining to visualize neurons (blue), their organization as layers, and determine which area of the body homunculus we are looking at in the primary somatosensory cortex (SSp). If you look closely, you can see major differences in the size, shape and orientation of the cells in each layer. Layer 1 has few cells, layer 2/3 has medium size, pyramidal-shaped cells, layer 4 has small, densely packed granular cells, layer 5 has big pyramidal cells, and layer 6 has cells that are more horizontally-shaped. The fact that cells have different shapes, sizes, and orientation have led to a lot of descriptive names and classifications. Some examples from across the brain:

Size:

Magnocellular: Magno = Big

Parvocellular: Parvo = small

Koniocellular: Konio = tiny

Shape:

Granule: small and round like grains of sand (granule layer =layer 4 in cortex)

Fusiform:  tapered at two ends like a spindle

Pyramidal: triangular shape like a pyramid

Oval: oval-shaped

Orientation:

Horizontal: cell body is oriented horizontal to a clear axis or landmark

Transverse: diagonally oriented

In addition, there are many cells that have a clearly distinct size and shape that get special names like Purkinje cells or get their name from the morphology of their dendrites or axons (basket cells, chandelier cells, tufted cells etc.).

Following this logic, different brain regions or nuclei are distinguished and defined by the different cells within them! For example, the paraventricular nucleus of the hypothalamus (PVH) is composed of different parvicellular and magnocellular subnuclei, which in turn, contain parvocellular and magnocellular neurons (note parvicellular brain regions contain parvocellular neurons). Parvocellular and magnocellular PVH neurons are also functionally-distinct as magnocellular neurons release posterior pituitary hormones (vasopressin and oxytocin) whereas parvocellular neurons release anterior pituitary hormones. An extreme example of this is the bed nuclei of stria terminalis (BST) which are a collection of more than a dozen small, but distinct subnuclei including oval, fusiform, transverse, and magnocellular subnuclei (see below).

BSTKluver

Kluver-Berrera-stained coronal section of the rat Bed Nuclei of Stria Terminalis (BST). Kluver-Berrera staining produces a blue color in myelinated axons whereas cell bodies are stained magenta. The BST is a collection of many small subnuclei each with distinct cytoarchitectural features. From Bienkowski, Wendel, and Rinaman, 2013.

In the case of the cortex, the entire cortex is one giant sheet of cells that are organized as several layers. Classically, most people would say isocortex (or neocortex) contains 6 layers, whereas allocortex contains 3 layers. Really, that’s not quite true, as many of the layers break down into sublayers (5a, 5b, 5c, etc.), but generally the number of layers and their relative thickness changes across the cortex and that allows us to define different cortical regions. Notably, visual cortex has a thick layer 4 and motor cortex doesn’t have a layer 4 (agranular; also motor cortex has really big layer 5 pyramidal neurons).

Overall, cytoarchitecture is not just about cells, it’s about tissue! Brain tissue is more than just a random smattering of cells, there is organization inherent to it and taking the cells out of the brain (in vitro experiments, cell cultures, etc.) means you lose something about how it all works. Even dead tissue can tell you a lot about how the brain works if you know how to look at it!

-M

Under the Microscope #1

SW140611-03Afibers

For the first Under the Microscope, we have the Pillars of the Mind banner image! In this case, we injected 3 anterograde tracers into different parts of the same brain region. The image shows the 3 topographic sets of fluorescently-colored axon fibers:

  1. Can you name the fiber pathway that’s labeled here?
  2. Can you guess where the injection sites are located?

 

I’ll update this post with the answers around 12:30pm PST!

 

-M

 

 

 

Under the Microscope Answer:

 

UndertheMicroscope1-01

Ok, here’s the original fluorescent image alongside the corresponding part of the mouse Allen Reference Atlas above (atlas on right side, Nissl stain on the left).

From the labeled image, we can see that there are two sets of fibers: 1) red, green, and magenta fibers traveling horizontally across the midline of the brain (ventral hippocampal commissure) after arriving via the fimbria (fi) and 2) vertically-oriented magenta fibers (dorsal fornix). In comparison to the atlas, we can see that the ventral hippocampal commissure fibers pass through the septofimbrial nucleus (SF) and triangular nucleus of the septum (TRS) and a close inspection of the fibers would reveal an absence of boutons on the fibers. This part of the brain has been difficult to study in the past because of the small size of the area coupled with confounding axon fibers of passage.

 

From this information, you might guess that the injection sites are located somewhere in the temporal lobe, particularly either hippocampus (CA3), entorhinal cortex, or the subicular complex, as these regions project to both sides of the brain and their fibers travel through dorsal or ventral hippocampal commissures. In this case, the injection sites for all 3 tracers are located in entorhinal cortex.

 

-M

Breaking the Ice

When I was a graduate student in the late 2000’s, I had many smart people tell me that neuroanatomy was a dead field of science. Many professors told me “we know enough neuroanatomy” so I should move on to study function.

Of course, I didn’t listen. I studied and trained in classic neuroanatomy anyway, because as corny as it sounds, I loved it. There was just something about it that always clicked with me and its led me to explore all over the brain. I started studying viscerosensory brainstem circuits to the hypothalamus. From the hypothalamus, I began studying the amygdala, bed nuclei of stria terminalis, and the other basal ganglia-like structures. Now, I’ve spent the last 5 years as a postdoc with a front row seat to one of the biggest databases of mouse connectivity data in the world. Through all of this, I’ve gained a pretty broad and somewhat unique view of the brain as a whole system and I want to share what I’ve learned with as many people as possible, because neuroanatomy is far from dead.

I think a big problem in neuroscience is that not a lot of graduate students are getting strong training in systems neuroanatomy these days (I’ll go into this in a later blog post) and too many students have listened to the ‘neuroanatomy is a dead field’ professors. It’s a shame because I believe neuroanatomy can be incredibly useful to many fields of neuroscience and help make your research better! Structure and function are two sides to the same coin and differences in connectivity allow you to form functional hypotheses that can be tested with new tools like optogenetics. As our toolbox gets more and more specific, the newest discoveries will come from those who understand the details!

Ok, so what do I want this blog to be. I want this blog to be a place where I can help explain neuroanatomy like we are just hanging out at the bar (where real learning takes place). I want to try to tear away the esoteric jargon and terminology that I think holds most people back from understanding neuroanatomy. I’ve got some ideas in place for several series of blog posts that I hope you’ll like:

Art and History of Neuroscience

Neuroanatomy is historically the oldest field of neuroscience and you could even date it back to the ancient Egyptians who actually had a hieroglyph for ‘brain’. As artistic abilities evolved, the depictions of neuroanatomy evolved with it. In this way, understanding neuroanatomy is intimately tied to our ability to visualize the brain.

Theories of Nervous System

How does the brain work as a whole? There are some pretty good theories about how the brain might work at the systems-level. These papers are not the kind of papers you can read in one afternoon. I’ll throw in some of my thoughts as well.

The Hitchhiker’s Guide

Inject something in the brain and see where it goes, right? It’s a little more complicated than that. I’ll do my best to explain all the nuances that separate good neuroanatomy data from bad neuroanatomy data.

Better Know a Brain Region

Like the Colbert Report, but with brain regions. An in-depth look at a specific brain region and how it relates to other parts of the brain along with a discussion of how they work together as a systems-level network.

Under the Microscope

I’ll show a microscope image. You guess the brain region and the labeling. Fun, right?

Of course, if you have any ideas you want me to talk about, let me know!

-M