2-Minute Neuroscience: Multiple Sclerosis

In this video, I discuss multiple sclerosis. Multiple sclerosis is a central nervous system disorder that can create a variety of symptoms ranging from visual disturbances to paralysis. It is characterized by damage to myelin, the insulatory material that surrounds neurons. This damage is linked to disruptions in healthy neuronal function, which are thought to lead to the symptoms of the disease. It is widely believed that the myelin damage that occurs in multiple sclerosis is due, at least in part, to the cells of the immune system targeting myelin. Thus, most of the treatments for multiple sclerosis involve drugs that suppress the immune response in some way.

2-Minute Neuroscience: Alzheimer's Disease

a coronal slice of a brain that has atrophied severely due to the effects of alzheimer's disease.

a coronal slice of a brain that has atrophied severely due to the effects of alzheimer's disease.

In this video, I discuss Alzheimer's disease---the most common form of neurodegenerative disease. In addition to the widespread neurodegeneration that occurs in Alzheimer's disease, there are specific neurobiological abnormalities that appear in the brains of Alzheimer's disease patients. For example, clusters of a misfolded form of a protein called amyloid beta develop around neurons; the clusters are called amyloid plaques. Additionally, clusters of misfolded tau protein develop inside neurons; these clusters are called neurofibrillary tangles. The most common treatments for Alzheimer's disease are acetycholinesterase inhibitors, which are drugs that inhibit the breakdown of the neurotransmitter acetylcholine. Acetylcholine is thought to be important to healthy cognition, but acetylcholinesterase inhibitors have relatively modest effects on the symptoms of Alzheimer's disease.

2-Minute Neuroscience: Parkinson's Disease

substantia-nigrae.jpg

In this video, I discuss Parkinson's disease---the second most common neurodegenerative disease behind Alzheimer's disease. Parkinson's disease is associated with the degeneration and death of dopamine neurons in the substantia nigra. The substantia nigra is a region of the brain that is part of a collection of structures known as the basal ganglia, which are important to movement. Parkinson's disease patients experience severe movement difficulties that become more problematic as the degeneration of substantia nigra neurons becomes more extensive. The most common treatment for Parkinson's disease involves the administration of L-DOPA, a precursor to dopamine that allows the brain to synthesize more of the neurotransmitter to replenish depleted dopamine levels.

The amygdala: Beyond fear

THE AMYGDALA SHOWN ALONG WITH OTHER LIMBIC SYSTEM STRUCTURES.

THE AMYGDALA SHOWN ALONG WITH OTHER LIMBIC SYSTEM STRUCTURES.

The amygdala---or, more appropriately, amygdalae, as there is one in each cerebral hemisphere---was not recognized as a distinct brain region until the 1800s, and it wasn't until the middle of the twentieth century that it began to be considered an especially significant area in mediating emotional responses. Specifics about the role of the amygdala in emotion remained somewhat unclear, however, until the 1970s and 1980s when it was studied in fear conditioning experiments in rodents. A typical fear conditioning experiment in rodents involves pairing an aversive stimulus (e.g. an electrical shock to the feet) with a previously neutral stimulus like an audible tone until the rodent begins to display signs of fear at simply hearing the tone. Using this experimental approach, researchers were able to demonstrate that functioning amygdalae are very important for rodents to learn the fear responses typically seen as a result of fear conditioning.

From this time on, research began to accumulate that identified the amygdala as having an integral role in fear in general. And thus was born the conception of the amygdala as a "threat-detector." According to this view, the amygdala helps us to identify threats in our environment and---if threats are present---to initiate a fight-or-flight response. This basic understanding of the function of the amygdala is repeated in many textbooks and classrooms---and has even found its way into popular culture. The problem is, however, that this is an oversimplified view of the amygdala. Yes, the amygdala seems to play a significant role in fear. But it is also likely involved in a slew of other behaviors and emotional responses.

An intricate structure with manifold connections

The name amygdala comes from the Greek word for almond, and the amygdala earned this designation because it is partially composed of an almond-shaped structure found deep within the temporal lobes. The almond-shaped structure, however, is just one nucleus of the amygdala (the basal nucleus)---for although it is often referred to as one entity, the amygdala is actually made up of a collection of nuclei along with some other distinct cell groups. The nuclei of the amygdala include the basal nucleus, accessory basal nucleus, central nucleus, lateral nucleus, medial nucleus, and cortical nucleus. Each of these nuclei can also be partitioned into a collection of subnuclei (e.g. the lateral nucleus can be divided into the dorsal lateral, ventrolateral, and medial lateral nuclei). 

Exactly how the amygdala should be divided anatomically has been the subject of some debate, and no clear consensus has been reached. Many researchers group the lateral, basal, and accessory basal nuclei together into a structure referred to as the basolateral complex, and sometimes the cortical and medial nuclei are aggregated as the cortico-medial region. However, there is even a lack of consistency in the application of these terms. For example, some investigators use the basolateral designation to refer to the complex mentioned above, while others use it to refer to just the basal nucleus or basolateral nucleus specifically. Thus, the anatomy of the amygdala is much more complex than is often implied in simple descriptions of the structure. Indeed, the complexity is significant enough that neuroanatomists still have a hard time agreeing on how the different components of the amygdala should be categorized.

In addition to its anatomical diversity, the amygdala has abundant connections throughout the brain---connections that are widespread and divergent enough to suggest many functions beyond just threat detection. For example, many areas of the prefrontal cortex as well as sensory areas throughout the brain have bidirectional connections with the amygdala. The amygdala also has projections that extend to the hippocampi, basal ganglia, basal forebrain, hypothalamus, and a variety of other structures.

Evidence for diversity of function

It is true there is ample evidence that suggests the amygdala is important in the processing of fearful emotions and the identification of threatening stimuli. However, there is also a significant amount of evidence pointing to functions for the amygdala beyond simple threat detection. For example, studies have found the amygdala to be active not just during fear conditioning, but also when learning to link a previously neutral stimulus with a positive experience. Indeed, these studies suggest the amygdala may be involved in learning to assign a positive or negative value to a neutral stimulus, suggesting it has a role in assigning value in general and in the formation of positive and negative memories.

Due to its role in assigning value to stimuli and then creating memories about such valuations, it may not be surprising that some have implicated the amygdala in addictive behaviors. The amygdala has been shown to interact with reward areas of the brain like the ventral striatum, and it seems to play an important role in forming memories associated with drug use. Studies have found, for example, that disrupting amygdala function can inhibit the ability of rodents to learn positive associations with drugs like cocaine. Thus, disrupting activity in the amygdala can also disrupt the acquisition of drug-taking behavior in rodents.

Therefore, instead of being involved only with aversive memories and the learning of conditioned responses to fearful stimuli, the amygdala has come to be considered an important region for the consolidation of memories that have any strong emotional component---whether positive or negative. And this is still really only scratching the surface of the function of this complicated structure. Some studies have suggested, for example, that the amygdala plays a key role in social interaction, others have linked it to aggressive tendencies, and still others have indicated that amygdala connectivity may help to predict sexual orientation.

It may be involved with all of these things. Because the amygdala is a complex structure made up of multiple nuclei, it is unlikely it would serve only one function like "fear detection." Indeed, it is probably unlikely it would even be involved with only one large category of function like emotions. Simplifying the functions of a structure like the amygdala does help to make the brain easier to understand on a superficial level, but it's important to keep in mind that when we do so we are avoiding a more complicated reality in order to make the details of the organ more comprehensible. Although this can be a useful tactic, if we forget we are using it we can hinder the attainment of a more complete understanding of a structure by focusing too much on the simplified model.

LeDoux, Joseph (2007). The Amygdala Current Biology

2-Minute Neuroscience: Glutamate

In this video, I discuss glutamate---the primary excitatory neurotransmitter of the human nervous system. Glutamate is an amino acid neurotransmitter that interacts with both ionotropic and metabotropic receptors. There are 3 identified ionotropic glutamate receptors: NMDA, AMPA, and kainate receptors, and 3 identified metabotropic glutamate receptors. Glutamate is removed from the synaptic cleft by excitatory amino acid transporters, or EAATs. Glutamate transported into glial cells is converted to glutamine before being sent back to the neuron to be converted back to glutamate, a process referred to as the glutamate-glutamine cycle.

Know your brain: Primary somatosensory cortex

Where is the primary somatosensory cortex?

primary somatosensory cortex (in blue)

primary somatosensory cortex (in blue)

The primary somatosensory cortex is located in a ridge of cortex called the postcentral gyrus, which is found in the parietal lobe. It is situated just posterior to the central sulcus, a prominent fissure that runs down the side of the cerebral cortex. The primary somatosensory cortex consists of Brodmann's areas 3a, 3b, 1, and 2.

What is the primary somatosensory cortex and what does it do?

The primary somatosensory cortex is responsible for processing somatic sensations. These sensations arise from receptors positioned throughout the body that are responsible for detecting touch, proprioception (i.e. the position of the body in space), nociception (i.e. pain), and temperature. When such receptors detect one of these sensations, the information is sent to the thalamus and then to the primary somatosensory cortex.

The primary somatosensory cortex is divided into multiple areas based on the delineations of the German neuroscientist Korbinian Brodmann. Brodmann identified 52 distinct regions of the brain according to differences in cellular composition; these divisions are still widely used today and the regions they form are referred to as Brodmann's areas. Brodmann divided the primary somatosensory cortex into areas 3 (which is subdivided into 3a and 3b), 1, and 2.

The numbers Brodmann assigned to the somatosensory cortex are based on the order in which he examined the postcentral gyrus and thus are not indicative of any ranking of importance. Indeed, area 3 is generally considered the primary area of the somatosensory cortex. Area 3 receives the majority of somatosensory input directly from the thalamus, and the initial processing of this information occurs here. Area 3b specifically is concerned with basic processing of touch sensations, while area 3a responds to information from proprioceptors.

Area 3b is densely connected to areas 1 and 2. Thus, while area 3b acts as a primary area for touch information, that information is then also sent to areas 1 and 2 for more complex processing. Area 1, for example, seems to be important to sensing the texture of an object while area 2 appears to play a role in perceiving size and shape. Area 2 also is involved with proprioception. Specific lesions to any of these areas of the somatosensory cortex support the roles mentioned above; lesions to area 3b, for example, result in widespread deficits in tactile sensations while lesions to area 1 result in deficits in discriminating the texture of objects.

somatotopic arrangement of the somatosensory cortex

somatotopic arrangement of the somatosensory cortex

Each of the four areas of the primary somatosensory cortex are arranged such that a particular location in that area receives information from a particular part of the body. This arrangement is referred to as somatotopic, and the full body is represented in this way in each of the four divisions of the somatosensory cortex. Because some areas of the body (e.g. lips, hands) are more sensitive than others, they require more circuitry and cortex to be devoted to processing sensations from them. Thus, the somatotopic maps found in the somatosensory cortex are distorted such that the highly sensitive areas of the body take up a disproportionate amount of space in them (see image to the right).

Purves D, Augustine GJ, Fitzpatrick D, Hall WC, Lamantia AS, McNamara JO, White LE. Neuroscience. 4th ed. Sunderland, MA. Sinauer Associates; 2008.

2-Minute Neuroscience: GABA

In this video I discuss the neurotransmitter gamma-aminobutyric acid, or GABA. GABA is the primary inhibitory neurotransmitter in the human nervous system; its effects generally involve making neurons less likely to fire action potentials or release neurotransmitters. GABA acts at both ionotropic (GABAa) and metabotropic (GABAb) receptors, and its action is terminated by a transport protein called the GABA transporter. Several drugs like alcohol and benzodiazepines cause increased GABA activity, which is associated with sedative effects.