Why We Need a Hippocampus: Anterograde Amnesia
Two kinds of amnesia discussed in the video lectures are are retrograde and anterograde amnesia. You have retrograde amnesia if you cannot recall events that happened before a trauma. You have anterograde amnesia if you can remember the past, but you no longer are able to form new permanent memories. It's also possible to have both kinds at once.
The weirdly shaped structure in the picture above is the hippocampus. The hippocampus is responsible for our ability to form long-term memories. This ability is called consolidation, which is the process of converting short-term memories into long-term ones. If we lost our hippocampus, we would have anterograde amnesia.
Anterograde amnesia can occur with disease or surgery, such as Korsakoff's syndrome or temporal-lobe damage or surgery. The patient is left with short-term memory (sometimes called working memory) and often intact long-term memory (LTM), but no way to consolidate new short-term memories into long-term memories. People with anterograde amnesia can recall old memories prior to the disease or surgery. They also can hold an event or information in short-term memory for a couple of minutes, until they’re distracted or stop thinking about it. However, they can't recall anything that happened after the disease or surgery -- they have lost the ability to form new declarative (explicit) memories but not non-declarative (implicit) memories. They can't remember what they ate for breakfast yesterday, but they may be able to implicitly learn a new motor task like mirror tracing, although they won’t remember actually doing so.
To explain anterograde amnesia and loss of consolidation, Dr. Suzuki in the video lecture discusses one of the most-studied patients in history, H.M. He had his temporal-lobe tissue removed to limit the spread of his epileptic seizures. (Click on “download audio” or “show transcript”.) Hippocampal damage in H.M. prevented the transfer of short-term memories to long-term storage (consolidation), even though STM and LTM remained largely intact. (Surgeons no longer remove both temporal lobes.) H.M. has since died in 2008, and neuroscientists are studying his dissected brain.
Another famous anterograde amnesiac, Clive Wearing, has both anterograde and a large degree of retrograde amnesia, due to loss of his hippocampus and parts of his temporal and frontal lobes, from an attack of encephalitis. You can see him in this fascinating video here and read more about him in The New Yorker.
Amnesia in the movies is rarely like real amnesia, except for the really good movie Memento from 2000. However, the movie 50 First Dates was pure fiction, but a case very similar to it was recently published.
Consolidation at the Synapse: Neuroplasticity
How does consolidation happen at the level of a neuron? The answer seems to lie in Long-Term Potentiation, or LTP, which was discovered in the hippocampus.
Most neural firings (action potentials) and the pathways that connect them don’t leave permanent traces. This is okay, because most of the information we encounter in a given day isn’t worth remembering. But there has to be a way for important events to leave a trace so that it can be remembered (reactivated) later on.
When an important event occurs, changes happen at the level of the synapse that strengthen the connection between two neurons. What does it mean to have a strong connection? Basically, it means that the presynaptic neuron is capable of producing a stronger EPSP in the postsynaptic neuron. (Remember that any neuron can be presynaptic at the axon terminals, and postsynaptic at the dendrites; the terms presynaptic and postsynaptic refer to the relationship between two neurons at a synapse.) This way, the neurons become more sensitive to the same input. When a rapid series of action potentials is fired into the hippocampus from another brain area, neurons within the hippocampus increase their own activity. For a long time afterwards—hours, days, weeks—those neurons will continue to fire with high sensitivity to normal input activity from other brain structures. They remember the high-frequency input that they reacted to in the first place.
The strengthening of synaptic connections through LTP in the hippocampus involves the AMPA and NMDA receptors for glutamate. Glutamate is the main excitatory neurotransmitter that typically produces EPSPs in postsynaptic neurons. The AMPA and NMDA receptors are ionotropic receptors (that directly open ion channels) for glutamate. How the AMPA and NMDA receptors are involved in LTP is explained here. When something important happens, the high-frequency stimulation of the hippocampus first depolarizes the dendrite membrane by releasing glutamate, which activates the AMPA receptors, which then allow the NMDA receptors to open channels for sodium and calcium to enter the cell, resulting in further depolarization and the creation of yet more AMPA receptors in the dendrite membrane. The additional AMPA receptors result from the calcium ions that enter the neuron through the NMDA receptor. Calcium activates enzymes called kinases, which insert AMPA receptors into the postsynaptic membrane – making the neuron more sensitive to glutamate than before. Confused? Take a look at the process in this tutorial (click on "step-through" or "narrated").
You can also hear Nobel-prize winner Eric Kandel talk about all of this in even more detail at this site: http://media.hhmi.org/hl/08Lect4.html (this ran slow on my computer but you might have better luck). The BBC ran a 3-part series of radio programs that includes this research here: http://www.bbc.co.uk/radio4/memory/programmes/making_memory1.shtml (Click on “programme two” and “programme three” in orange for the rest.)
1. How would you distinguish amnesia from normal forgetting? When would you call an absent-minded person amnesic?
2. Different types of conditioning – a form of learning – are described in the NOBA “Conditioning and Learning” and in the Lecture 18 video lecture. See if you can describe an everyday example of conditioning. What kind of conditioning is it? What brain areas are involved?
2. The field of language research has grown from the idea of localizing one single brain area to one function, to determining the interdependence and connections between brain areas. We are still trying to understand the complex function and relationships between different brain areas used for language. Understanding and speaking language is extremely complex.
Other animals communicate, but many researchers believe that only humans have the capacity for true language. If you have an hour, you can listen to Jeff Elman talk about the uniqueness of human language, and how we learn and produce it: YouTube - Grey Matters: Understanding Language. He talks about Broca’s area (with an example of a Broca’s aphasia patient) starting at 22 minutes and the KE family at 40 minutes.
You can read an overview of language and the brain at the Neuroscience for Kids website. For explanation and example of Broca’s aphasia, you can watch this video: YouTube - Broca's aphasia.
Here are the questions (answer both):
1. The definition of specific aphasias have been refined over the years. What is it about this Woman: http://www.youtube.com/watch?v=gocIUW3E-go&feature=related or Man: http://www.youtube.com/watch?v=f2IiMEbMnPM&feature=related that leads to a diagnosis of Broca’s aphasia? What is it about this Gentleman: http://www.youtube.com/watch?v=aVhYN7NTIKU or this Lady: http://www.youtube.com/watch?v=dKTdMV6cOZw&feature=related that leads to a diagnosis of Wernicke's aphasia?
2. Pretend you are a neuropsychologist, and that you have been asked to determine the abilities and deficits of people with aphasia. What tasks would you include in your examination to test for the presence of particular language deficits?
|Due By (Pacific Time)
||09/24/2015 12:00 am