|WEEK #||TOPICS||LECTURE SUMMARIES|
The students and instructors will introduces themselves and review the course syllabus and objectives. An introduction will be given about neurons, synapses, selected brain regions, experiments linking learning and memory to brain regions, and linking learning and memory to neuronal activity and synapses. These concepts will be discussed in greater detail during the course.
|2||Fundamentals of learning and memory: pre- and post-synaptic mechanisms|| |
It is widely believed that long-term changes in the strength of synaptic connections underlie learning and memory. These changes can strengthen or weaken pre-existing synapses, or they can involve formation of new synapses or elimination of old ones. In class today, we will discuss two ways in which pre-existing synaptic connections can be strengthened or weakened, exemplifying two different locales at which alterations in the strength of synapses can be expressed.
|3||Mechanisms of learning: activity-regulated genes|| |
Neuronal activity driven by sensory stimulation induces the expression of activity-regulated genes in active brain areas. Many of these genes have been shown to encode proteins that enact changes in the strength of synaptic connections, which are believed to underlie learning and memory. Thus, the identification and functional characterization of activity-regulated genes has been an invaluable approach to shedding light on synaptic plasticity mechanisms.
|4||Forms of Learning and Memory I: Procedural and Episodic|| |
Starting this week, we will learn about different forms of learning and memory and their biological bases. We begin by discussing two contrasting types of memory: memories that we recall consciously, such as specific events and places (episodic), and memories that are recalled 'sub-consciously,' such as knowing how to ride a bicycle (procedural).
|5||Forms of Learning and Memory II: Non-Associative vs. Associative|| |
In our everyday lives, sometimes we enhance our behavioral response to repeated stimulation. This is called sensitization, and it requires repeated exposure to the stimulus to occur. For instance, we get annoyed if someone interrupts us again and again on a busy day. Our reaction could become worse for any additional interruption, even though we do not dislike the person who interrupted us. Since our aversive response was specific to the stimulus (interruption) and was not associated with another stimulus presented alongside (the person who interrupts), this can be considered as non-associative learning. In contrast, an aversive reaction to that person could continue even when that person is no longer interrupting us. In this case, the two stimuli have been associated with each other (interruption and the person who is interrupting). This can be considered associative learning. The papers this week will discuss the biological bases for these two kinds of learning.
|6||Lab visit — role of activity-regulated genes in experience-dependent plasticity||We will visit the laboratory of Professor Elly Nedivi in the MIT Picower Institute for Learning and Memory. We will have a tour of the lab and discuss one of the lab's projects investigating the role of an activity-regulated gene called cpg15 in experience-dependent synaptic plasticity.|
|7||Forms of Learning and Memory III: Drug Addiction and Perceptual Learning|| |
A common phenomenon in biology is the conservation of the same molecular mechanisms for seemingly unrelated processes. One example involves drug addiction. During drug exposure, many of the molecular and synaptic plasticity mechanisms underlying normal learning and memory are recruited to yield robust and long-lasting changes in the brain, which account for the intense drug-seeking behaviors of the drug user. We will explore how and where these changes occur in today's class. Like many other forms of learning, the changes in the brain that occur after drug exposure become stronger with each use of the drug. Based on the second paper of today's class, we will discuss how repeated exposure to the same stimulus can induce long-lasting synaptic changes during everyday life. This form of learning, called perceptual learning, can occur in response to many ordinary stimuli, from hearing a popular song to tasting a favorite food.
|8||Learning through others' experience and observational learning|| |
Most behavioral adaptations are a consequence of one's own experience. However, we also learn from the experience of others. The first paper discusses the mechanisms of observational learning. New research has indicated that the experience of future parents, even before the conception of their offspring, can modify the behavior of progeny. We will find out how this happens in this week's second paper.
|9||Synapse formation and stabilization||
Learning alters the existing representation or creates novel representations of information in the brain. This happens, in part, by forming new connections (synapses) between neurons. This week, we will look at two papers that report contradictory findings with respect to the time scale for synapse formation. We will discuss why they might have arrived at different conclusions and and also consider potential implications of their findings.
|10||Experience-dependent plasticity: Visual Cortex|| |
Making the right connections is very competitive even for neurons. When more than one neuron vies for the same postsynaptic partner, the neuron with activity that correlates with that of the partner makes lasting synapses. In other words, neurons that fire together wire together. Axonal inputs carrying information from each eye terminate in alternating columns in the visual cortex. As a consequence, the neurons in a column preferentially respond to information from one eye or the other (ocular dominance). Ocular dominance columns are an end result of synaptic competition, wherein correlated firing of inputs (with respect to postsynaptic neuronal activity) from one eye are retained and non-correlated firing of inputs from the other eye are eliminated. There is a time window in development, called the critical period, during which cortical connections are permissive to remodeling driven by activity-dependent synaptic plasticity mechanisms. Closing one eye during the critical period for eye-specific preference in the visual cortex leads to smaller deprived eye columns and larger non-deprived eye columns. However, evidence for non-competitive mechanisms to establish connection strengths have also emerged. This week we will consider two papers that discuss the mechanisms related to competitive and non-competitive plasticity.
|11||Occlusion of synaptic plasticity by learning|| |
One of the best ways to test the hypothesis that synaptic plasticity and learning are part of the same process is to show that they both cause the same change in the brain. If synaptic plasticity underlies learning, then, after learning, synaptic plasticity might not be able to be induced because it would have already been expressed during learning. (It could be, in effect, occluded if the synapses had already been strengthened or weakened to their greatest extent). In this week's breakthrough papers, the authors have shown just that in two different brain regions and after different types of learning.
|12||Creating false memory, erasing specific memory|| |
The ultimate test to whether we are on the right path to understanding how learning and memory are encoded in the brain is by artificially creating or erasing specific memories. This week we will discuss papers that report creation or erasure of a specific memory trace.
|13||Understanding a disease: Fragile X Syndrome|| |
Fragile X Syndrome (FXS) is an X-linked heritable form of intellectual disability resulting from mutation of the fragile X mental retardation gene (FMR1). The fragile X protein (FMRP) is a postsynaptic mRNA-binding protein involved in translational suppression at synapses. The absence of FMRP is thought to result in unregulated synthesis of proteins, with severe consequences for the regulation of synaptic activity. We will discuss the protein synthesis phenotype of a mouse model for FXS and the use of a drug to reverse this phenotype and its downstream effects.
|14||Oral presentations and course discussion||
After the oral presentations, we will end the semester with a discussion of the course.