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.

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.

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.

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.

Written assignment due

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.

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.

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.