This section is an advanced explanation of how the brain processes auditory input with a focus on current cutting edge research in synaptic plasticity and auditory learning. By the end of this section you should be able to:
For an introduction to senses and hearing visit: Grades K-5
For a more in-depth explanation of the brain’s role in hearing visit: Grades 6-12
In the previous sections we discussed that hearing, like all senses, involves not only your sense organs, but also your brain. We also discussed how the brain receives signals from the ear via neurons, and how learning requires synaptic plasticity – changes in how neurons connect to one another. Let’s dive deeper into the complexities of auditory learning.
Learning, in the context of behavioral neuroscience, can be defined as the acquisition and maintenance of memories concerning a specific event, task, or sensory experience. The physical manifestation of memory consists of groups of neurons throughout different brain regions that are connected to one another. Synaptic plasticity is required to form new connections and to strengthen, weaken existing connections.
When a neuron experiences a plasticity-inducing event (learning), this immediately induces the transcription of plasticity-related activity-induced Immediate-Early Genes (IEGs). IEGs do not require de novo protein synthesis in order to begin transcription from DNA to mRNA. These genes encode proteins essential to synaptic plasticity. One plasticity-related IEG is of particular interest: Arc/Arg3.1 (Activity-related cytoskeleton-associated protein). Arc is required for the consolidation of Long-Term Potentiation (LTP); in other words, it is necessary to preserve short-term memory as long-term memory for hippocampal-dependent learning. The temporal dynamics of Arc transcription following a plasticity-inducing event are well studied. Arc mRNA is only transcribed for a very brief time after induction, about 5 minutes, so it is very useful for a technique called catFISH (cellular compartment analysis of temporal activity using fluorescence in situ hybridization). By looking for the presence of Arc mRNA within the nucleus of individual neurons, populations of neurons (neuronal ensembles) that experienced activity at the same time can be identified. Activity in these neuronal ensembles can be temporally correlated with behavioral manipulations to study the effect of behavior or the administration of drugs and other compounds that may alter normal physiological function.
One of the ways researchers investigate biological processes is to interfere with normal function of a system and observe the resulting outcome. There are several important ways to interfere with synaptic plasticity in the brain that are helpful in understanding the processes behind normal function; studying the effects that this has on learning reveals the underlying roles performed by different processes.
One way to alter plasticity is to interfere with gene expression, the transcription of DNA to mRNA and the translation of mRNA to protein. Oligodeoxynucleotides (ODNs) are short sequences of synthetic DNA which can be inserted into cells to alter the normal function of DNA and RNA. For activity-induced IEGs such as Arc, transfecting neurons with anti-sense ODNs prevents translation of Arc mRNA to protein. In transfected neurons, new learning is not consolidated from short-term memory to long-term memory. The ODNs prevent translation by binding the target mRNA; the ODNs can be precisely infused into brain regions of interest, such as primary auditory cortex.
When a synapse experiences plasticity it undergoes structural changes. Post-synaptic neurotransmitter receptors are moved to and from the cell surface, this requires the alteration of the cytoskeleton, the molecular structures that determine the size and shape of a synapse and also serve a role in the transportation of molecules and structures within the cell. The cytoskeleton is primarily composed of microfilaments and microtubules. The protein actin polymerizes into filaments (F-actin); interfering with actin polymerization and depolymerization can interfere with synaptic plasticity. The sea sponge toxins latrunculin and jasplakinolide both interact with actin. Latrunculin prevents actin polymerization and enhances depolymerization while jasplakinolide binds to actin, enhancing polymerization. Infusing neurons with either of these toxins can result in altered learning.
Another way to interfere with synaptic function is by altering the function of neurotransmitter receptors. Receptor agonists, antagonists, and other modulators can have many varied effects on cellular function. The use of cell-type specific receptor antagonists in localized infusions is very useful for blocking communication between neurons in a specific brain region.
Research into the mechanisms of synaptic plasticity in auditory learning is ongoing. There is still much to be learned from the research already conducted as part of this project. This page will be updated as more published research is available.
