Genetic Underpinnings of Synaptic Disease

Overview

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This course explores how genetic variation shapes synaptic function, neural circuits, and behavior. Learners will examine how specific gene mutations alter communication between neurons and how these molecular changes scale up to influence cognition, development, and addiction. The course begins by investigating genetic disruptions of synaptic proteins using Fragile X syndrome as a central example. Learners will explore how mutations in key regulatory genes impair synaptic plasticity, alter neural development, and contribute to neurological symptoms, while also examining current challenges and emerging therapeutic strategies for genetic brain disorders. The course then introduces genetic knockout models as powerful tools for identifying gene function, highlighting research on nicotinic acetylcholine receptor subunits and human genetic mutations that serve as natural experiments in understanding disease mechanisms. In the final module, learners integrate these concepts to study complex synaptic modulation within the brain’s reward pathway, using nicotine addiction and smoking as case studies. The course explores how multiple neurotransmitter systems interact within reward circuits to drive motivation and reinforcement, and concludes with an overview of smoking cessation therapies, emphasizing the pharmacokinetic and pharmacodynamic principles that determine their clinical effectiveness. This course is designed for learners with a background in biology who are interested in neuroscience, genetics, pharmacology, or addiction science. It is especially well suited for learners preparing for careers in medicine, biomedical research, psychology, pharmacy, or other health sciences.

Syllabus

Genetic causes of synaptic disease: Fragile X Syndrome

This module explores how genetic alterations affect synaptic function, using Fragile X syndrome as a key example. We will learn about the genetic mutations that cause Fragile X syndrome, how these changes disrupt synaptic activity, and the current challenges and promising advances in treating genetic forms of neurological disease.

Determining function using genetic knockouts

This module examines the use of genetic knockout models in identifying the roles of specific genes, highlighting studies of nicotinic acetylcholine receptor subunits as a case example. The accompanying reading discusses human genetic mutations that act as natural experiments, offering insight into gene function and disease mechanisms.

Complex synaptic modulation

In this module, we will bring together concepts from the course to examine complex synaptic modulation using nicotine addiction and smoking as examples. We will introduce the brain’s reward pathway and the key neural circuits involved in motivation and reinforcement. Within each synapse of this simplified reward circuit, we will explore how different neurotransmitters influence overall circuit activity. The module will also include a brief overview of the history of the cigarette epidemic and conclude with a discussion of common drugs used for smoking cessation, examining their pharmacokinetics and pharmacodynamics as key aspects of their efficacy.