Question

Describe two ways in which biological influences can lead to depression.

Answer 1

1. Genetics: The results from family and twin studies make a strong case for a moderate genetic contribution to the causal patterns depression. Attempts to identify specific genes that may be responsible for these genetic influences have not yet been successful, although there are some promising leads. One very promising candidate for a specific gene that might be implicated is the serotonin-transporter gene—a gene involved in the transmission and reuptake of serotonin, one of the key neurotransmitters involved in depression. There are two different kinds of versions or alleles involved—the short allele (s) and the long allele (l), and people have two short alleles (ss), two long alleles (ll), or one of each (sl). Prior work with animals had suggested that having ss alleles might predispose a person to depression relative to a person having ll alleles, but human work on this issue had provided mixed results.

2. Neurochemical factors:  Ever since the 1960s, the view that depression may arise from disruptions in the delicate balance of neurotransmitter substances that regulate and mediate the activity of the brain’s nerve cells has received a great deal of attention. A large body of evidence suggested that various biological therapies that are often used to treat severe mood disorders—such as electroconvulsive therapy and antidepressant medications—affect the concentrations or the activity of neurotransmitters at the synapse. Such early findings encouraged the development of neurochemical theories of the etiology of major depression. Early attention in the 1960s and 1970s focused primarily on two neurotransmitter substances of the monoamine class—norepinephrine and serotonin—because researchers observed that antidepressant medications seemed to have the effect of increasing these neurotransmitters’ availability at synaptic junctions.  This observation led to the once influential monoamine theory of depression—that depression was at least sometimes due to an absolute or relative depletion of one or both of these neurotransmitters at important receptor sites in the brain. This depletion could come about through impaired synthesis of these neurotransmitters in the presynaptic neuron, through increased degradation of the neurotransmitters once they were released into the synapse, or through altered functioning of postsynaptic receptors. Collectively, these neurotransmitters are now known to be involved in the regulation of behavioral activity, stress, emotional expression, and vegetative functions (involving appetite, sleep, and arousal)—all of which are disturbed in mood disorders.