Stanford’s Robert Sapolsky On Depression

Published on May 25, 2014 (edited for improved sound: noise and stereo issues, and miscellaneous parts taken out) Stanford Professor Robert Sapolsky, posits that depression is the most damaging disease that you can experience. Right now it is the number four cause of disability in the US and it is becoming more common. Sapolsky states […]

Published on May 25, 2014
(edited for improved sound: noise and stereo issues, and miscellaneous parts taken out)

Stanford Professor Robert Sapolsky, posits that depression is the most damaging disease that you can experience. Right now it is the number four cause of disability in the US and it is becoming more common. Sapolsky states that depression is as real of a biological disease as is diabetes.


Neurotransmitters

The neurotransmitter serotonin is involved in regulating many important physiological (body-oriented) functions, including sleep, aggression, eating, sexual behavior, and mood. Serotonin is produced by serotonergic neurons. Current research suggests that a decrease in the production of serotonin by these neurons can cause depression in some people, and more specifically, a mood state that can cause some people to feel suicidal.

In the 1960s, the “catecholamine hypothesis” was a popular explanation for why people developed depression. This hypothesis suggested that a deficiency of the neurotransmitter norepinephrine (also known as noradrenaline) in certain areas of the brain was responsible for creating depressed mood. More recent research suggests that there is indeed a subset of depressed people who have low levels of norepinephrine. For example, autopsy studies show that people who have experienced multiple depressive episodes have fewer norepinephrinergic neurons than people who have no depressive history. However, research results also tell us that not all people experience mood changes in response to decreased norepinephrine levels. Some people who are depressed actually show hyperactivity within the neurons that produce norepinephrine. More current studies suggest that in some people, low levels of serotonin trigger a drop in norepinephrine levels, which then leads to depression.

Another line of research has investigated linkages between stress, depression, and norepinephrine. Norepinephrine helps our bodies to recognize and respond to stressful situations. Researchers suggest that people who are vulnerable to depression may have a norepinephrinergic system that doesn’t handle the effects of stress very efficiently.

The neurotransmitter dopamine is also linked to depression. Dopamine plays an important role in regulating our drive to seek out rewards, as well as our ability to obtain a sense of pleasure. Low dopamine levels may in part explain why depressed people don’t derive the same sense of pleasure out of activities or people that they did before becoming depressed.


subject

A subject is a being who has a unique consciousness and/or unique personal experiences, or an entity that has a relationship with another entity that exists outside of itself (called an “object“). A subject is an observer and an object is a thing observed. This concept is especially important in continental philosophy, where ‘the Subject’ […]

A subject is a being who has a unique consciousness and/or unique personal experiences, or an entity that has a relationship with another entity that exists outside of itself (called an “object“). A subject is an observer and an object is a thing observed. This concept is especially important in continental philosophy, where ‘the Subject’ is a central term in debates over human autonomy and the nature of the self.[citation needed]

The sharp distinction between subject and object corresponds to the distinction, in the philosophy of René Descartes, between thought and extension. Descartes believed that thought (subjectivity) was the essence of the mind, and that extension (the occupation of space) was the essence of matter.[citation needed]

In the modern continental tradition, debates over the nature of the Subject play a role comparable to debates over personhood within the distinct Anglo-American tradition ofanalytical philosophy.


risk perception

Risk as Analysis and Risk as Feelings: Some Thoughts about Affect, Reason, Risk, and Rationality

Paul Slovic,

Melissa L. Finucane,

Ellen Peters,

Donald G. MacGregor

Risk as Analysis and Risk as Feelings: Some Thoughts about Affect, Reason, Risk, and Rationality

  • Paul Slovic,

  • Melissa L. Finucane,

  • Ellen Peters,

  • Donald G. MacGregor


The ventral pallidum

The ventral pallidum is a structure within the basal ganglia of the brain. It is an output nucleus whose fibres project to thalamicnuclei, such as the ventral anterior nucleus, the ventral lateral nucleus, and the medial dorsal nucleus. The ventral pallidum is a component of the limbic loop of the basal ganglia, a pathway involved […]

The ventral pallidum is a structure within the basal ganglia of the brain. It is an output nucleus whose fibres project to thalamicnuclei, such as the ventral anterior nucleus, the ventral lateral nucleus, and the medial dorsal nucleus. The ventral pallidum is a component of the limbic loop of the basal ganglia, a pathway involved in the regulation of motivation, behaviour, and emotions. It is involved in drug addiction.


long-term potentiation

In neuroscience, long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between twoneurons.[2] The opposite of LTP is long-term depression, which produces a long-lasting decrease in synaptic strength. It is one of several phenomena underlying […]

In neuroscience, long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between twoneurons.[2] The opposite of LTP is long-term depression, which produces a long-lasting decrease in synaptic strength.

It is one of several phenomena underlying synaptic plasticity, the ability of chemical synapses to change their strength. As memories are thought to be encoded by modification of synaptic strength,[3] LTP is widely considered one of the major cellular mechanisms that underlies learning and memory.[2][3]

LTP was discovered in the rabbit hippocampus by Terje Lømo in 1966 and has remained a popular subject of research since. Many modern LTP studies seek to better understand its basic biology, while others aim to draw a causal link between LTP and behavioral learning. Still others try to develop methods, pharmacologic or otherwise, of enhancing LTP to improve learning and memory. LTP is also a subject of clinical research, for example, in the areas of Alzheimer’s disease andaddiction medicine.


The hippocampus

The hippocampus (named after its resemblance to the seahorse, from the Greek ἱππόκαμπος, “seahorse” from ἵππος hippos, “horse” and κάμπος kampos, “sea monster”) is a major component of the brains of humans and other vertebrates. Humans and other mammals have two hippocampi, one in each side of the brain. It belongs to the limbic system […]

The hippocampus (named after its resemblance to the seahorse, from the Greek ??????????, “seahorse” from ????? hippos, “horse” and ?????? kampos, “sea monster”) is a major component of the brains of humans and other vertebrates. Humans and other mammals have two hippocampi, one in each side of the brain. It belongs to the limbic system and plays important roles in the consolidation of information from short-term memory to long-term memory and spatial navigation. The hippocampus is located under the cerebral cortex;[1] and in primates it is located in the medial temporal lobe, underneath the cortical surface. It contains two main interlocking parts: the hippocampus proper (also called Ammon’s horn)[2] and the dentate gyrus.

In Alzheimer’s disease, the hippocampus is one of the first regions of the brain to suffer damage; memory loss and disorientation are included among the early symptoms. Damage to the hippocampus can also result from oxygen starvation (hypoxia), encephalitis, ormedial temporal lobe epilepsy. People with extensive, bilateral hippocampal damage may experience anterograde amnesia—the inability to form and retain new memories.

In rodents, the hippocampus has been studied extensively as part of a brain system responsible for spatial memory and navigation. Many neurons in the rat and mouse hippocampus respond as place cells: that is, they fire bursts of action potentials when the animal passes through a specific part of its environment. Hippocampal place cells interact extensively with head direction cells, whose activity acts as an inertial compass, and conjecturally with grid cells in the neighboring entorhinal cortex.

Since different neuronal cell types are neatly organized into layers in the hippocampus, it has frequently been used as a model system for studying neurophysiology. The form of neural plasticity known as long-term potentiation (LTP) was first discovered to occur in the hippocampus and has often been studied in this structure. LTP is widely believed to be one of the main neural mechanisms by which memory is stored in the brain.