Biopsychology — .: 3iCreative :.

Biopsychology of Drug Addiction

05/04/2011 by 3icreative

Specificity of Drug Tolerance

Drug Tolerance is a decreased sensitivity to a drug that develops due to exposure. In short, more and more of a drug is needed to achieve the same response. It can also be shown when the same dose has effect over time. This is sown by a shift to the right in the dose-response curve.

Cross Tolerance – Exposure to one drug can produce tolerance to other drugs that act by the same mechanism
Drug Sensitization – Increases in the sensitivity to a drug. You can become tolerant to some effects of a drug, but not others.
Not a unitary phenomenon – When a drug is administered at active doses, all kinds of changes can occur to reduce its effects.

How Drug Tolerance Happens

Metabolic Tolerance – Changes that reduce the amount of the drug getting to an activation site (increasing the rate it is broken down in the liver)
Functional Tolerance – Results from changes that reduce the reactivity of the sites of action to the drug; tolerance to psychoactive drugs (those that change your thoughts, feelings, perceptions and behaviors) is typically functional, and shown by many experiments to be the result of Pavlovian conditioning. In one experiment (Crowell, Hinson & Siegel, 1981), rats injected with alcohol only demonstrated hypothermic effects (temperature reducing) only when they were given alcohol in the same room as it was previously administered. This, and many other experiments, demonstrates the Situational Specificity of drug tolerance.

Conditioned Compensatory Responses – According to Siegal, conditional stimuli that predict drug administration elicit conditional responses opposite to the unconditional effects of the drug – ie, if someone is in a situation where previous drug use has occurred, changes in the nervous system occur to counteract the effects. The day you experience a Conditioned Compensatory Response, you have a craving or physiological need for a drug.

Physical Dependence on Drugs

Occurs when people suffer from withdrawal symptoms when they stop taking a drug, and it is eliminated from their system. Withdrawal symptoms are almost always the opposite of the initial effects of a drug, which suggests that they are produced by the same neural changes that produce drug tolerance.

Biological Theories of Drug Addiction

What is Drug Addiction?

Addicts are habitual users; however, not all habitual users are addicts. The difference is that addicts continue to use a drug despite adverse on their health/life, and repeated, failed efforts to stop using it.

Physical Dependence Theory of Addiction

The earliest models of addiction were based on a theory that suggested drug addicts are driven by an aversion to withdrawal symptoms. However, attempts to gradually curtail drug use in addicts show that nearly all detoxified addicts return to former drug-taking habits. Another piece of evidence is that some drugs, like cocaine and amphetamines, do not produce withdrawal symptoms. Finally, some drugs involve cycles of binges and detoxification, which indicated detoxification does not prevent addicts from renewing their habits.

Positive Incentive Theory

The Positive Incentive Theory suggests that addiction is caused by the anticipated pleasure of taking a drug. Robinson and Berridge’s Incentive Sensitization Theory argue that it isn’t the liking of drug taking, but the anticipated pleasure, that creates addiction, so that in cases of chronic use, the incentive value is often disproportionate to the actual pleasure derived from it. Hence, even though the drugs result in misery, addicts continue to crave them even more.

What Causes a Drug Addict to Relapse?

Stress – The major factor in relapse.
Priming – Users who have abstained believe that their addiction is under control; however, one use and they often plunge back into addiction;
Environmental Cues – Anything previously associated with the drug (times, places, people, objects) associated with the drug can induce relapse.

Facts About Commonly Used Drugs

Tobacco and alcohol have much larger negative health effects on Americans than marijuana, cocaine and heroin

Tobacco

Nicotine is the major psychoactive ingredient
Responsible for over 3 million deaths per year worldwide (about 450,000 in the US, and about 20% of all deaths in Western countries)
High tolerance develops
70% of experimenters become addicted versus 10% for alcohol and 30% for heroin
Only 20% of attempts to quit are successful for 2 years or more
Nicotine addiction has a genetic component with 65% heritability
Smokers are actually more tense than non-smokers; stress level increase between cigarettes
Buerger’s Disease – Blood vessels in the legs constrict when nicotine enters the system, leads to gangrene and amputation
Smoking during pregnancy increases the risk of miscarriage, stillbirth and early death of a child; levels of nicotine in breastfed infants is nearly as high as in the blood of their smoking mothers

Alcohol

100,000 Americans die each year from alcohol-related diseases and accidents, and is involved in about 3% of all deaths in the US
Alcohol is classified as a depressant because it decreases neural firing; at low doses, it can stimulate neural firing and sociability
Alcohol has a major genetic component; 55% heritability
Blood levels at 0.5% causes risk of death from respiratory depression
A hangover is actually alcohol withdrawal
Delirium tremens (DTs) – third phase of withdrawal which starts about 1 to 2 days after cessation, and lasts 3 to 4 days, causes hallucinations, delusions, agitation, confusion, high temperature, and increased heart rate
Chronic alcohol consumption is associated with extensive brain damage
Korsakoff’s Syndrome – neuropsychological disorder characterized by severe memory loss, sensory and motor dysfunction, and dementia

Marijuana (Cannabis Sativa)

Psychoactive ingredient is THC (delta-9-tetrahydrocannabinol) which are in the form of a sticky resin on the leaves and flowering part of the plant; when extracted, this is called hashish
Can be smoked, or baked into an oil-rich substrate and ingested orally
Usage goes back 6,000 to China
George Washington grew cannabis for rope
Some laws classify marijuana as a narcotic; however, the structures of the active ingredients, physiological and behavior effects bear no resemblance to other narcotics
High doses impair psychological functioning – short term memory impairment and ability to perform multi-step tasks, slurred speech, limited ability to have a meaningful conversation
Seems to curb aggressive behavior
Low addiction potential, but tolerance does develop, no obvious withdrawal symptoms
Most scientists agree that small amounts have few, if any, permanent adverse effects, and long-term adverse effects are fewer than legal drugs like alcohol and nicotine
Respiratory problems are common, as is elevated heart rate
Anadamide is a clone of the THC-like chemical that binds to the receptor, but function is still unknown; it may protect the brain from excitotoxicity; mice without these receptors are more susceptible to seizures

Cocaine & Stimulants

Stimulants increase neural and behavioral activity
Coca-Cola is a mild stimulant that uses caffeine, but originally contained small amounts of cocaine
Cocaine is derived primarily in Peru and Bolivia from the coca bush
Cocaine hydrochlorida is the white powder most people are familiar with, and it is usually snorted or injected
Crack is an impure form of cocaine residue that is usually smoked
1.5 million Americans used cocaine or crack in the last month
Often consumed in binges, like alcohol
Cocaine psychosis is similar to paranoid schizophrenia
Extremely addictive, but mild withdrawal symptoms
Blocks the reuptake of catecholamines (dopamine, norepinephrine, and epinephrine)
Amphetamines (speed) has effects similar to cocaine; methamphetimines (METH) and MDMA/Esctacy are other popular forms of amphetamines
Stimulants are neurotoxins and a large cause for concern; MDMA has been shown to have toxic effects on serotonergic and dopaminergic neurons, and has been shown to cause brain damage
Women who use stimulants while pregnant often have children with lower IQs

Opiates: Heroin & Morphine

Opium contains morphine and codeine, a weaker derivative
Unmatched at painkillers, and can be used to treat coughs
Also highly addictive
Practice of eating opium became popular in the Middle East around 4000 B.C.
Harrison Narcotics Act 1914 made it illegal to sell or use opium, morphine or cocaine, but not heroin, which can penetrate the blood-brain barrier
In 1989, Bayer Drug Company marketed heroin, which was available without a prescription, as a non-addictive super-aspirin; it became illegal in 1942
About 130,000 Americans currently use heroin
Direct health hazards of chronic exposure are fairly minor
Dr. William Stewart Halsted, one of the founders of John Hopkins, is rumored to have regularly used opiates
Moderate withdrawal symptoms comparable to the flu; sometimes exaggerated in media; not as dangerous or terrifying as withdrawal from barbiturates or alcohol
Treatment programs report about a 10% rate

Addictions: Neural Mechanisms of Motivation

Drug Self-Administration Paradigm – Laboratory rats and primates can learn to self-administer addictive drugs, just like humans do
Conditioned Place Preference Paradigm – Drug-free rats will prefer the less comfortable compartment in which drugs were previously administered; importance is that they are tested while drug-free to avoid effects of drugs on behavior

Dopamine & Drug Addiction

Mesotelencephalic Dopamine System – The neurons which compose the brain’s dopamine system are the substantia nigra and ventral tegmental areas in the brain. Most of the axons of dopaminergic neurons have cell bodies in the substantia nigra and project into the dorsal striatum (nigrostriatal pathway). The degeneration of this pathway is associated with Parkinson’s disease.

Get Help for Drug Addiction

If you, or someone you know, suffers from Drug Addiction, get help from a professional. Each drug addiction counseling session an addict undergoes is a step towards building a brighter future without drugs.

Biopsychology: Genetic Disorders vs Exposure Disorders

03/12/2011 by 3icreative

Genetic Disorders

Down Syndrome (also known as Trisomy 21)

A person with Down Syndrome has 3 chromosomes on #21. The mom’s egg has an extra chromosome. There are 2 types of Down Syndrome:

MM1 – Mutation of mom’s egg occurs while mom was developing
MM2 – Mutation of mom’s egg occurs as mom ages. Under age 30, chances of Down Syndrome are less than 1 in 1000. Over age 50, the chances are 1 in 12. The only option is prenatal testing, or in vitro fertilization.

Phenylketonuria (PKU)

A person with Phenylketonuria cannot break down phenylalnine because they do not produce an enzyme. Phenylalnine is used in artificial sweeter, and found in diet sodas. When excess phenylalnine builds up, it causes mental retardation. There are strict dietary restrictions (low protien diet & Phenyl-free milkshare mix) for protein replacement). Most critical time to monitor is before age 30.

Fragile X Syndrome

More common in males
Facial features
Associated with hyperactivity, and attention deficit disorder

Exposure Disorders

Spina Bifida

Occurs due to maternal lack of folic acid
Neural tube does not close (day 23)
Severity depends on opening size. Severe can lead to paralysis, limb deformity, and mental retardation
Some forms may be genetic

Fetal Alcohol Syndrome

Physical abnormalities: wide eyes, flat bridge of nose, longer space from from nose to lips with no ridge, thin upper lip
Mental retardation
The more you drink, the more likely fetal alcohol syndrome will occur

The Forebrain: Telencephalon & Diencephalon

03/12/2011 by 3icreative

The forebrain is split into 2 sections: The telencephalon and the diencephalon.

Parts of the telencephalon

Cerebral cortex – The cerebral cortex is the “gray matter” of your brain, and is comprised of the fissures (valleys) and gyri (hills). Most information processing occurs in the cerebral cortex. Each of its 6 layers has different composition in terms of neurons and connectivity. However, there are 2 types of basic neurons: Star-shaped cells (small interneurons with no tail) and triangular cells (large multipolar neurons). There are 4 lobes in the cerebral cortex:
- Frontal lobe – The frontal lobe is associated with personality, conscience (right/wrong/consequences), planning and is the source of inhibitions. Moniz won a Nobel Prize for developing the prefrontal lobotomy. It was later replaced by Walter Freeman’s transorbital lobotomy. They were both later replaced with safer alternatives (drugs like thorazine).
- Parietal lobe – The parietal lobe is in charge of somatosensory processing (touch). See Oliver Sack’s case study about the man who fell out of bed.
- Occipital lobe – The occipital lobe processes visual memory, and is associated with migraine headaches.
- Temporal lobe – Auditory and language processing occurs in the temporal lobe; about 90% on the left side.
Corpus callosum – The white matter in the brain that connects the left and right hemispheres. Split brain occurs when the connection in the corpus callosum is severed.
Limbic system – The limbic system is the collective name for the parts of the brain that control emotion, motivation, and emotional association with memory, and includes the hippocampus, cingulate cortex, mammillary bodies, amygdala, fornex and septum.
- Hippocampus – It’s easy to remember where the hippocampus is because it’s shaped like a seahorse. The hippocampus is associated with short and long term memory indexing (moves memories in and out), and is one of the first parts of the brain affected in Alzheimer’s. Damage to the hippocampus can cause amnesia, preventing the formation of new memories (anterograde amnesia), as well as recollection of old ones (retrograde amnesia). Elderly people with shrinkage of the hippocampus tend to have memory problems (episodic and working memory). Abnormalities in development of the hippocampus are associated with schizophrenia.
- Anterior cingulate cortex (ACC) – In PTSD, there is lower activity and fewer neurons in the the anterior cingulate cortex.
- Amygdala -The amygdala is shaped like an almond, and located on the fatter end of the hippocampus. It is responsible for emotional processing, and associated with conditioned learning, especially fear/anger/rage. Dysfunction of the amygdala is linked to anxiety, autism, depression, post-traumatic stress disorder, phobias and binge drinking. PTSD is now being treated with small doses of esctasy (plus counseling). Also see case study below of Little Albert by John Watson.
- Olfactory bulb – Sense of smell, connected to the amygdala, which is why smells are strong sources of memories.

Parts of the diencephalon

Thalamus – The thalamus has 2 lobes, and is responsible for sensory relay in your brain. Essentially, it is the “traffic cop” that directs information. It does NOT help with recognition.
Hypothalamus – The hypothalamus controls motivated behavior by regulating the release of hormones from the pituitary gland. It is responsible for the 4 F’s: Fighting, fleeing, feeding and sex.
Pituitary gland – Small pea-sized gland of the endocrine system, often called the “Master Gland.” The pituitary gland hangs from the hypothalamus.
Pineal gland – Small gland of the endocrine system that controls melatonin (a hormone that affects the modulation of wake/sleep patterns and seasonal functions) production that’s sometimes referred to as the “third eye.”

Biopsychology & the Development of the Nervous System

03/04/2011 by 3icreative

Embryonic Cell Layers - 3iCreative In order to understand psychology from a biological perspective, we must understand the development of the nervous system, starting from conception.

Each of us began as a single-celled zygote which multiplied to become an embryo (day 10 to 8 weeks), and then a fetus. In order for us become “us” — and not a blob of cells — many things had to happen, including development of the nervous system.

The development of the nervous system begins during the embryonic stage, about 2 to 2.5 weeks post-conception, when the neural plate forms from the inner layer, called the ECTODERM. Here’s a quick review of embryonic cell layers:

Embryonic Cell Layers

Ectoderm – The inner layer of the cell which forms the nervous system
Mesoderm – The middle layer of the embryonic cell which becomes connective tissue, bone, muscles, etc.
Endoderm – The outer later of cells which develops into bodily organs

In order for proper development to occur, 3 things must happen, starting with the formation of the NEURAL PLATE, a small path of tissue on the dorsal (back).

1) Cell Differentiation

Differentiation refers to the creation of different types of cells. So, for example, some cells will need to become muscle cells, and some will need to become glial cells, etc.

TOTIPOTENT – During the earliest stages of embryonic development, most cells are totipotent, which means that they are able to develop into any type of cell.
MULTIPOTENT – As the embryo develops, cell differentiation becomes more specified. For example, cells in the neural plate can only mature into nervous system cells. These cells are often referred to as embryonic stem cells.

2) Neuronal Migration & Aggregation

The second thing that must occur for proper development is neuronal migration – the movement of different types of cells to the proper location (migration). Once the cells are in the right location, they must align (aggregation). There are 2 ways this can happen:

SOMAL TRANSLOCATION – During somal translocation, cells migrate to the appropriate location by developing extensions that look for cues to point in the right direction. As the cells move, the “tail” or extension they have disappears behind them. Many chemicals have been identified that guide cells in the right direction. The 2 most important:
- Glycoproteins
- Chemoattractants
GLIAL MEDIATED MIGRATION – As the walls of the neural tube thicken, a temporary network of glial cells (RADIAL GLIAL CELLS) develops inside the tube. During glial medial migration, cells latch onto the framework and inch along like a little worm as it guides them in the right direction.

3) Formation of Neural Connections (Axon Growth & Synapse Formation)

Once the cells are properly aligned, the neural pathways must be “hooked up” correctly. So, in the next step of the process, axons and dendrites grow out from the cell’s GROWTH CONE (swelling on one side of the cell which extends and retracts in search of the right direction). Guided by NEUROTROPINS (NGF – Nerve Growth Factor), FILOPEDIA protrude out

AXON GROWTH – In the 1940s, Sperry cut the optic nerves of frogs, rotated their eyeballs 180 degrees, and waited for the axons to regenerate. When he dangled a lure behind the frogs, the struck forward, suggesting that their visual world had also rotated. The same was true whether or not the optic nerve was cut. This behavioral evidence suggests that each retinal cell had grown back to the same point where it was originally connected. This was confirmed in 2000.

Sperry’s Chemoaffinity Hypothesis of Axonal Development – Each post synaptic surface in the nervous system releases a unique chemical label, which attracts a growing axon. However, this hypothesis does not account for the fact that some axons follow the same circuitous route to reach their target in every member of a species, rather than going directly from point A to point B.
- Elaboration of hypothesis based on new research indicates that axon growth is influenced by a series of chemical signals along the route. These guidance molecules are called CHEMOATTRACTANTS. Others repel (CHEMOREPELLANTS). Other signals comes from adjacent growing axons. The PIONEER GROWTH CONES lead the way, and others follow in their path. FASCICULATION is the tendency of developing axons to grow along the paths established by preceding axons. When pioneer axons die before reaching their destination, subsequent axons of the same nerves tend to die also.
Topographic Gradient Hypothesis – Axons growing from one topographic surface to another are guided to specific targets arranged on the terminal surface in the same way the axon’s cell bodies are arranged on the original cell surface (guided to destination by 2 intersecting gradients on original surface).

SYNAPTOGENESIS (synapse formation) – It takes the coordination of 2 axons to create a synapse between them. Recent discovery – Astrocytes (star-shaped glial cells in the brain and spinal cord) are necessary for this process.

Neuronal Death

The death of neurons is a normal part of the development process, and operates on a “survival of the fittest” principle. We produce about 50% more neurons than we need, and those that die generally lose the competition for the chemicals (target sites) they need. The ones that don’t get hooked up properly or used, die.

Implanting new chemicals (target sites) reduces neuron death
Destroying neurons in a particular area before the period of cell death increases the survival rate of the remaining neurons
Increasing the number of axons that initially innervate a target reduces the number that survive

NECROSIS – Passive cell death

APOTOSIS – Active cell death; this is the safer process because the internal structures of the cell are packaged in membranes before the cell breaks. The membranes attract scavenger cells that prevent inflammation. If the process is inhibited, cancer can develop. If the process is overstimulated, neurogenerative diseases may develop.