PSYC 302: Biopsychology11/27/07-Announcements:1. Review Session today.2. Final exam next Tues (12/4).Substance Abuse and AddictionReward pathway-- Dopaminergic neurons have their cell bodies in the ventral tegmental area (VTA), and their axons extend into various brain areas, including the nucleus accumbens. The nucleus accumbens is part of a structure called the striatum that includes the caudate nucleus and putamen. Although it's a small structure, it's a very important "pleasure center."Olds & Milner- stuck an electrode accidentally in a rat's nucleus accumbens and they found that the rat would forego sleep and food to self-stimulate.Alcohol-- From a psychopharmacological perspective, alcohol inhibits the flow of sodium ions into neurons, making it a CNS depressant. Decreases serotonin (excitatory) activity and facilitates response by the GABA (inhibitory) receptors. It blocksglutamate (excitatory) receptors and increases dopamine (excitatory; key to the reward pathway) activity.Type I vs Type II- Type I is late onset, and so it appears to be less genetic in basis, and less severe than Type II, which is largely genetic.Type II alcoholism has greater concordance in monozygotic vs. dizygotic twins. Plus, there is a strong correlation between the occurrence of Typ II alcoholism in biological fathers and sons, even when the son is adopted and raised in a non-alcoholic family.One of the treatments for alcoholism is antabuse, which has a low adherence rate. The drug causes the user to become severely nauseated when they drink alcohol.Alcohol metabolism: alcohol ---> acetaldehyde ---> acetic acidAcetaldehyde is very toxic and causes nausea and vomiting.Methadone in the treatment of heroin addiction:Methadone is just a substitute opiate for heroin. When taken orally, it crosses the blood-brain barrier much more slowly than heroin, and so it produces its effects more slowly, including withdrawal, and it's far less addictive. BUT if you inject methadone, itbecomes pretty similar to heroin in its effects.Solution: Mix naloxone with methadone. Naloxone is an antagonist that blocks opiate receptors. But when it's taken orally, it's broken down in the stomach and rendered ineffective. If it's taken in any other way, it blocks the effects of methadone or any other opiate.DEPRESSIONIs there a genetic component?There are two genes implicated in depression: One gene results in lowered serotonin production and the other gene increases the efficiency of serotonin reuptake.What are anatomical/structural differences in the brains of depressed individuals?Depressed people have less activity in the LEFT prefrontal cortex and more in the RIGHT.Drug treatments:1. tricyclics (e.g. Tofranil)-- prevents the presynaptic neuron from reuptaking serotonin, dopamine and norepinephrine.2. selective serotonin reuptake inhibitors (SSRIs; e.g., Paxil, Zoloft, Prozac)-- they block the reuptake of serotonin but not of other monoamines.3. Monoamine oxidase inhibitors- Monoamines are a class of neurotransmitters that includes dopamine, serotonin, epinephrine, and norepinephrine. Monoamine oxidase (MAO) is an enzyme that breaks down these neurotransmitters. By blocking MAO, you leave the neurotransmitters in the synapse longer so that they exert a greater effect.4. atypical antidepressants (Wellbutrine) inhibits dopamine and norepinephrine reuptakeComparing different treatments for depression, we see the following efficacy rates:Antidepressants- 50-60%Psychotherapy- 50-60%Placebo- 30%Electroconvulsive therapy (ECT; as seen in "Ordinary People" and "One Flew Over the Cuckoo's Nest"). Nobody knows exactly why it works. It has certain side effects, including memory loss, which can be minimized by administering the current only to the right hemisphere), and it has a high relapse rate.Depressed people have sleep maintenance insomnia (trouble getting back to sleep when they awaken) and enter REM more quickly. This suggests that they are "phase advanced", that their sleep-waking cycle has shifted so that their body temperature starts to decrease earlier in the day.In some cases, if you keep the patient awake for an entire night, their sleep-wakingcycle will return to normal and depression symptoms will decrease.Seasonal Affective Disorder (SAD)- phase delay in the sleep-waking cycle, meaning that sleep occurs later and temperature rhythms are altered so that temperature decreases happen later, as well. Bright full-spectrum light.Bipolar disorders- manic and depressive episodesBipolar I-- The manic episodes are more severe, and can include restlessness, excitement, rambling thought, loss of inhibitionsBipolar II- much milder manic phases (hypomania), which include agitation and anxietyTreatments for bipolar:Lithium, carbamazepine (Depakote) and Valproate-- all block the synthesis of arachidonic acid (a precursor of cannabinoids in the brain), which is produced when the brain is inflamed. Lithium does not increase GABA activity, but the other two do. Since GABA is inhibitory, we assume that these drugs reduce manic symptoms by inhibiting brain activity. Valproate stimulates growth of axons and dendrites.SchizophreniaAcute-- sudden onset, good prospects of recovery ("Eden Express" by Mark Vonnegut)Chronic-- gradual onset, long-term course, harder to treatTwo classes of symptoms of schizophrenia:1. Positive symptoms-- Psychotic cluster (delusions, hallucinations); disorganized cluster-- inappropriate behavior, emotional displays, bizarre behavior, thought disorder)2. Negative symptoms-- flat affect, weak social interactions, problems with speech and working memoryIs schizophrenia genetic? There is evidence for and against:FOR: greater concordance in dizygotic twins than in other siblingsAGAINST: The concordance rate for monozygotic twins is only 50%Neurodevelopmental hypothesis-- Brain abnormalities that occur in prenatal or neonatal development. Evidence for this hypothesis:1. A number of different neonatal complications have been linked to schizophrenia.2. Schizophrenics show certain brain abnormalitiesa) decreased volume in the left temporar and frontal cortexb) larger ventriclesc) smaller cell bodies, especially in the neurons of the hippocampus and right prefrontal cortexd) unlike most people, who have a larger planum temporale in the left hemisphere, schizophrenics have a larger right p.t.e) lower than normal left hemisphere activity3. abnormalities in development have