BLOA

1. BLOA 1. Examine one study related to LOF in the brain 2. Explain, using one or more examples, the effects of neurotransmission of human behaviour

2. Aphashia • Loss of ability to understand or express speech, caused by brain damage.

3. Broca’s Aphasia • Paul Broca (1824-1880) • Damage to a specific part of the brain was responsible for the loss of ability to produce coherent speech. • Severe articulation delay • Sarah Scott Youtube • Broca (1861) found that people suffering from damage in an area (that was eventually called the Broca’s area) were unable to understand and make grammatically complex sentences. Their speech consists of almost entirely content words. • Patients have a difficult time producing speech but could understand it.

4. Wernicke’s Aphasia • (1874) – First described the area that appears to be crucial for language comprehension. People who suffer from damage to Wernicke’s area are unable to understand content words while listening, and they are unable to produce meaningful sentences. • Patients could produce speech, but not understand it.

5. Your Turn… • You already have the outline for the SAQ prompt (2.2 handout). Apply the same outline to a different study. The following could be used on your exam: • Broca (Tan) • Sperry • Gazzainga • Phineas Gage • Ogden (2005) – Janet • Wernicke • Explain the study (Aim, Method, Results/Findings) • What can be learned about LOF from the study? • Evaluation of the study

6. Natural Experiment or Case Study? • Sperry’s work is sometimes considered a natural experiment, although others argue it is a case study. • Corpus Callosum is a part of the brain that joins the two hemispheres and it appears to be responsible for communication between them. • What do you think? • Can the findings be generalized to the rest of the human population? Explain.

7. Physiology & Behaviour: Neurotransmission • Neuron Transmission

8. How do nerve cells communicate? • There are 3 main parts to the transmission process at the synapse • 1. Neurotransmitters are stored in vesicles inside the terminal button of the axon; the vesicles are transported to the edge of the button and the neurotransmitters are released into the synaptic gap • 2. In the synapse, neurotransmitters can bind with a receptor site on the next neuron if they fit (lock & key). If enough of the NT binds to the receiving neuron’s receptor sites, the neuron will ‘fire’ (meaning it will transmit the info across its cell body electronically) • 3. Any unused NT’s are reabsorbed back into the neuron of origin (REUPTAKE….RECYCLED to be used again)

9. The transmission process can be altered by drugs when: • 1. Certain drugs introduced to the nervous system can encourage or prevent the production and release of NT’s, thus, increasing or decreasing the amount of NT’s available in the synapse. • 2. Certain drugs can occupy receptor sites that would normally receive a neurotransmitter. When a drug does this, it has its own effect on the receiving neuron as well as preventing the naturally occurring NT from from completing the transfer. • 3. Certain drugs can prevent the reuptake of NT’s which allows them more time so bind to receiving neurons.

10. Caffeine… • Caffeine follows rule #2. When a person begins to feel sleepy, a neurotransmitter called ADENOSINE is being released into the synaptic gap in a specific part of the brain. • Adenosine acts to inhibits activity and prepare the body for sleep. • When caffeine enters the synaptic gap, it binds with the receptor sites that adenosine normally uses, and prevents the normal inhibition of activity. • In addition, caffeine actually stimulates brain activity, which means that a person’s movements and thoughts may become faster

11. Drugs & Behaviour • Our body easily develops tolerance to drugs (adaptability) requiring higher doses to achieve the same effect as the brain compensates for the drug use • Once the effects of the drug wears off, the symptoms of withdrawal occur in force and the effect you were blocking by taking the drug takes hold. • Much drug research has been done through experimentation with animals and humans.

12. Dopamine Levels • Neurotransmitter involved in a goal-directed behaviour (motivation) such as pleasure-seeking, control of movement, emotional response and addictive behaviour • Released into the brain’s reward system • High levels of Dopamine have been associated with Schizophrenia • Low levels of Dopamine have been associated with Parkinson’s Disease

13. Dopamine • L-Dopa was a breakthrough in treatment for Parkinson’s Disease ( a degenerative condition that usually involves a resting tremor, a difficulty initiating movement, and difficulty in controlling directed movement such as picking up a spoon or cup). • Drug was designed to relieve the symptoms by increasing the amount of dopamine available would have a positive effect.

14. Dopamine & Addictive Behaviour • Dopamine released in the brains reward system and associated with pleasure seeking and addiction • Addictive drugs increase amount of dopamine in reward system • Can be released by environmental triggers b/c of association with pleasure • Nicotine increases levels of dopamine in the reward circuit, creating feelings of pleasure/relaxation

15. Serotonin Levels • Prozac was founded to be effective in reducing symptoms of depression, theoretically because depression is associated with low levels of serotonin in specific regions of the brain responsible for mood regulation. • Prozac’s action of blocking serotonin reuptake is able to increase the amount of serotonin available and therefore facilitate the transmission of mood regulation messages in the brain. • How does LSD work? It works against serotonin activity by blocking serotonin receptors. It seems that one of the main functions of serotonin is to inhibit dreaming while we are not sleeping.

16. Serotonin and Depression • Delgado & Moreno (2000) • Correlational Study • Found lower levels of noradrenaline (norepinephrine) and serotonin in patients with major depression • Indicates there is a relationship between neurotransmitter levels and depression but does not demonstrate cause-effect relationship

17. Acetylcholine (ACh) • ACh is a neurotransmitter linked to synaptic to synaptic plasticity in the hippocampus • Plays an important role in learning and STM via the cholinergic system • Cholinergic system is a system of nerve cells using ACh in transmitting nerve signals • Memory processing / higher cognitive functions depend on cholinergic system