1. Differentiate between positive and negative reinforcement. Explain how they differ from punishment.
The difference between positive and negative reinforcement is subtle, but very important.
A behaviour that is reinforced by discontinuing, subtracting, or evading a negative result or aversive stimulus is a negative reinforcement. As an example, doing something helpful (the behaviour) in order to stop an authority figure from shouting (aversive stimulus). Similarly, B.F Skinner used a Skinner box to support his theory, by the rat pressing a lever in order to escape a foot shock. Another example would be blasting the car horn to remove a car in front of you in traffic.
Whereas, positive reinforcement involves the addition of a reinforcing stimulus following a behaviour which then makes it more likely that the behaviour will occur again in the future. In other words positive reinforcement is a reward for doing something well, which leads to an increase in behaviour. For example, in 1974, B.F. Skinner had trained pigeons to peck the left side of a disc enable to get food. This also links with the method of giving a child a ‘treat’ for a good school report, as this would then encourage the child to behave better at school; or even working hard in class and receiving an good grade, which you are praised for in front of the whole class.
However, not all positively reinforced behaviours are desirable behaviours. Our reactions to an undesirable behaviour can accidentally lead to reinforcing that behaviour. In the end, it all comes down to pain versus pleasure in the end.
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2. Describe in detail the process of communication between neurons.
Neurons send signals to other neurons through specialised contacts known as synapses. A chemical synapse is the more usual type inside of the nervous system. It’s typically a chemical synapse existing between the axon terminal of the neuron sending the message, and the dendrites/cell body of the neuron receiving the message. The neuron sending the message is called the presynaptic cell and the one receiving the message is the postsynaptic cell. In a chemical synapse, the presynaptic and postsynaptic cell don’t actually touch each other, but are separated by a very tiny gap called a synaptic cleft.
A chemical synapse transforms an electrical signal (which is the action potential in the presynaptic cell’s axon) into a chemical signal (the neurotransmitter) and back to an electrical signal (the postsynaptic potential) in the postsynaptic cell. When the action potential reaches the axon terminal buttons, calcium (Ca++) pathways open in the presynaptic membrane allowing an influx of Ca++. Vesicles including the neurotransmitter fuse with the presynaptic membrane (exocytosis). Neurotransmitters spill out, diffusing across the synaptic cleft, then binding with receptor cites on the dendrites of the post-synaptic membrane ‘lock and key’ fashion.
Neurotransmitter-gated channels on the postsynaptic membranes allows the specific ions to come through, changing the membrane potential (a difference in charge across the membrane). If excitatory sodium channels open depolarising the post-synaptic neuron (EPSP), which is more likely to fire. If inhibitory potassium channels open hyper-polarising the postsynaptic neuron (IPSP), which is less likely to fire.
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3. Contrast agonist and antagonist drug effects.
Agonist was originated from late Latin word ‘agnista’, which means contender. Antagonist was derived from the Latin word ‘antagonista’ and from the Greek word of ‘antagonistes’, which translates to competitor and opponent.
An agonist and an antagonist behaves in opposite directions. For example, when an agonist produces an action, an antagonist opposes the action; an agonist works when the muscles relax but an antagonist works when muscles contract; while agonist stimulates an action, an antagonist sits idle and does nothing at all. In addition to this, an agonist ties itself to a receptor site and causes a response (binds to the postsynaptic membrane (mimics the NT), whereas an antagonist works in opposition to the drug and cuts the response (blocks the receptors on the postsynaptic membrane). Agonists are the chemicals or reactions, which aids in binding and also altering the function of the activity of receptors. Even though antagonists help in binding receptors, they don’t alter its activity. An agonist also increases the pre-cursor of a neurotransmitter (NT), destroys degrading enzymes, prevents re-uptake. Whereas, in contrast to this, an antagonist effects (inhibitory) blocks synthesis of the NT, breaks down the vesicle containing NT’s, blocks release of the NT from the terminal buttons.
Full agonist opioids activate the opioid receptors in the brain fully resulting in the full opioid effect. E.g. heroin, oxycodone, methadone, hydrocodone, morphine, and opium. However, antagonists cause no opioid effect and block full agonist opioids. E.g. naltrexone and naloxone. Naloxone is sometimes used to reverse heroin overdose.
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4. What evidence is there to suggest that using a mobile phone whilst driving or even walking has a negative impact on attention?
Mobile phones keep us connected with the world, but they also cause a disconnection that creates sometimes very dangerous lapses in attention. There’s many studies that have provided us clear evidence that using a mobile whilst driving or walking has a negative impact on our attention, such as, Caird et al. (2008) wrote a literature review of studies involving driving simulation tasks and mobile phone use. It showed that there was a mean increase in reaction time of .25s which was found to all types of phone-related tasks. E.g, a vehicle breaking, and similar for handheld and hands free.
Strayer et al. (2011) conducted an observation study of drivers approaching road junction. Which found 75% of drivers using mobiles failed to stop, and the likelihood of driver being in an accident was 4x greater when using a mobile.
Whilst using your mobile, you will recognise less objects. Hymen et al. (2010) compared mobile phones and mp3s, in pairs and alone. The mobile user was found to change direction more often, didn’t acknowledge others, and their walking slowed. The mobile user was also less likely to notice a clown riding a unicycle than other conditions. Authors argue that walking should use few cognitive resources, but there was evidence of inattentional blindness (failure to perceive unexpected objects/changes in environment).
Thornton et al. (2014) found that the mere presence of a mobile phone causes distraction. Strayer & Drews (2007) also supported this when 30 objects were presented during driving simulation tasks.
Word count: 250
Student Number: 21336229
5. Evaluate the evidence for the existence of different types of long-term memory.
Memory research has been advanced by:- human brain injury studies, nonhuman animal lesion studies, research looks for ‘dissociations’, and technology that allows us to study the brain in action. Before memories can form, learning must occur. Different types of long-term memory include: declarative and procedural memory. Procedural memory includes how to do things. Whereas, declarative memory includes facts, general knowledge, and personal experiences. Two subtypes of declarative memory are episodic and semantic memory. The most famous study demonstrating the separation of the declarative and procedural memories, was about a patient named “H.M.” in 1953. Parts of his medial temporal lobe, hippocampus and amygdala were removed to attempt to cure his uncontrollable epilepsy. Post-surgery, H.M. could still form new procedural and short-term memories, but enduring declarative memories couldn’t be made anymore. The nature of the exact brain surgery he faced, and types of amnesia he suffered, provided great understanding of how certain areas of the brain are linked to specific processes in memory formation. Specifically, his capability to recall memories from prior to his surgery, but his incapability to create new long-term memories, suggests that encoding and retrieval of long-term memory information is mediated by distinct systems within the medial temporal lobe, particularly the hippocampus. The fact he was able to learn hand-eye coordination skills like mirror drawing, despite having no memory of learning or practising the task before, also suggested the existence different types of long-term memory (declarative and procedural memories).
Word count: 250
6. Discuss the impact that past experience can have on problem solving.
When it comes to reproductive problem solving, the positive transfer effect usually shows that past experience is beneficial to solving problems. Whereas, the negative transfer effect suggests that past experience is actually a hindrance to solving problems. Functional fixedness applies here.
If past experience can hinder problem solving, we might expect younger children may be less affected. For example, by factional fixedness.
Defeyter & German (2003) studied children aged 5-7, asking them to remove an object from a tube. Several objects including a stick are presented. When there was no suggested use for the stick, there was no evidence of functional fixedness. But, a suggested use for the stick, lead to evidence of functional fixedness. However, there wasn’t evidence of functional fixedness in the younger children as they have less experience of problem solving.
Additionally, the negative transfer effect implies is that both the mental set and learned helplessness is applied here. Mental set can make it simple to solve a certain problem, but attachment to the wrong mental set can hinder problem-solving and creativity. For example, Luchins (1942), the Water Jar Problem. Participants were given 3 water jars, each able to hold a different, fixed amount of water; they had to discover how to measure a certain amount of water using these jars. This found that they used methods they’d used before to find the solution even though there were quicker and more efficient methods. This experiment showed how mental sets can hinder the solving of novel problems.
Word count: 250
Total word count: 1,500