Changes in Synapses That Happen During Classical Conditioning
The first scientific study of animal learning demonstrated a form of associative learning – classical conditioning; it can be described as a process of learning where a neutral stimulus (e. g. bell) is paired with an unconditional stimulus (e. g. food) and as a consequence, the neutral stimulus becomes conditioned and comes to elicit the same response (e. g. salivation) as the unconditional stimulus even when presented alone (Murphy & Naish, 2006).
It has been proposed that “…classical conditioning…is quite easy to explain on the basis of simple changes in synapses. ” In order to assess the merit of this claim, it is necessary to describe the simple changes that occur in synapses during classical conditioning. All forms of learning require some synaptic change, however it isn’t clear whether these can always be explained by the same kind of synaptic changes that happen in classical conditioning (Murphy & Naish, 2006). Some forms of learning will be explored in terms of synaptic changes.
At a neurobiological level, learning is “created” by the interconnectedness between neurons (synapses). Hebb proposed that if the postsynaptic neuron fired while the presynaptic terminal was releasing neurotransmitter (NT), the presynaptic neuron would be more likely to influence the postsynaptic neuron on subsequent occasions, i. e. when previously unassociated neurons fire simultaneously on repeated occasions, new links are formed which increase synaptic efficiency (Hebbian learning).
Hebbian learning explains Pavlov’s associative learning – classical conditioning. Pavlov carried out experiments with dogs and noted their salivation reflex in response to food presentation (unconditioned response), later he repeatedly paired the presentation of food (unconditioned stimulus) with the ringing of a bell (neutral stimulus) and finally he sounded the bell (conditional stimulus) without presenting the food and that alone triggered salivation (conditioned response) (Murphy & Naish, 2006).
Repeated activity in two neurons simultaneously (e. g. bell, food) strengthens the synapses and eventually activity in one of the two neurons alone will produce activity in the other because new effective links are formed by the repeated and simultaneous firing, creating an auto-associated pattern (bell and food repeatedly presented together lead to a conditioned learning response). The conditioning of an eye-blink to a buzzer is another example that can be supported by Hebb’s proposal of changes in synaptic efficacy.
Activation of the neutral (presynaptic) neuron that fires to the sound of a buzzer at the same time that a puff of air occurs (unconditioned neuron) causes an eye-blinking response (blinking neuron). At first, the connection between the neutral neuron and the postsynaptic neuron is very weak, so the release of NT by the neutral neuron is unlikely to trigger firing in the postsynaptic neuron. However, the unconditioned (presynaptic) neuron has an efficient synapse with the postsynaptic neuron i. e. this presynaptic neuron causes the postsynaptic neuron to fire thus producing a blinking response.
If both presynaptic neurons are repeatedly activated at the same time that the air-puff occurs, an excitatory postsynaptic potential is elicited in the blinking neuron and the previously weak synapse will become stronger to the point that, this synapse alone can trigger firing in the postsynaptic neuron that responds to the air-puff and causes eye-blinking (Murphy & Naish, 2006). Classical conditioning was originally interpreted as an automatic response linking a new stimulus to an existing reflex behaviour (S-R sequence).
However, further research into conditioning found the process to be more complex, Pavlov realized that his dogs came running to be fed when they heard the bell. But, running isn’t an automatic reflex; this could perhaps be seen as instrumental conditioning, which happens when behaviour is rewarded. This kind of learning appears more complex than classical conditioning, as previously interpreted, as the animal has to acquire what appears like a declarative memory (a memory of “knowing what”). Thus, this process of learning is likely to involve a more complex system of adjusting Hebbian synaptic efficiency.
Instrumental conditioning is often used when teaching new tricks to a dog, e. g. teaching a dog to “shake hands”; upon hearing the command the dog sits down and raises a front paw, then the dog receives a reward (Murphy & Naish, 2006). Applying Hebbian learning to this example isn’t straightforward, however as the time between triggering the behaviour and receiving the reward has to be almost instantaneous, or the dog won’t learn the trick, this can be linked to Hebbian learning – both neurons (human voice and reward) have to be simultaneously activated for the behaviour to take place, i. . synaptic strength will increase only if both pre- and postsynaptic neurons are simultaneously activated (Murphy & Naish, 2006). Perhaps “reward” neurons fire while there is activity in the neurons that direct the behaviour. The dog may anticipate the reward which leads to the “shaking-hands” behaviour and is likely to strengthen associated synapses. The theory that learning can induce changes in neural networks is supported by recordings from the sea slug aplysia while the animal is learning (Murphy & Naish, 2006).
Aplysia is perhaps the most simple example of biological changes at synapses resulting in encoding environmental events and thus learning. This animal is able of non-associative learning brought about by changes in synaptic connections between sensory and motor neurons. If a mild stimulation is applied to the siphon, it withdraws its gill, however repeated mild stimulation decreases its reponse, i. e. habituation occurs, due to a reduction in the number of synaptic connections which leads to a decrease in synaptic efficiency. But, if an intense stimulus is applied to the tail or head this results in withdrawal of the gill, i. . sensitization occurs, due to an increase in the number of synaptic connections, leading to increased synaptic efficiency (Murphy & Naish, 2006). The different examples of learning presented can to some extent be supported by Hebb’s proposal of changes in synaptic efficiency. Since synaptic changes are all we have available as a physical basis of learning they could perhaps be further explored as the physical basis of all forms of learning. Word count: 984 References Murphy, K. , Naish, P. (2006). Learning and Memory, Learning and Language, 2nd ed. , pp. 1-29, 42-48, The Open University, Milton Keynes.
QUESTION 2 a. i. For dopamine (DA) to “skyrocket”, it means that high levels of it were released by the dopaminergic system and as this substance plays a role in the appetitive phase of feeding motivation, will likely motivate the person to obtain food in order to bring their body nutrients back to optimal level (homeostasis). The increase in DA levels is caused by the activation of the mesolimbic dopaminergic pathway which increases its neural activity. a. ii. A PET scan procedure with a participant who is a cheeseburger eater (non-meat eaters might not experience a DA rise).
The participant should fast for 8-12 hours (to make sure he/she feels hungry). A radioactively-labelled marker is injected intravenously into the participant and his/her brain is scanned before waving a hot cheeseburger in front of his/her nose/mouth and scanned again while this is happening. Brain scans will compare DA levels “before” and “during” the food stimulation. The comparison will look both at brain regions/neurons affected and activity levels. As the marker competes with the brain’s released DA to bind to receptors, the scans will provide an inverse measure of the brain’s DA levels, i. . an increase in DA will show a low signal from the marker and vice-versa. Word count: 200 b. i. This could happen either because of genetic reasons i. e. the person was born with fewer dopamine D2 receptors or because the repeated use of certain substances/drugs has led to a decrease in D2 receptors. It is also possible that the combination of genetic factors and drug use contribute to a decrease in D2 receptors. b. ii. The best kind of evidence would be brain imaging (e. g. PET scans) of addicts; ideally from before and during the addiction.
In order to compare the same individual(s) levels of D2 receptors so as to decide whether D2 receptors decreased with drug use or were originally low. Brain imaging of close relatives or genetic studies would also be useful in deciding if fewer D2 receptors were inherited. b. iii. The notion of “desensitization” in the extract indicates that the repeated use of addictive drugs decreases the amount of dopamine D2 receptors causing the dopaminergic system to become less sensitive to DA, thus leading the addict to seek greater amounts of the drug.
This concept contrasts with “incentive sensitization”, i. e. the repeated exposure of the NS to addictive drugs leads to increase in dendritic spines which “pulls” the addict towards drug-related incentives e. g. syringes, locations associated with drug-taking. Word count: 199 c. i. In terms of incentives what might be involved is: pleasure, cues paired with food e. g. smell, sight of food, location. A spike in dopamine levels caused by presentation of a conditional stimulus e. g. tress, pain, watching TV etc, if the person tends to eat when these occur. c. ii. The “much more” and hunger interact as external and internal factors in the feeding motivation. The internal factors reflect an internal deficit of energy (e. g. nutrients, glucose levels), the external factors are related to things like, sight or smell of food, changing in available diet. c. iii. The functional significance is to pull the person to seek food and restore homeostatic balance, thus lowering the body’s perceived risk to physical integrity.
Word count: 100 d. Schizophrenia is associated with abnormalities in the anatomy of the brain and the network connections within it (made of small building blocks called neurons), thus producing abnormal levels of certain brain chemicals. From this point of view it might be considered a brain disorder, however the abnormality or dysfunction that occurs in the brain leads to particular patterns of thinking and feeling which cause abnormal psychological experiences. This second aspect may point to a classification of schizophrenia as a mind disorder.
From a biological psychology perspective brain structure/activity and thoughts/feelings constitute different aspects of a highly complex phenomenon where a dysfunctional brain affects an individual’s psychological experience. While major symptoms like: hallucinations, delusions, thought disorder, affective flattening and social withdrawal tend to be the focus of attention and may seem like the confirmation of a mind disorder, there are subtle and ongoing cognitive difficulties which tend to be ignored: problems with coordination, attention, concentration and willed action.
Evidence shows: lower IQ levels, abnormal patterns of eye movement when following a target, unusual EEGs. PET and MRI scans provide detailed evidence of deep measurable brain abnormalities at the level of: structure, cells and chemicals which affect brain functioning in schizophrenics. Word count: 199W