Psyc20006 - Biological Psychology

The probing excitability approach which tests the responsiveness of the motor system during a cognitive task. If the motor cortex is required for a cognitive task then it should already be activated when single-pulse TMS is delivered. The measure of interest is how strongly the motor cortex reacts to the pulse itself and how strongly the body part will move in response to the additional stimulation. 

The paired pulse approach first activates the brain using a sub-threshold stimulation and then interferes with neuronal transmission using a second supra-threshold stimulation and aims to answer the question of how strongly the first stimulation affects the second.

Schizophrenics have an increased Cortical Silencing Period (CSP), meaning that the cooling off period is reduced after excitation and thus there is hyperexcitability and problems with getting rid of muscular activation.

The virtual lesion approach involves repeated TMS (rTMS) which can inhibit functions for a longer period of time. 

The Z distribution uses the population SD

The t statistic takes into account both the expected mean and a measure of the standard error of the mean based on the sample

The bottom of the above equation refers to the standard mean of the population

The x value with a hat refers to the sample mean

Great temporal resolution but poor spatial resolution

Can't test causality

Electrode cap signals are amplified and EEG is recorded during experimental stimulation

EEG reflects post-synaptic potentials (voltages that arise when NT bind to receptors of the post-synaptic cell). This causes ion channels to open/close, leading to graded change sin the potential across the membrane.

EEGs pick up the summation of charges

Folding within the brain (gyrus) destroy signals, therefore there is not an accurate representation

Signal is band-pass filtered to remove low (<.5-1Hz) and high frequencies (>35-70Hz) because they do not reflect brain activity

EEG is biased to signals generated in superficial layers of cerebral cortex

The meninges, CSF and skull make it difficult to localise the source

The inverse problem: you can reconstruct scalp configurations if sources are known, but you cannot reconstruct the source if the scalp configuration is known

A) Artefact rejection and occular correction must occur in order to clean the raw signal

B) The signal is unaffected by sweating and electrical noise

C) Mathematical algorithms remove most of the noise and artefacts but cannot remove the noise generated from muscle clenching

D) Event related potentials involve multiple trials

A and D

B and D

MRI is utilised in reverse inference of cognitive processes based off the presence of activation

A magnetic field of 3T is usually used for functional imaging

Magnetisation on the z-axis is easily  measured because the movement is in the same direction as the magnetic current from the MRI

The head coil is used to send and receive radio frequency pulses

The Hydrogen protons precess either parallel of antiparallel and the precession frequency of protons depends on the strength of the magnetic field.

Phase coherence occurs when the protons are all doing the same thing

A radiofrequency (RF) pulse is applied perpendicular to the magnetic field which matches the precession frequency of the protons and is thus absorbed.

The RF pulse has two effects: 1) it tilts the magnetisation vector to the transverse plane and 2) it aligns the precession of the spins which means that the protons' rotations are "in phase". The transversely rotating magnetisation vector can then be recorded as a signal.

When the RF pulse is switched off the longitudinal magnetisation decays and the transversal magnetisation is re-established. This is known as the "relaxation" phase

The transversal magnetisation decays with different speeds depending on the tissue as a result of the differing density of protons, as they lose coherence because they will be influenced by other protons in their environment.

The signals from different protons will get out of phase with each other and begin to cancel each other out

Resonance means that protons will only absorb the RF that matches their precession frequency. By allowing the magnetic field to vary linearly, we can cause the resonance frequency to vary throughout the brain, this can be achieved using gradients.

1) divide the brain into slices and use a slice selecting gradient through the gradation of the RF pulse. 2) form a  phase encoding gradient gives us the y axis coordinate. 3) frequency encoding gradient gives us the x axis coordinate

Fourier transformation allows for the measurement and reconstruction of the 3D brain, but takes just under 1 second

Deoxygenated blood increased the signal (it is paramagnetic)

Neural activity is accompanied by a local oversupply in oxygenated and therefore provides a better BOLD signal

You can track which brain regions are active during cognitive tasks through oxygen levels

There is a temporal lag in the bold response (8 secs - haemodynamic response function) and the BOLD signal requires 16 secs to restore to baseline

High blood flow may mean relatively less oxygen is extracted

It is not valid to compare signals between different regions as the signal change is different

Excitation inhibition networks (EIN) are small and highly interconnected functional microunits. If they equal 0 it means the excitatory neurons and inhibitory neurons have cancelled each other out, and thus are not observed in the BOLD signal.

FMRI displays brain activities as blobs of activation, but for the most part the brain is not modular

Although we interpret the results of fMRI correctly it us not clear whether we have not accounted for extraneous variables

Temporal resolution is poor and spatial resolution is limited by the relatively large size of a voxel, which may contain up to 100,000 neurons

There is a multiple comparison meaning that a bonferroni correction must be made by dividing the alpha level by the number of t tests (50,000)

FMRI has been utilised to confirm how the human visual system represents information and how the visual content becomes available to higher level visual areas in the cortex

Kanwisher and colleagues (1997) discovered that the fusiform gyrus responded strongly to faces, indicating that the visual areas of the brain are modular 

It would be simply impossible if the brain had modules for everything

Kanwisher and colleagues (2002) suggested that the visual system might not be organised by specific object categories, rather it may be organised by where we encounter things in our visual field

Malach and colleagues (2002) argued that coding is driven by resolution needs and the fusiform face area is good for everything that requires high resolution

Gauthier and colleagues (1999) discovered that the the FFA responded strongly to greebles indicating that it is a specialised area for expertise rather than a modular area for faces

Reverse inference is a problem because: task A shows that brain region Z is active in this study. In other studies, cognitive process X is occurring when brain region Z is active. Therefore, in this study activity in brain region Z means that there is engagement of cognitive function X.

Brain region Z may not be exclusively used in cognitive function X, it may be active in other tasks.

Some researchers suggest that anterior regions of the brain is associated with abstract information and is more diffuse and harder to map, as compared to the posterior regions which represent more specific content

The frontal lobe may be recruited more strongly during more difficult tasks

A lot of brain regions are a part of a "multiple demand" network. This means that if we see activation of one of these, we still do not know what each individual brain region is responsible for

If the brain region is activated by many cognitive functions we learn very little about it, however, if the experimental setup succeeds in manipulating the cognitive process of interest, it can still provide useful information about the process

Only a few neurons in a voxel may be showing differences which can only be detected through more sensitive tasks.

The quality of the task to measure the cognitive process

When the null hypothesis is accepted we don't know the significance because statistic tests are designed to make the alternative hypothesis  difficult, not the null hypothesis, therefore we cannot interpret the null hypothesis results

The specificity of region for this cognitive process

Epileptic seizures arise from sudden excitation in groups of neurons with a loss of inhibitory potential

Intermittent derangement of the nervous system presumably due to a sudden, excessive, disorderly discharge of cerebral neurons

Temporal lobe epilepsy involves recurrent unprovoked seizures originating from medial or lateral areas of the temporal lobe

Simple partial seizures (with loss of awareness/consciousness)  and complete partial seizures (no loss of awareness/consciousness)

Surgical removal of the lesioned hippocampus can't cure, but can reduce the number of seizures.

The most common pathophysiology of TLE is hippocampal sclerosis and results from neuronal loss and gliosis

Partial seizures often originate from a  particular past of the brain and often spread to the whole brain.

Often occurs early in life (2 years plus)

Other aetiologies include past infections, tumours and vascular malformations

The temporal lobe includes the superior temporal gyrus, middle temporal gyrus and inferior temporal gyrus

He was having 10-20 major seizures per day due to bilateral hippocampi sclerosis and thus had both hippocampi removed

HM struggled with procedural memory, however, his declarative memory came back over time.

After his surgery he had fewer seizures, a normal IQ, a normal attention span and retrograde and anterograde amnesia

Retrograde amnesia leads to an impairment in one's ability to recall memories prior to an event, whilst anterograde amnesia leads to an impairment in creating new memories after an injury

Intact memory function relies on a neuroanatomical network, involving functional asymetry many brain regions including the temporal lobes which are the engine of memory

Medial temporal lobe structures are essential for memory

Medial temporal structures are more essential for anterograde memory

There is a distinction between declarative and procedural memory

The hippocampus was the region of the brain first identified to support memory and the hippocampal formation includes the dentate gyrus, CA1-CA3 and the subiculum

Patients have material-specific memory deficits related to involved medial temporal lobe (MTL)

Left MTL lesion results in verbal memory impairment whilst right MTL lesion results in non-verbal/visual memory impairments

The hippocampus is also known as Cornu ammonis and can be labelled CA1 to CA5

They are all correct

The above image is a schematic representation of the Medial Temporal Lobe

Information is integrated in sensory systems and is sent to the hippocampal formation for long term storage

Memories can be accessed by reciprocal connections between the hippocampal formation and the temporal neocortex

The  subcortex is part of the limbic system and is involved in higher order thinking. (sensory perception, generation of motor commands, spatial reasoning, conscious thought and in humans, language)

The hippocampal formation and surrounding structures are essential for learning and consolidating novel information.

The consolidation theory suggests that after a period of consolidation, information may be retrieved independent of involvement from the hippocampal formation

The multiple trace theory suggests that autobiographical/episodic experiences always require the hippocampal formation

The hippocampal formation is not necessary in relational memories between two arbitrary pieces of information.

Information must move through the hippocampal formation and surrounding structures for learning to occur, thus the hippocampal formation in the MTL are fundamental structures of declarative memory

Papez's circuit, frontal lobes and the diencephalon are all involved in memory

Papez's circuit and the amygdala form the limbic system which is integral in emotional memory formation

Regardless of the strength of an emotional experience the storing of the memory is always the same

Lesions of the limbic system result in a loss of conditioned fear, an impairment of fear learning and reduced memory for emotionally laden events

Papez's circuit is comprised of mamillary bodies (part of the hypothalamus), fornix, anterior thalamic nuclei, cingulate gyrus and the hypothalamas

Declarative memory impairment is least reliable when the hippocampus or the Anterior Thalamic Nuclei are lesioned

Lesions to Papez's circuit result in declarative memory impairment (poor relational memory/encoding)

The frontal lobe is involved in developing and implementing strategies for appropriate memory, encoding and retrieval

Dorsal Lateral Pre-Frontal cortex damage results in an impairment in remembering contextual detail i.e. the source of information, the chronological order of memories can result in confabulation (the production of statements involving bizaar distortions of memory)

There are a lot of connections withing the pre-frontal cortex that go to the peririhinal cortex

Diencephalon means interbrain and is comprised of the thalamus and the hypothalamus

The thalamus is connected to all regions of the brain and damage to a specific location will mean damage to a connection of a specific brain region and the damage results in the same problem as would occur id that brain region itself was damaged

Anterior and medial lesions are more likely to cause memory deficits than posterior or lateral lesions. This is because parts of the thalamus have a direct connection to the temporal lobe

Dense amnesic syndrome is associated with damage to the mammillo-thalamic tract, as it connects to the posterior thalamus and hippocampus

If the Medio Dorsal Nucleus and or the Internal Medullary Lamina is damaged but the MTT is spared, then there will be specific retrieval difficulties but preserved recognition

They are all correct

Dorsal Medial Thalamus damage results in deficits in selecting the appropriate information to be retrieved (active retrieval) due to reduced mental flexibility, whilst damage to the intralaminar results in deficits seen in semantic memory and memory retrieval

Lesions of the frontal lobe lead to impaired abilities to organise the encoding, retrieval and maintenance of memories

Learning involves synaptic plasticity which refers to the biochemistry of synapses changing, thus altering the effects on the post-synaptic neuron

Long term potention  refers to a long term increase in the excitability of a neuron in response to a a particular synaptic input , caused by repeated high frequency of that input

None of them are incorrect

Hebb's rule referes to growth processes and metabolic changes which occur in a pre-synaptic and post-synaptic neuron in order to increase the efficiency of firing in the post-synaptic neuron

LTP occurs in the hippocampus (particularly CA5 and the dentate gyrus, but also in the entorhinal cortex) and  in the prefrontal cortex, the motor cortex, thalamus, amygdala and visual cortex

LTP causes more glutamate receptors to be inserted in the post-synaptic neuron, more glutamate to be released and bushier dendrites

Sensitization refers to a single noxious stimuli causing an exaggerated synaptic response to repeat presentation of the noxious stimulus

Long term depression is resultant of low frequency stimulation at synapses and can decrease synaptic strength

Habituation refers to the process in which repeated stimulation reduces the strength of the synaptic response and thus reduces neurotransmitter

They're all correct

Maintaining information over time, in one's mind

The mental processes of acquiring and retaining information for later retrieval

The process of encoding information for sustained use

The ability to correctly recall something explicitly or implicitly learnt

A and c

A and b

C and d

Implicit memories cannot be recalled unless conditions are the same as when the information was encoded

Implicit and explicit memories were derived from dissociable cognitive theories

Procedural and declarative were named through analysis of performance on particular tasks

In studies of amnesia procedural/declarative distinction is less meaningful

Procedural memory is important in motor performance. And is supported by memory systems that are independent of the hippocampal formation.

Declarative memory can be independent of the environment, is relational and can trigger the remembering of related memories.

Declarative memory is of semantic knowledge i.e. how to perform a task

There are essentially 4 models of memory, 3 serial and 1 parrallel.

Attkinson and Shiffron Model (1968): Is depicted in the above picture. Sensory memory = echoic and visual. Working memory capacity = 5-9 chunks of information, and is the site where associations are formed between old and new information. Long term memory = stable system, structural and neural changes. Over time memories change. Memories are subjective.

Levels of processing model - Craik and Lockhart (1972): Information is retained according to the level of processing it has undergone. Shallow to deep continuum. Features maintenance and elaborative rehearsal.

Tulving's Model of Memory (1972-2001): From ablation studies. utilised Atkinson-Shiffron model. Separated LTM into components: procedural, episodic and semantic.

Parallel Distributed Processing: memory is the activation of connections in different areas (distribution) simultaneously (parallel). The pattern of activation is defined by the memory or knowledge. Learning means that the strength of connections between relevant sites is changed. Emphasis is not on the elements, but rather the connections and their strengths.

They're all correct

A) All models account for all data from research

B) Parallel models are more useful in amnesia studies

C) Tulving's model maps onto the amnesia state the best

D) Memory refers to the knowledge of an event or a fact, of which in the meantime we have not been thinking about, with the additional consciousness that we have thought of or experienced it before.

E) Semantic memory works by allowing an individual to re-experience, through autonoetic awareness, previous experiences and project similar experiences into the future (mental time travel)

B and c

C and d

C,d and e

The episodic context associated with a semantic memory fades over time

Episodic memories share many features with the semantic system, but is not a parallel system. (Tulving)

The systems are entirely parallel within declarative memory, which is dependent on the hippocampal system. Therefore, damage to the hippocampal system leads to the equal impairment of both the memory systems. Therefore, the systems are dissociable. (Squire and Zola)

Serial Parallel Independent Hypothesis (Tulving): Encoding into episodic memory relies on the semantic memory system, thus, episodic memory is a unique extension of semantic memory where retrieval can be supported by either or both systems.

They're all correct

No dissociation: damaging X or Y affects A and B equally

Single Dissociation: You damage X and if affects A but not B, when you damage Y is affects both

Double Dissociation: You damage X and it affects A and not B, you damage Y and it affects B and not A

Double dissociations mean that the systems are completely independent of each other

All are correct

It investigated three patients who had suffered very early bilateral medial temporal lobe injuries

All three had abnormally small bilateral hippocampi and relatively intact extra-hippocampi temporal lobes

All three cases have significantly impaired memory function , relative to intellectual capacity

Their everyday memory deficits included: spatial memory, temporal memory and episodic memory. But all had factual knowledge within the normal range

Despite their impairments they were able to be left alone

They had intact semantic memory but impaired episodic memory, which fit with Tulving's SPI model

Double dissociations exist but are rare

Individuals with down's syndrome have a reduced risk of developing DAT

The most common primary dementing illness, where neural tissue itself is affected by the disease

Definitive diagnosis can only be made on pathology and in life only a diagnosis of dementia of the alzheimers type may be made (DAT)

ApoE is present in late onset AD (60 years +), however, there are rare autosomal dominant cases involving mutations in three genes: amyloid precursor protein (APP), presinilin 1 (PSEN1), presinulin 2 (PSEN2). All of which alter production of amyloid beta peptides, which is the principle component of senile plaques

Strokes or head trauma may bring forward the time of onset of DAT

Onset is gradual and the course of the illness features a slow deterioration, which can be categorised into three main phases. 

Phase 1 lasts 2-3 years and includes the following symptoms: failing memory, muddled inefficiency in Activities of Daily Living. Spatial disorientation and mood heightening.

Phase 2 features a more rapid progress of deterioration. Intellect and personality deteriorate, dysphasia (problems with language), dyspraxia (trouble sequencing motor movements), agnosia (difficulty identifying objects) and acalulia (a loss of ability to understand mathematical functions) occurs. In addition, disturbance of posture and gait, increased muscle tone (even when relaxed) and delusions and hallucinations occur.

Phase 3 - terminal stage. Symptoms include: profound apathy, becoming be ridden, loss of neurological function, bodily wasting and pneumonia, as a result of inhaling food.

They're all correct

Probable AD: Deficits in 2 or more areas of cognition, progressive worsening of memory and other cognitive functions, no disturbance in consciousness, onset between 40-90, in the absence of any other causes and the presence of biomarkers (elevation or depletion in a blood profile)

Possible AD: Made on the basis of Dementia syndrome, can be made in the presence of another disorder, which is not considered to be the cause of dementia

Definite AD: Histopathological evidence of AD obtained through a biopsy or autopsy 

Pathology of AD: Grossly atrophied brain, mainly affecting the frontal, temporal and parieto-occipital lobes. Extensive degeneration of neurons, glial cell proliferation, extensive amounts of senile plaques, extensive amounts if neurofibrillary tangles.

AD commences in the hippocampus/Medial Temporal Lobes. It then spreads to the frontal cortex, and then to the parietal cortex 

Clinical patterns of cognitive impairment include: Anterograde memory (difficulties learnming new things, impaired delayed recall and poor recognition memory), Retrograde memory (temporal gradient - old memories are the sharpest), Wernicke's aphasia (difficulties finding the right words), visuospatial deficits and behaviour change

Behaviour change is due to the spread to the frontal lobe, Visuospatial deficits are due to the spread to the parietal lobes and anterograde memory impairments are due to the spread to the hippocampus and MTL

Treatment only improves the quality of life for the individual, it does not stop the progression of the illness

When bound by a specific neurotransmitter, Ion channels open and allow a specific ion to flow through

The influx of positively charged ions increases the likelihood of the firing of the post-synaptic neuron

GPCR utilise second messengers which act to either open a channel or alter the expression of genes in the nucleus

The terms neurotransmitter and neuromodulator can be used interchangeably in most cases

Excitatory pathways are mostly found in long projections throughout the cortex, whilst inhibitory pathways are mostly short local neurons, which form a dense web around and between the excitatory neurons.

Neuromodulation alters neurotransmitter release and neurotransmitter action at the post synaptic neuron

Neuronmodulation may cause changes in neural function or structure and sustained neuromodulation can drive changes in the brain related to synaptic plasticity.

GABA is the inhibitory neurotransmitter, whilst glutamate is the excitatory neurotransmitter

Serotonin (5-HT) in synthesised in the Raphe Nuclei and is cluster released to the entire brain, including the hippocampus, amygdala, brainstem and cortex

Noradrenaline (NA) is synthesised in the Locus Coeruleus and released to the thalamus, amygdala, hypothalamus and cortex

Dopamine (DA) is synthesised in the substantia niagra and the ventral tegmental area and is distributed to the amygdala, nucleus accumbens, pre-frontal cortex and striatum

Acetylcholine (Ach) is produced in the nucleus basalis of Meynert and the medial septal nucleus and is projected to the thalamus, neocortex and hippocampus

Histamine (HA) system: the neurons are located to the posterior hypothalamus

They're all correct

Drugs are either agonistic, prolong activation and increase the impact of the pathway, or antagonistic block the receptor and reduce activation and decrease the impact of the pathway

Neurotransmitters function can be altered by increasing or decreasing the synthesis of the neurotransmitter. An increase in some neurotransmitters lead to a decrease in production via negative feedback.

Both synthesis, transport and release of NT are fast 

Peptides, nucleosides, lipids and gases are non-traditional NT as they do not satisfy all the criteria

Glutamate is the same as glutamic acid and is synthesised in the brain from glutamine, which is released by cells neighbouring the neuron

The effects of alcohol on memory loss and sedation is a result of the agonist effects of alcohol on GABA

There are four major types of  glutamate receptors. 3 ion channels (NMDA, AMDA and Kainate receptors) and 1 GPCR (metabotrophic)

The NMDA receptor has at least 6 different binding sites, and therefore it has lots of complex functions. For example, it will only open if glycine is bound and magnesium isn't

Alcohol is an NMDA antagonist and blocks the signal of glutamate, whilst increasing GABA inhibition

Phencyclidine (PCP) and Ketamine  both are NMDA antagonists. Both  cause dissociative hallucinations and increase the risk of suicidal behaviour

Alcohol, PCP and ketamine all have different effects on the mind despite affecting the same receptor

The link between glutamate and psychosis is well known, there have also been other links to dopamine

NMDA receptors are associated with learning and memory and are likely to be relevant to schizophrenia and IQ

Inhibitory networks reduce the likelihood of neurons firing for their non-preferred stimulus

GABA is synthesised from glutamatic acid and can also be converted to and from glutamate

There are two types of GABA receptors: GABAa ion channel and GABAb GPCR

Epilepsy is caused by an abnormality in GABA neurons or receptors

They're all correct

The ventral Tegmental Area is associated with motivation and emotional response and reward, desire and addiction

Dopamine synthesis: tyrosine - DOPA - Dopamine - Noradrenaline

If an unexpected  reward occurs DA neurons become more active and release a burst of DA

After repeated associations between the reward and the beep, no DA will be released 

If a reward is expected and not provided DA neurons will be suppressed. Therefore DA doesn't code the actual reward, rather it codes reward vs expected)

If the gain or loss is unexpected then the feelings associated are often more  intense

The aversive feeling of cognitive effort reflects "opportunity cost"

Incentives can help with motivation because they counterbalance opportunity costs

Opportunity cost refers to everything else rewarding that you could be doing

Unpredictability adds to the boost of DA (better than expected)

For something to be addictive you must code losses as equally significant than gains

Cocaine blocks the re-uptake o dopamine after it is released, therefore increasing the dopamine signal as perceived by the post-synaptic neuron

Amphetamine (ice = pure, speed = less pure) reverse the uptake transporter causing the active expelling of DA and NA out of the neuron. They also prevent DA uptake.

Addictive dopamine drugs are always coded by the brain as better than expected as DA is released at the time of the beep and at the time when it enters the blood stream. This means that every time the dopamine drug is used the reward system codes it as better than before.

More addictive drugs are released slower than less addictive drugs

Drugs initiate wanting and cravings

Cognitive control is reduced by impaired function of the prefrontal cortex as a result of excessive dopamine

Failures of top down control contribute to the loss of control over the urge to take drugs

DA system might be less important in the behavioural/habit and cognitive aspects than the pleasant feeling

Noradrenaline is synthesis: tyrosine - DOPA - Dopamine - noradrenaline

High Locus Ceruleus (LC) /NA activity is involved in fight, flight, freeze and fornicate

NA causes a state of hyperarousal adapted for evolutionary important situations where individual or sexual fitness is involved

High levels of LC/NA activity can lead to stress, anxiety, panic attacks and mania

Stress and arousal can be depicted on an inverted U with high anxiety and sleep on either end

Moderate levels of LC and NA act to consolidate decisions of either exploring or exploiting one's environment

A burst of NA tips the balance and commits the individual to a particular behaviour or action

Neurons in the Locus Coeruleus are inhibited after firing due to a refractory period which acts to inhibit all other choices

The more salient the stimulus the smaller the burst of LC neurons and NA