Biopsych (unfinished)

The Nervous System (NS)

The human NS is a complex network of nerve cells and fibres that enables the brain to receive information about the environment and to command responses.

Nerves are cylindrical bundles of several thousand neuron axons (fibres)

Neurons are specialised cells in the brain and NS that transmit electrical impulses, enabling thought, speech, movement etc.

The CNS is the major division of the NS that includes all nerves in the central system. Its 2 main processes are controlling behaviour and regulating the body’s physiological processes.

The brain and the spinal column/ cord are the 2 main components of the CNS, but the brain stem is often included too. The brain is responsible for the integration and co-ordination of information received and decision making in response, whereas the spinal column is a column of nerves that links the brain stem with the PNS.

The PNS includes all the nerves external to the CNS. The Somatic NS carries both sensory information about the internal and external environment to the CNS and motor instructions from the CNS to the PNS. This means it can control skeletal (voluntary) muscle movements. The Autonomic NS works with smooth (organ) muscle to affect action and control involuntary bodily processes.

The Sympathetic NS is responsible for explosive action, and the fight/freeze/flight response to perceived threats. Whereas the Parasympathetic NS works to rest and digest to preserve homeostasis. These work on a principle of reciprocal inhibition.

Neurons and synaptic transmission

Neurons communicate through the process of synaptic transmission, where the electric action potential is briefly carried by chemical neurotransmitters. When the action potential reaches the axon terminal of the pre-synaptic neuron, neurotransmitters in the vesicles are released to diffuse across the synaptic gap to the post synaptic neuron. If an inhibitory neurotransmitter is received at the specialised receptor cells, IPSP is generated, which leads to a decrease in voltage. Whereas if the neurotransmitter is excitatory, EPSP is generated and the resting pd increases.

Whether the post-synaptic cell fires is determined by the summation or calculation of these charges.

Spatial summation is where EPSPs are generated from many different pre-synaptic neurons, while temporal summation is the high frequency action potentials of a single pre-synaptic neuron. If the membrane potential reaches -55mV (from its resting potential of -70mV) the post-synaptic neuron fires an action potential and the process continues.

This graph demonstrates the membrane potential of a post-synaptic neuron before, during and after an action potential is generated.

Endocrine System

Similarities and differences between the NS and endocrine system

Similarities:

• both use chemical messengers
• they work together to regulate body processes
• receptors are specialised in both systems (cells or parts of post-synaptic neurons)

Differences:

Glands and hormones in the endocrine system

The pituitary gland is seen as the main gland in the endocrine system, however this is controlled by the hypothalamus. The hypothalamus is significant because it can create instructions in both the endocrine and nervous systems (it brings the systems together).

The pituitary gland is responsible for the release of hormones from glands in the body. These hormones travel through the blood stream and bind to the receptors at their target organs or glands, to influence behaviour.

The endocrine system uses a negative feedback loop (this means the system responds when the conditions are no longer ideal) to maintain homeostasis (the regulation of internal bodily functions in an optimal state).

Cortisol

Note: I need to be able to give an example of a hormone - not adrenaline

Gland Hormone

The hypothalamus releases CRH in the brain, which travels to the pituitary gland and instructs it to release ACTH. ACTH then travels through the blood stream, when it reaches the adrenal cortex, the cortex is instructed to secrete cortisol.

Cortisol release is generally used as a second fight or flight wave: it is referred to as chronic stress (plan C) or the HPA axis.

Cortisol release evolved because of its adaptive nature, so cortisol in the short term can have many benefits:

• increased brain performance
• better memory
• changes to salt and water levels in body (to fight the predator)
• increase of blood pressure

However, in the long term, this can become dangerous and lead to many problems:

• difficulty concentrating
• heart disease
• more susceptible to diseases - lower immunity
• exhaustion

Fight-or-flight response

Stress can either be acute or chronic. Chronic (plan C - there is no plan B) is explained with the release of cortisol, and is not 100% necessary.

Plan A demonstrates how the NS can work with endocrinal back up.

Evaluation

• Fight or flight are not the only responses to stress in humans: the freeze response is a momentary parasympathetic brake on the motor system as a form of behavioural inhibition (Gray et al). It is controlled by the periaqueductal grey, in the brain, and consists or a temporary heart rate deceleration amongst other things. Neuroimaging studies in humans have demonstrated the importance of this area of the brain, and furthermore the importance of shifting between freezing and active defence modes. This means that the fight or flight theory does not fully describe the stress response in all humans: it does not recognise the protective element of the freeze response.
• When in a stressful situation, females tend to have a release of oxytocin that was not studied at the time fight or flight was theorised. The oxytocin release is important because it is linked to the “tend and befriend” response to stress, due to its link to affiliative behaviours. This provides an extra step that the fight or flight explanation doesn’t refer to. Furthermore, in humans oxytocin has been seen to inhibit glucocorticoids (stress hormones), suggesting it could protect against the effects of chronic stress - this is important real world application.
• Luckow et al (1998) found that “seeking and using social support” was massively significant in females (but not at all in males), (p<0.0000001). This is significant because it represents the importance of oxytocin as a limitation of the fight or flight explanation, because the fight or flight response doesn’t refer to other stress responses in those with XX chromosomes.
• There may also be different stress responses for different stressors: participants who experienced acute social stress were more likely to engage in prosocial behaviours (Von Dawans et al), thus a tend-and-befriend response may be present in some situations for non-females. Furthermore, prosocial behaviour may actually be a protective pattern against stress.

Localisation of function

Localisation of function is the theory that particular regions of the brain are responsible for specific functions such as language. It means that behaviours originate from specific, discrete regions. The antonym of this is that function is distributed.

Cortices

FM (radio - the motor cortex is in the frontal lobe)

PS (play station - the somatosensory cortex is in the parietal lobe)

wTAf (teaching assistant/ wtf - Wernicke’s area in the auditory cortex in the temporal lobe can cause fluency aphasia)

OV (ovulation - visual cortex is in the occipital lobe)

Visual information is received as light energy in the photoreceptors in the retina, before being translated in the ganglion cells in the retina. It travels along the optic nerve as an impulse before being received in the thalamus (relay station). Then it is directed and interpreted in the visual cortex in the occipital lobe.

Auditory information is received in the cochlea in the inner ear, and is translated in the Organ of Corti. It travels along the auditory nerve and is first received in the brain stem (where basic decoding takes place), then the thalamus then the auditory cortex in the temporal lobe.

The somatosensory cortex is the part of the brain that receives and interprets information relating to touch, whereas the motor cortex is the part of the cortex with motor origin. Both cortices have the whole body represented, but it is represented contralaterally, upside down and not proportionally. The size of the body part on the cortex is due to the sizes of sensory receptors and muscle effectors, not the actual size of the body part.

Note: the somatosensory has some features that the motor doesn’t because you cannot move them e.g. gums or head.

This is called the somatosensory and motor homunculus.

Language centres

There are two main language centres in the brain: Broca’s area and Wernicke’s area.

Broca’s area is responsible for the production of language and is found in the posterior portion of the left frontal lobe. It was theorised by Paul Broca who studied patients who could understand but not produce language, during post-mortem analyses it was found that these patients had lesions in one specific area. There are two regions of Broca’s area: language and demanding cognitive tasks (Fedorenko et al, 2012).

Wernicke’s area is responsible for the understanding and comprehension of language. It is located in the posterior portion of the left temporal lobe. Wernicke suggested that language involves separate motor and sensory regions located in different cortical regions. This was supported when there was a neural loop found which ran between Broca’s and Wernicke’s areas (the arcuate fasiculus).

When either of these areas become damaged, a person can develop aphasia. This is a language deficit. There are 3 types:

• Broca’s aphasia aka Expressive aphasia. This is when there is damage to Broca’s area so a person struggles to produce language
• Wernicke’s aphasia aka Fluency aphasia. This is when a person cannot comprehend or interpret language, however they can often produce something that sounds like language because it uses the same sounds.
• Global aphasia. This is when both language capabilities are lost due to extensive damage.

Evaluation (preference for localisation, over-ridden by a drive for adaptation)

• The initial PM research on aphasia led to the theories about specialised language centres, especially Broca’s area.
  • But these are case studies which cannot allow researchers to establish cause and effect between the lesions and the language deficits.
  • Furthermore, Dronkers et al (2007) used MRI scans and found that the damage was more extensive than initially concluded so the damage was not as localised. They suggested that language is significantly more complex and can involve numerous regions of the brain.
• Case study of VJ, whose convulsions led to bilateral hippocampal atrophy. Even after convulsions ended, his performance seemed normal however, his episodic memory suffered. This is similar to the studies of HM who had his hippocampus removed. Some memory function was recovered, however the cortex was unable to compensate for the damage to the hippocampus. It seems like the hippocampus is an area of the brain that doesn’t perform as expected, this may be because it is the only area of the brain that can form new neurons - only some areas of the brain are very localised.
• Echolocation is something that blind people can learn to do to “see” the surroundings. The auditory information from the clicking is received by the visual cortex (not the auditory), which demonstrates that the cortex is adapting to maximise functioning.
• Lashley experimented on rats with surgically induced brain lesions and created 2 significant theories. Mass action suggests that the degree of impairment after damage is directly proportional to the amount of brain damaged, not the location. The Principle of Equipotentiality suggests that every aspect of the cortex has equal potential to perform a function (this is how there can be a recovery of function without neural - cortex recovery)

Lateralisation and split-brain research

Hemispheric lateralisation is the theory that each hemisphere is specialised for distinct ways of processing and particular functions. Even though the two hemispheres are separate, they are connected by the corpus callosum, which is a bundle of nerve fibres which allows the communication of signals between the two hemispheres.

There are somatosensory, auditory and visual cortices in both hemispheres, and the control of movement and reception is contralateral. However there are some differences in the functions associated with each hemisphere:

• LEFT: detail-oriented (supported by lots of research); language functioning is localised to the left (in 95% of right handed individuals); planning; analytical thought etc
• RIGHT: bigger picture concepts; facial recognition; non-verbal cues; emotions; impulsivity and creativeness

Remember that piece of research where there was damage to one of the hemispheres, and then the patient was asked to draw shapes e.g. M made of zs or triangles etc.

There are more similarities than differences between the brains of XX and XY individuals, but note that XX individuals tend to have more connected brains whereas XY are more likely to be “left-oriented”.

Evaluation

• There is more evidence for language being specialised to the left hemisphere. While the right hemisphere has some linguistic capacity e.g. short words, simple grammatical comparisons (e.g. did they/didn’t they), it is unable to process long sentences or words that cannot be broken down. This is important because it means that, while there is a degree of flexibility, language functioning is specialised to the left hemisphere.
• Research on JW found that while recognition of familiar others is specialised to the right hemisphere, the left hemisphere has a preference for self-recognition (to a very high degree of significance). Speaking about lateralisation too simply is a problem, but this provides evidence for it but in a more complex way.
  • It was found, however, that both hemispheres were capable of self-recognition so hemispheric lateralisation is not 100% determined.
• EB had his entire left hemisphere removed at 2.5 yrs and after intensive rehab was able to recover most of his language functions. This suggests that the brain is very able to adapt.
  • However, he had a low IQ and systematic testing revealed difficulties with grammar which suggests that while the right hemisphere was able to create a left-like neural blueprint (copy what would have been on the left hemisphere), it was unable to fully take on the role of the left hemisphere.
• Split brain research (below) can be used for this
• Szaflarski et al (2006) found that language became more lateralised to the left hemisphere as age increased, but after 25 it became increasingly less lateralised. This means that lateralisation doesn’t appear to be constant in an individual’s life and changes as they experience normal development.

Split brain research (supports hemispheric lateralisation)

Split-brain research refers to the studying of individuals who have had split-brain surgery, in order to understand more about the individual specialisms of each hemisphere. In this surgery the corpus callosum is severed or burned in order to minimise the frequency and intensity of epileptic seizures (to stop them spreading between the two hemispheres). However, using split brain patients is difficult because the surgery is rare, so it has the same limitations as case studies.

Sperry’s research into SB patients contained 11 participants with commissurotomies (severing of the CC) and a control group that did not have any hemispheric disconnection. It was a natural experiment with elements of case-studies (due to a small sample size) where participants were measured on their performance of certain tasks in a laboratory.

Participants were asked to look at a focal point in the screen and there was a brief showing of a visual stimulus in either the left or right field of vision. If it was in the left FoV (RH), the participant was unable to name it (sometimes they even claimed they couldn’t see anything), but could identify it from a list of words, or draw it with their left hand then name it. When a stimulus was shown to the right FoV (LH), participants could name the stimulus.

The two hemispheres appeared to work independently, e.g. if a stimulus was shown to the LH, then the RH, it would not be recognised and was perceived to be new. Similarly when an object was “shown” to each hand then placed in a grab bag, each hand would often pick up and reject the object the other hand was looking for - they worked completely separately.

Later research showed that when the L FoV (RH) was shown an Arcimboldo fruit face, it saw the face first, but when the same painting was shown to the R FoV (LH), it only recognised the fruit.

Evaluation of SB research:

• High internal validity because the brief duration of the visual stimulus ensured that there was not enough time for the FoV to shift so the other hemisphere would have access to the information. This is significant because it stops information travelling between the hemispheres both internally and externally which means that we can be sure of what part of the brain performs which task.
• Another strength is that the small sample size allowed experimental data to be collected along side information from case studies. This is good because rich information could be collected e.g. SB patients often had STM deficits, difficulties with concentration and orientation problems.
  • This is also a limitation but because there is such a small number of individuals who have had commissurotomies, this is not that significant.
• There was significant variation in the SB sample: there was non-standardised CC severing (e.g. sometimes it was partial etc) so not all the variables were controlled and this could have impacted the performance in tasks.
• Furthermore, there is a confounding variable in the control group. Not only did they have intact CCs, but they also did not have epilepsy. This means that researchers cannot be sure whether the observed differences in performance were due to long lasting and severe epilepsy (which was also treated by ineffective drug therapy in the long term) or the CC severing. This significantly challenges the validity of the study.

Plasticity and functional recovery of the brain

Plasticity

Plasticity refers to the brain’s ability to adapt in response to experience. Any experience or change in the environment can lead to plasticity, but a key one is learning: neural challenge.

When an individual practises a skill, or revises, neural networks in the brain can be established and each time this behaviour is repeated, this pathway is strengthened. Neurons in these pathways can have preferences for connections (they like to keep doing the same thing), which can lead them to adapt e.g. strengthen or change pathways to make a skill more efficient. Even accidental interaction between neurons (it doesn’t need to be an intentional practising of a skill) can demonstrate plasticity. Going through life provides the brain with many opportunities to adapt.

Evaluation (of methodology - we know it happens)

• Kemperman put rats into an enriched environment with notable cognitive challenge (difficult maze etc) and saw that there were new neurons in the rats’ hippocampi. Since it was a lab study, cause and effect can be found with certainty. This is an example of neuroplasticity.
• Draganski used MRIs of medical students before and after their final exams and saw that there was a change in volume of the hippocampus. This cannot be used to provide causal inferences, however the degree of similarity between the findings of this research and Kemperman’s are significant. They both have high reliability and when you combine the research it suggests that cognitive challenge can alter the hippocampus, which demonstrates the nature of plasticity.
• McGuire et al found that London taxi drivers had more grey matter in their brain, and a bigger posterior hippocampus than the control group when tested using MRI machines. This is linked to their extensive spatial navigation. This data has a high reliability, but it cannot be used to draw causal inference between taxi work and hippocampal growth. However, there was a dose-response relationship between the length of time being a taxi driver and the significance of difference in the brain.
• Even though there is a rapid growth of synaptic connectivity in childhood, followed by a pruning during the teen years, plasticity can still occur as humans age. It is important to note that after early adulthood, more effort is required to maintain plasticity (e.g. practising new skills), but it can still happen. This demonstrates that the process of neuroplasticity is can still be influenced by individual differences.

Functional recovery

Functional recovery is when the brain can restore skills or behaviours after damage has occurred. This can happen because of the plasticity of the brain and it often works with structural reorganisation by moving the functions of areas damaged by trauma to other undamaged areas.

Ways the brain can reorganise:

• Re-routing: a neuron that has lost its target seeks a new connection to enable communication around the damaged area
• Sprouting: nerve fibres grow and become bushier to make new connections and enable connection
• Recruitment: the homologous area on the opposite hemisphere begins to perform specific tasks previously undertaken by the damaged are. Note: this tends to be a last resort because it is a difficult (metabolically) and drastic change.
• Denervation super-sensitivity: this is when intact cells become hyper-sensitive to stimulation so larger results are experienced from the same amount of neurotransmitters.
• Unmasking: dormant synapses which were functionally blocked (e.g. as a result of under-stimulation) are “revealed” when input increases

Congenital damage is when brain damage resulted from development so it was present at birth.

Acquired damage is whem brain damage results from later trauma or insult.

Evaluation (what factors can affect FR - is it universal and the same all the time?)

• As with plasticity, the more effort you tend to put in, the more significant recovery can be. This can be in the form of practise or therapy/rehabilitation. An example of this is EB (left hemisphere removal at 2.5 years) who had intensive rehab from 5 years until his fluency improved. Later, he had no significant language problems but his IQ was still lower than expected.
  • Low IQ is not 100% because of loss of LH, but it is likely that it could be. This would mean that functional recovery does not mean any damage is undone.
• In an acquired damage group, the best predictor of subsequent IQ was lesion size. Regardless of age or time since damage, the larger the lesion, the poorer the IQ. This links to Lashley’s Mass Action principle which suggests that it is the amount of damage, not the location of damage that can predict whether or not function will recover.
• The Kennard Principle suggests that the younger the individual is when the damage occurs the better their chances of recovery.
  • However, this is only true for acquired damage. For congenital damage, there was seen to be a negative relationship between a child’s IQ and their age. This is when as they got older, the difference in functioning between them and their peers became clearer because they “struggled to keep up”
  • This links to the crowding hypothesis: this suggests that a brain which is damaged congenitally, can often initially compensate with maximal rewiring, however this individual would struggle significantly more if there was more damage. Or alternatively they would have difficulties adapting to acquire further mental skills (e.g. onset of school). It’s as if they “ran out of wiring”
• Based on a study of 769 patients on the US traumatic brain injury systems database, Schneider found that individuals are 7x more likely to be disability free after a moderate to severe brain injury if they have a college level education. He called this “cognitive reserve”. We could assume that the brain has learnt how to use plasticity then they have an ability to recover.
  • However, in America you have to pay more for college, so it can be assumed that these families were wealthier. They may have been able to afford better medical care etc. This provides a confounding variable.
  • Also the data is secondary, non-experimental data so not only can it not be used to draw causal inferences, but it could also lack a level of validity as a result.
• Not every part of the brain can recover with the same levels of success. E.g. HM or VJ were unable to mend parts of their hippocampus because regions with specialised circuitry cannot mend in the same way.

Ways of studying the brain

PM: post-mortem examinations involve studying the actual, physical brain of a deceased individual to look for lesions or causes for any phenomenological afflictions or mental health disorders an individual may have struggled with e.g. Broca’s work with Tan. They are used to find the underlying neurobiology of a particular behaviour. It is useful for learning about the ways that certain psychiatric disorders can physically affect the brain e.g. increased ventricular size in schizophrenic patients.

To analyse brains, the brain of a patient can be compared to a neurotypical control.

fMRI: functional magnetic resonance imaging measures changes in brain activity by looking for changes of blood flow to certain areas. This allows researchers to create a visual map of activity in the brain, rather than just anatomy, to deduce that certain regions are involved in task performance.

EEG: Electroencephalograms measure electrical activity in the brain using electrodes on the scalp. Signals are graphed over a period of time and abnormal patterns or arrhythmias (no particular rhythm) can be used to diagnose disorders e.g. epilepsy. Data is gathered and summated or superposed to create a graph where different types of waves (alpha, beta, delta and theta) can be identified by their frequency.

From this data you get rhythmic patterns of neural oscillations because the neurons are in synchrony. It provides generalised information on the activity of many neurons.

ERP (event-related potentials): this relies of EEG data to pinpoint/ time-lock certain spikes or troughs of brain activity to specific stimuli. It is difficult to detect, but after a stimulus is shown it is possible to see tiny voltage changes which must be averaged together to see the impact. These responses can be divided into 2 categories: sensory responses (signals are generated before the first 100ms) or cognitive responses (signals are generated after the first 100ms).

Note: the strengths and limitations of each of these methods can often offset each other.

Clarity of data:

• Spatial resolution: region/ locality
• Temporal resolution: time

Biological rhythms: circadian, ultradian and infradian and the differences between them

Note: you could have an essay on 1 or more bio rhythms, or even circadian. But for infradian and ultradian by themselves, it shouldn’t be more than 8 ish marks.

Biological rhythms are patterns of physiological processes that occur and recur with a predictable regularity. They govern the activity of cells and organs.

There are 3 types of biological rhythm:

• Circadian (circa dian - approx 24 hours)
• Ultradian (under 24 hours e.g. BRAC)
• Infradian (any rhythm in excess of 24 hours e.g. menstrual cycle)

In the exam you must stress the rhythmicity.

Circadian

Circadian rhythms are any bodily cycle that lasts about 24 hours, even in the absence of environmental stimuli (if there are no environmental cues, a rhythm is said to be free running). Circadian rhythms influence so many aspects of our body including sleep-wake cycles, body temperature and hormone secretion.

Irregular rhythms, or when the CR is not in sync with the environment (e.g. jet lag or shift work), can lead to things like low mood and motivation, poor cognitive functioning, or other more serious conditions such as heart health, diabetes or bipolar disorder.

Circadian rhythms are governed by the suprachiasmatic nucleus which sits close to the hypothalamus. The SCN is entrained (synchronised to stimuli) by light signals from the brain: when the SCN receives signals of light in the morning, the “master clock” is reset in a time-dependent manner. When the SCN is reset, it sends signals to the peripheral oscillators (other cells in the body, each with their own body clock) to ensure there is synchrony.

Note: sleep and wakefulness are not governed by circadian rhythms alone, homeostatic sleep pressure is what makes us want to sleep more and more the longer we have been awake.

Evaluation (not discussing whether this exists, but the effects and individuals differences etc)

• Xie et al (2019) found that participants held in a circadian misalignment condition experienced many negative problems e.g. glucose imbalances, insulin action and appetite control.
• Links between a lack of synchrony and harmful side effects throughout life. During pubescence, this lack of regulation can impact brain development and lead to a susceptibility to mood disorders.
• Chronotypes are people’s natural inclinations for wake and sleep patterns, so the technicalities about the precise time of the circadian rhythm can be partly influenced by genes. Approx 1/3 are larks, 1/3 are night owls and 1/3 have a mixed pattern. The societal need to follow a 9-5 work day leads many night owls to becoming chronically socially jet lagged, this can result in diminished integrity of white matter in the brain and increased risks for things like depression and alcohol use.
• Nikbakhitian et al (2021) used an accelerometer (objective measure) derived sleep onset time (SOT) for over 100,000 participants. An association was discovered between cardio-vascular disease and SOT either before 10pm or after 11pm, irrelevant of sex, previous CVDs etc. (RWA)

Ultradian

An example of an ultradian rhythm is the BRAC: Basic Rest Activity Cycle - a 90 minute cycle of alertness and sleep stages (Kleitmann).

#ladder of sleep cycles diagram

Sleep progresses through 5 (sometimes 4 because stage 4 is difficult to distinguish from 3) key stages in a ladder process. The evolutionary benefit of this is that is someone was woken up early, they will have had the benefits of each stage of sleep.

NREM sleep: non-REM sleep. It is slow-wave sleep (stages 1-4)

REM sleep: Rapid Eye Movement sleep. This is significant because it is paradoxical (the EEG of someone in REM sleep looks almost indistinguishable from someone who is awake), and desynchronised (there is no predictable pattern of electrical activity over the cortex). Humans dream when they are in REM sleep, this is also where emotional processing occurs. Heart rate increases and breathing gets shallower.

Stage 1: light sleep where we feel drowsy and muscle activity slows down: the brain has alpha waves

Stage 2: slightly deeper sleep, breathing and heart rate slows. Neural activity is characterised by theta waves

Stage 3: deep sleep where theta waves begin to turn into delta waves

Stage 4: very deep sleep where healing and repair occur. This is also where sleep-walking occurs

As the night progresses, the length of stage 4 sleep decreases, while the time spent in REM increases. This is also true of a lifespan.

Evaluation

Infradian

There is some (slightly sketchy) evidence for weekly infradian cycles, but this is limited so we focus on the menstrual cycle instead.

Make sure you focus on the fact that this is a biological rhythm for reproduction, not just a period thing.