Bio psychology L6-10 Flashcards

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1
Q

Describe localisation of function

A

refers to the principle that functions (e.g. vision, hearing, memory, etc.) have specific locations within the brain

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2
Q

Where are the visual centres
What do they do (brief)

A

Visual Cortex – The visual cortex processes information such as colour and shape. It is in the occipital lobe of BOTH hemispheres of the brain.

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3
Q

Describe the process which occurs within the visual cortex

A

Visual processing starts in the retina where light enters and strikes the photoreceptors. Nerve impulses from the retina are transmitted to the brain via the optic nerve. The majority terminate in the thalamus, which acts as a relay station, passing the information onto the visual cortex.

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4
Q

Where are the auditory centres located
What do they do

A

Auditory Cortex – The auditory cortex processes information such as pitch and volume. It lies within the temporal lobe in BOTH hemispheres of the brain

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5
Q

Describe the processes within the auditory centres

A

The auditory pathway begins in the cochlea in the inner ear, where sound waves are converted to nerve impulses, which travel via the auditory nerve to the auditory cortex. Basic decoding occurs in the brain stem, the thalamus carries out further processing before impulses reach the auditory cortex.

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6
Q

Where is the motor cortex located, what is it responsible for ?

A

The motor cortex is responsible for voluntary movements. It is located in the frontal lobe of BOTH brain hemispheres.

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7
Q

Describe control within the motor cortex

A

Different parts of the motor cortex control different parts of the body. These areas are arranged logically next to one another. Damage to this area can cause a loss of muscle function/paralysis in one or both sides of the body (depending on which hemisphere/hemispheres have been affected)

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8
Q

Where is the somatosensory cortex

A

It is located in the parietal lobe of BOTH hemispheres.

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9
Q

What is the somatosensory cortex responsible for

A

The somatosensory cortex is responsible for processing sensations such as pain and pressure

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10
Q

What are the language areas?

A

Broca’s area
Wernickes area

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11
Q

Describe the Broca’s area

A

– This area is named after Paul Broca who treated patients who had difficulty producing speech

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12
Q

What does damage to the Broca’s area cause? Why?

A

He found that they had lesions to the LEFT hemisphere of the frontal lobe. Damage to the Broa’s Area causes Expressive Aphasia. This disorder affects language production but NOT understanding. Speech lacks fluency and patients have difficulty with certain words which help
sentences function (e.g. ‘it’ and ‘the’).

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13
Q

Where is the Wernickes area?

A

This area is in the LEFT hemisphere of the temporal lobe.

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14
Q

Describe the wernickes area

A

Carl Wernicke found that patients with a lesion to this area could speak but were unable to understand language. Wernicke concluded that this area is responsible for the processing of spoken language.

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15
Q

What does damage to the wernickes area cause?

A

The Wernicke Area is connected to the Broca’s Area by a neural loop. Damage to the Wernicke’s Area causes Receptive Aphasia. This disorder leads to an impaired ability to understand language.

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16
Q

What are the strengths of localisation of function?

A

There aren’t any :o

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17
Q

What are the weaknesses of localisation of function?

A
  • Motor and somatosensory functions are highly localized to specific cortex areas, while higher functions like personality and consciousness are widely distributed. Language functions involve networks of brain regions, though components like speech production may be localized to areas such as Broca’s Area.
  • The equipotentiality theory (Lashley, 1930) posits that higher mental functions are not localized. It suggests that intact cortical areas can assume the functions of damaged areas.
  • Dronkers et al. (2007) re-examined Broca’s patients’ brains with MRI, finding multiple damaged areas. Lesions in Broca’s Area cause temporary speech disruptions but not severe language impairment, indicating that language is more widely distributed (less localised)
  • Communication between brain areas may be more crucial than specific regions. Dejerine (1892) described a patient who couldn’t read due to damage between the visual cortex and Wernicke’s area.
  • Bavelier et al. (1997) found individual differences in brain area responsibilities, with silent reading activating different regions, including the right temporal lobe, left frontal lobe, and occipital lobe, suggesting that silent reading lacks a specific brain location.
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18
Q

what is contra lateral organisation?

A

The hemispheres of the cerebrum mainly represent the opposite side of the body,

For example, the left hemisphere of the cerebrum controls movement, sensations and visual and auditory processing on the right side of the body and vice versa.

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19
Q

Define hemispheric lateralisation

A

certain functions are principally governed by one side of the brain

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20
Q

What has research shown us about hemispheric lateralisation?

A
  • in most people language centres are lateralised to the left hemisphere. Whereas, the right hemisphere is dominant for visuo-spatial functions and facial recognition.
  • The Broca’s Area was thought to be responsible for the production of speech, however, this is now thought to involve a wider network than just the Broca’s Area. Damage to the Broca’s Area leads to expressive aphasia.
  • The Wernicke’s Area is considered to play a vital role in understanding language/interpreting speech. Damage to the Wernicke’s Area leads to receptive aphasia.
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21
Q

How are our hemispheres connected?

A

By a bundle of nerve fibres known as the corpus callosum which enables information to be communicated between the two hemispheres. Many researchers suggest that the two hemispheres work together to form most tasks as part of a highly integrated system

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22
Q

What are the strengths of hemispheric lateralisation?

A
  • It makes sense from an evolutionary perspective. It increases neural processing capacity, which is adaptive. By using one hemisphere to engage in a particular task it leaves the other hemisphere free to engage in another function. Rogers et al. (2004) found that hemispheric lateralisation in chickens is associated with an ability to perform two tasks simultaneously (finding food and being vigilant for predators).
  • Patients who have extensive damage to their left hemisphere can experience global aphasia (loss of speech production and speech comprehension). This suggests that language is lateralised to the left hemisphere.
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23
Q

What are the weaknesses of hemispheric lateralisation?

A
  • Lateralisation patterns shift with age (Szaflarski et al 2006) with most tasks generally becoming less lateralised in healthy adulthood.
  • JW (split-brain patient) developed the capacity to speak using his right hemisphere, so that they could speak about information presented in either the left visual field or the right visual field (although he was more fluent if information was presented in the left). This shows language is not lateralised entirely to the left hemisphere (Turk et al. 2002).

-If one hemisphere is damaged, the opposite hemisphere can compensate. Danelli et al. (2013) studied EB, a 17-year-old Italian boy who had nearly his entire left hemisphere removed at age 2.5 due to a benign tumor. EB’s language appeared almost normal in everyday life, but testing revealed subtle grammatical issues and lower scores in picture naming and reading loan words. This shows that language function can be largely preserved after left hemisphere removal in childhood, though the right hemisphere alone cannot perfectly master all language components.

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24
Q

Be able to draw and label areas of the brain

A
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25
Q

What is a loan word?

A

Words adopted from another language e.g. café

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26
Q

What is the purpose of cutting the corpus callosum in patients with epilepsy?

A

Cutting the corpus callosum prevents the violent electrical activity caused by epileptic seizures from crossing from one hemisphere to the other, creating split-brain patients.

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27
Q

Who investigated split-brain patients and how is information processed in their brains?

A

Sperry and Gazzaniga (1968) investigated split-brain patients. Information from the left visual field goes to the right hemisphere, and information from the right visual field goes to the left hemisphere.

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28
Q

What happens in split-brain patients when the corpus callosum is severed?

A

In split-brain patients, the severed corpus callosum prevents information presented to one hemisphere from traveling to the other.

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29
Q

How did Sperry and Gazzaniga conduct their split-brain patient experiments?

A

Patients stared at a dot in the center of a screen, receiving visual information in either the left or right visual field. They responded using their left hand (right hemisphere), right hand (left hemisphere), or verbally (left hemisphere), without seeing their hands.

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30
Q

What is the result when split-brain patients see an image of a dog in their right visual field?

A

When shown an image of a dog in their right visual field, split-brain patients can verbally identify “dog” because the information reaches the left hemisphere’s language centers.

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31
Q

What is the result when split-brain patients see an image of a cat in their left visual field?

A

When shown an image of a cat in their left visual field, split-brain patients cannot verbally identify “cat” because language centres exist in the left hemisphere. But they can draw it with their left hand, controlled by the right hemisphere.

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32
Q

What are the strengths of split-brain research?

A
  • Experiments on split-brain patients are highly controlled and scientific.
33
Q

What are the weaknesses of split-brained research?

A
  • the disconnection between the hemispheres was greater in some patients than others.
  • Some split-brain patients have experienced drug therapy for much longer than others.
  • The comparison groups were not considered to be valid as they were often people with no history of epileptic seizures.
  • Many studies using split-brain patients have as few as three participants, making it hard for results to be generalised to the target population.
  • The data from this research is very artificial. In the real world a severed corpus callosum can be compensated for by the unrestricted use of both visual fields. This means the research lacks ecological validity.
34
Q

What is brain plasticity.

A

the ability of the brain to modify the structure and function based on experience.

Plasticity allows the brain to cope better with the indirect effects of brain damage, such as swelling or haemorrhage following a road accident, or the damage resulting from inadequate blood supply following a stroke.

35
Q

Evaluate brain plasticity

A

+ Kuhn et al. (2014) found a significant increase in grey matter in the hippocampus, visual cortex and cerebellum of the brain after participants played video games for 30 minutes a day over a two-month period.

+ Davidson et al. (2004) demonstrated the permanent change in the brain generated by prolonged meditation. Buddhist monks who meditated frequently had a much greater activation of gamma waves, which coordinate neural activity, than students who had no experience of meditation.

+ Maguire et al. (2000) found that the posterior hippocampal volume of London Taxi drivers’ brains was positively correlated with their time as a taxi driver and there were significant differences between taxi drivers’ brains and those of a control group

36
Q

Define and briefly describe functional recovery

A

Functional recovery is where the brain recovers abilities previously lost due to brain damage, it is an example of plasticity.

Research suggests that young brains are more plastic, however, the brain is capable of plasticity and functional recovery at any age.

Studies have suggested that women recover from a brain injury quicker than men do.

37
Q

Define and describe the three stages of functional recovery.

A
  1. Neuronal Unmasking - Dormant synapses are activated to compensate for damaged areas of the brain.
  2. Neural Reorganisation - Transfer of functions from damaged areas of the brain to undamaged ones. Neural reorganisation is greater in children than in adults.
  3. Axon sprouting – Growth of new neurons and/or connections (axons and dendrites) to compensate for damaged areas.
38
Q

Describe in detail neuronal unmasking

A

Dormant synapses are activated to compensate for damaged areas of the brain.

Structural changes support neuronal unmasking, such as axon sprouting (when undamaged axons grow new nerve endings to reconnect the neurons whose links were severed by damage thus making new neural pathways), reformation of blood vessels (facilitates the growth of new neural pathways) and recruitment of homologous areas (the intact hemisphere takes over the functions of the damaged hemisphere).

39
Q

Describe recovery

** in the context of functional recovery and brain plasticity

A

Full recovery is not passive, it depends on the extent of the damage and on various internal and external factors over time.

Spontaneous recovery from a brain injury tends to slow down after a number of weeks so treatment (e.g. physiotherapy) may be required to maintain improvements in functioning.

40
Q

Evaluate functional recovery

A

Strength: Functional recovery has practical applications in neurorehabilitation, it has led to the development of techniques such as motor therapy and electrical stimulation of the brain to counter the negative effects and deficits in motor and cognitive functions following accidents, injuries and strokes.

Weakness: Variable factors affect recovery after trauma:
University EDUCATION = better recovery from a brain injury. Going to university provides a cognitive reserve (Schneider et al., 2014).
AGE is another important factor. Elbert et al. (2014) concluded that the capacity for neural reorganisation is much greater in children than in adults.
GENDER also has an impact, women are more likely to recover from a brain injury than men (e.g. Ratcliffe et al., 2007).
Physical exhaustion/STRESS/alcohol can all impair functional recovery (e.g. Fleet & Heilman, 1986).

41
Q

What are the different ways of studying the brain?

A

Post-mortem examinations

Functional Magnetic Resonance Imaging

Electroencephalogram

Event-Related Potentials

42
Q

Describe post mortem examinations

A

Psychologists may study a person who displays an interesting behaviour by looking for abnormalities in the brain that might explain their behaviour after they die.

Post-mortem studies have found a link between brain abnormalities and psychiatric disorders, for instance, there is evidence of reduced glial cells in the frontal lobe of patients with depression.

43
Q

Evaluate post-mortem examinations

A
  • strength: It allows for more detailed examination of anatomical and neurochemical aspects of the brain than other methods. They have enabled researchers to examine deeper regions, such as the hippocampus and hypothalamus.
  • Studies using post-mortems may lack validity because people die in a variety of circumstances and at varying stages of disease. Similarly, the length of time between death and the post-mortem, and drug treatments, can all affect the brain.
  • Weakness: these studies have small sample sizes (as special permission needs to be granted). Hence, the sample is unlikely to be representative of the target population and so it is problematic to generalise the findings to the wider population.
44
Q

Describe Functional Magnetic Resonance Imaging (fMRI)

A
  • provides an INDIRECT measure of neural activity using magnetic fields and radio waves to monitor blood flow in the brain.
  • It measures the change in the energy released by haemoglobin, reflecting brain activity (oxygen consumption) to give a moving picture of the brain; activity in regions of interest can be compared during a base line task and during a specific activity
45
Q

Evaluate Functional Magnetic Resonance Imaging (fMRI) p

A
  • strength. fMRIs captures dynamic brain activity as opposed to a post-mortem examination which purely show the physiology of the brain.
  • strength: fMRIs have good spatial resolution (refers to the smallest feature that a measurement can detect).
  • Weak: Interpretation of fMRI is complex and is affected by poor temporal resolution (resolution of a measurement with respect to time), biased interpretation, and by the base line task used.
  • Weak: fMRI research is expensive leading to reduced sample sizes which negatively impact the validity of the research.
46
Q

Describe Electroencephalograms (EEG)

A

DIRECTLY measures GENERAL neural activity in the brain, usually linked to states such as sleep and arousal.

Electrodes are placed on the scalp and detect neuronal activity directly below where they are placed; differing numbers of electrodes can be used depending on focus of the research.

When electrical signals from the different electrodes are graphed over a period of time, the resulting representation is called an EEG pattern. EEG patterns of patients with epilepsy show spikes of electrical activity. EEG patterns of those with brain injury show a slowing of electrical activity.

47
Q

Evaluate Electroencephalograms

A
  • strength: An EEG is useful in clinical diagnosis, for instance it can record the neural activity associated with epilepsy so that doctors can confirm the person is experiencing seizures.
  • weak: EEGs are cheaper than an fMRI so can be used more widely in research.
  • weak: EEGs have poor spatial resolution.
48
Q

Describe Event-Related Potentials

A

Electrodes are placed on the scalp and DIRECTLY measure neural activity (below where they are placed) in response to a SPECIFIC stimulus introduced by the researcher.

Event-related potentials are difficult to pick out from all the other electrical activity being generated within the brain. To establish a specific response to a target stimulus requires many presentations of this stimulus and the responses are then averaged together. Any extraneous neural activity that is not related to the specific stimulus will not occur consistently, whereas activity linked to the stimulus will.

49
Q

What are the strengths of ERPs?

A

+ ERPs can measure the processing of a stimulus even in the absence of a behavioural response. Therefore it is possible to measure ‘covertly’ the processing of a stimulus.

+ ERPs are cheaper than an fMRI so can be used more widely in research.

+ ERPs have good temporal resolution (unlike fMRI)

50
Q

What are the weaknesses of ERPs?

A
  • ERPs have poor spatial resolution (unlike EEG).
  • Only sufficiently strong voltage changes generated across the scalp are recordable. Important electrical activity occurring deeper in the brain is not recorded. The generation of ERPs tends to be restricted to the neocortex.
51
Q

Define and describe Biological rhythms

A

Biological rhythms are cyclical changes in physiological systems. They evolved because the environments in which organisms live have cyclical changes e.g. day/night, summer/winter etc. There are three types of biological rhythms, circadian, ultradian and infradian.

52
Q

Define circadian rhythm (why it it needed?)

A

Circadian rhythms are any cycle that lasts 24 hours. Nearly all organisms possess a biological representation of the 24 hour day. These optimise an organism’s physiology and behaviour to best meet the varying demands of the day/night cycle.

53
Q

Describe how the circadian rhythm is coordinated

A

Circadian rhythms are driven by the suprachiasmatic nuclei (SCN) in the hypothalamus.

This pacemaker (controls the rate at which something occurs) must constantly be reset so that our bodies are in synchrony with the outside world.

Natural light provides the input to this system, setting the SCN to the correct time in a process called photoentrainment. The SCN then uses this information to coordinate activity of circadian rhythms throughout the body.

54
Q

What external signals determine the sleep-wake cycle?

A

Light and darkness determine when we feel the need to sleep and wake up. The rhythm dips and rises, with the strongest sleep drives between 2:00-4:00am and 1:00-3:00pm.

55
Q

When is melatonin released and what does it do?

A

Melatonin release from the pineal gland peaks during darkness. It induces sleep by inhibiting neural mechanisms that promote wakefulness. Light suppresses melatonin production.

56
Q

How does homeostasis affect sleep and wakefulness?

A

Homeostasis controls sleep and wakefulness by signaling an increasing need for sleep as we use energy during wakefulness. This drive increases throughout the day, peaking in the late evening.

57
Q

How do circadian rhythms and the homeostatic system interact?

A

Circadian rhythms keep us awake during daylight and prompt sleep as it gets dark. The homeostatic system increases sleepiness the longer we are awake, regardless of the time of day.

58
Q

What happens to the circadian rhythm without natural light?

A

Even without natural light, the internal circadian rhythm maintains a cycle of 24-25 hours.

59
Q

What is a strength of the circadian rhythm?

A

One practical application of circadian rhythms is chronotherapeutics, which focuses on the timing of medication to improve treatment success. It is crucial that the drug reaches the target area in the right concentration at the optimal time. For example, the risk of heart attack is highest in the early morning after waking. Thus, medications have been developed to be taken before sleep but released around 6:00 am when the risk is greatest.

60
Q

What are some weaknesses of circadian rhythms?

A
  • Research on circadian rhythms has not differentiated natural and artificial light. It was believed that only natural light had an impact but Cziesler et al. (1999) altered participant’s circadian rhythms from 22 to 28 hours using artificial light.
  • There are individual differences in the length of circadian rhythms. (Czeisler et al, 1999) found that cycles can vary from 13 to 165 hours
  • Another individual difference in circadian rhythms is when they reach their peak. ‘Morning people’ vs ‘evening people’
  • Studies of individuals who live in Artic regions, where the sun does not set in the summer months, show normal sleeping patterns despite the prolonged exposure to light. This shows that the exogenous zeitgeber of light can have very little bearing on our internal biological rhythms
61
Q

What are ultradian rhythms, and what is an example?

A

Ultradian rhythms are cycles that span less than 24 hours. An example is the sleep stages, which alternate between Rapid Eye Movement (REM) sleep (stage five) and Non-Rapid Eye Movement (NREM) sleep (stages one to four), repeating every 90 minutes.

62
Q

What distinguishes each sleep stage in terms of EEG patterns?

A

Each sleep stage shows a distinct EEG pattern. Brainwaves slow and breathing and heart rate decrease as a person enters deep sleep. REM sleep (stage five) exhibits an EEG pattern similar to wakefulness and is when dreaming occurs.

63
Q

What was proposed about the 90-minute cycle during sleep and wakefulness?

A

Kleitman (1969) referred to the 90-minute cycle during sleep as the Basic Rest Activity Cycle (BRAC). He suggested this cycle continues during wakefulness, where the mind can focus for about 90 minutes before physiological fatigue sets in, causing loss of concentration, fatigue, and hunger.

64
Q

Evaluate ultradian rhythms

A
  • strength: Ericsson et al. (2006) studied a group of elite violinists and found that their practise sessions were limited to 90 minutes at a time. Violinists frequently napped to recover from practise, with the best violinists napping more. The same pattern was found among athletics, chess players and writers. This fits with the BRAC.
  • Tucker et al. (2007) suggests individual differences in ultradian rhythms which are biologically determined and/or genetic in origin. Over 11 consecutive days+nights in a laboratory environment, researchers assessed sleep duration, time taken to fall asleep and the amount of time in each sleep stage. They found differences in all of these characteristics.
65
Q

What are infradian rhythms, provide an example?

A

Infradian rhythms span longer than 24 hours; examples include cycles lasting weeks, months, or a year. One example is the menstrual cycle, which typically lasts about 28 days but ranges from 23-36 days (Refinetti, 2006).

66
Q

How are hormones involved in regulating the menstrual cycle?

A

Ovulation occurs approximately halfway through the cycle when estrogen levels peak, lasting 16-32 hours. After ovulation, progesterone levels rise in preparation for potential embryo implantation in the uterus.

67
Q

Evaluate infradian rhythms

A
  • strength: Penton-Voak (1999) found that women express a preference for feminised male faces when choosing a partner for a long-term relationship. However, they showed a preference for masculinised faces during ovulation. (behaviour impacted)
  • weakness: The menstrual cycle depends on other factors e.g. pheromones. When several women of childbearing age live together, and do not take oral contraceptives, their menstrual cycles synchronise. In one study samples of sweat were collected from one group of women and rubbed onto the upper lip of, another group of women, their menstrual cycles became synchronised.
68
Q

What are pheromones

A

These are a chemical substance produced and released into the environment by an animal which affects the behaviour of others of the same species

69
Q

What two things help regulate biological rhythms?

A

endogenous pacemakers (internal): body clocks (e.g. the suprachiasmatic nuclei) which regulate biological rhythms

exogenous zeitgebers (external): cues (e.g. light) that entrain our biological rhythms.

70
Q

What is the suprachiasmatic nucleus (SCN) and what role does it play?

A

The SCN is a cluster of nerve cells in the hypothalamus, serving as the primary endogenous pacemaker. It generates circadian rhythms, acting as the master clock that synchronizes other brain regions controlling sleep, arousal, and all biological clocks in the body.

71
Q

How do neurons within the SCN coordinate with each other?

A

Neurons within the SCN synchronize to send time-coordinated signals to peripheral clocks throughout the body. These peripheral clocks can maintain circadian rhythms independently but rely on the SCN for coordination.

72
Q

How does the SCN respond to light levels, and how does it affect our biological clock?

A

The SCN receives light level information through the optic nerve. Morning light shifts our biological clock if it’s running slow. The SCN has its own circadian rhythm that only needs resetting when external light levels change.

73
Q

What role does the SCN play in regulating melatonin production?

A

The SCN regulates melatonin production in the pineal gland by the interconnecting neural pathway. It signals the pineal gland to increase melatonin production and secretion at night, promoting sleep by inhibiting wakefulness-promoting brain mechanisms.

74
Q

Evaluate endogenous pacemakers

A

Strength: Folkard (1996) studied Kate Aldcroft, who spent 25 days in a laboratory with no access to the exogenous zeitgebers of light to reset the SCN. However, at the end of 25 days her core temperature rhythm was still at 24 hours. This indicates that we DO NOT need the exogenous zeitgebers of light to maintain our internal biological rhythms.

Weakness: Kate Aldcroft’s sleep-wake cycle extended to 30 hours, with periods of sleep up to 16 hours. This suggests that we DO need the exogenous zeitgebers of light to maintain our internal biological rhythms.

75
Q

What are exogenous zeitgebers, and what is their primary role?

A

Exogenous zeitgebers are environmental events outside the organism that maintain its biological clock. Light is the most crucial zeitgeber for most animals.

76
Q

How does light influence the biological clock through the SCN?

A

Light-sensitive receptors in the SCN detect changes in light levels throughout the day. This information synchronizes the activity of organs and glands, resetting the internal biological clock to a 24-hour cycle. Melanopsin is critical in this system.

77
Q

What role does melanopsin play in the synchronization of biological rhythms?

A

Melanopsin, a protein in the retina sensitive to natural light, is critical for detecting light changes. It helps synchronize the biological clock by signaling the SCN about external light levels.

78
Q

What happens to biological rhythms when individuals experience changes in light exposure due to night shifts or travel to different time zones?

A

When individuals shift to night shifts or travel across time zones, their endogenous pacemakers attempt to maintain their internal sleep rhythms. However, they become desynchronized from the external light zeitgeber, leading to disrupted sleep patterns, increased anxiety, and decreased alertness.

79
Q

Evaluate Exogenous Zeitgebers

A
  • strength: The majority of blind people who still have light perception have normal circadian rhythms. Blind people without light perception show abnormal circadian rhythms. This shows the vital role that the exogenous zeitgeber of light levels play in maintaining our internal biological rhythms.
  • strength: Burgess et al. (2003) found that exposure to bright light prior to an east-west flight decreased the time needed to adjust circadian rhythms to local time.
  • weak: studies of individuals who live in Artic regions, where the sun does not set in the summer months, show normal sleeping patterns despite the prolonged exposure to light. This suggests that there are occasions where the exogenous zeitgeber of light may have very little bearing on our internal biological rhythms