Lecture 17 - Higher function 1: Sleep and waking Flashcards

1
Q

EEG

A

electroencephalogram

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2
Q

EEG measures

A

Brain electrical activity (synaptic potentials)
Electrical activity from inside from the excitable cells recorded from the outside of the body
Result of synaptic currents flowing through the dendrites

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3
Q

EEG is used to (clinically)

A

Used to (clinically)
Monitor behavioural state (coma, vegetative state, sleep stages)
Local changes may indicate abnormality
Diagnose epilepsy (abnormal synchronous brain activity, it is abnormal large amplitude activity)
Localise brain areas active in different tasks

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4
Q

Magnetoreception in humans

A

Alpha wave decrease shows processing of stimulus

Can be used to determine when someone is paying attention to something

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5
Q

EEG reflects

A

states of consciousness

alpha and beta rhythms

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6
Q

Alpha rhythm

A

Relaxed with eyes closed

Neurons are synchronisly active

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7
Q

Beta rhythm

A

Alert
Open eyes and pay attention
Not less active but it is just more distributed in time
Desynchronised

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8
Q

Seizures

A

(From the onset of the seizure) Neurons begin to excite each other because in generating action potential they are altering the extracellular potassium concentrations which causes depolarisation which makes them release more excitatory neurotransmitter which makes more action potential so it is like a positive feedback loop because rhythmic self activation causes the action potential generation locally

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9
Q

Sleep stages

A

Awake (activity is all over time and space) - stage 1 - stage 2 - stage 3 - stage 4 - REM (paradoxical sleep)
Dreaming occurs in REM/paradoxical sleep)
Over time get rhythmic activation of neural circuits in the brain

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10
Q

Sleep cycle

A

Emerge out of deeper stages of sleep at a cycle of about 1 hour
Eyes can become very mobile in REM sleep
Can record EMGs at the same time, REM sleep muscles become very relaxed, allows us to dream and run scenarios and participate in that state of consciousness but there is a disconnection from our motor output system

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11
Q

Control of sleep/waking cycle

A

Basic rhythm generated by “clock” in hypothalamus
Suprachiasmatic nucleus generates sleep waking cycle of about 24 hours, even in complete darkness
Accurate “entrainment” to day length via input from visual pathway

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12
Q

Orexins

A

Hypothalamic neurons release proteins called orexins, needed to keep us awake. People with narcolepsy unexpectedly fall asleep, because of defective orexin neurons

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13
Q

Neurons in reticular formation

A

Neurons in reticular formation (brainstem) - active = awake, reduced activity = sleep

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14
Q

Mechanisms of wakefulness

A

Reticular activating system icons - in the brainstem and distributed widely in the cortex which is responsible for waking us up and producing arousal

“Clock” neurons in hypothalamus
Intrinsic cycle, reset by retinal input
Approximately 24 hour cycle but it is reset/entrained by input from the retina

Neurons in reticular formation
Active = awake
Reduced active = sleep

Thalamus - gating of sensory inputs

Hypothalamic neurons release proteins called orexins, needed to keep us awake. People with narcolepsy unexpectedly fall asleep, because of defective orexin neurons.
Cannot make this particular protein orexin in their hypothalamus neurons

Reticular activating system directs input to the thalamus (relay system for directing the information to the correct regions of the cortex) so when we fall asleep there is a disconnect here as well from sensory inputs that might be entering the body from the periphery and they cannot access the cortex to wake us up

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15
Q

Functions of sleep hypotheses

A

Recuperation/homeostatic housekeeping ? (deprivation gives decreased immune function, psychosis)
Seems important - permeability of the BBB changes during sleep such that more fluid is transferred between the vasculature and the cells of the brain (washing out of the brain by the glialymphatic system which is the glia and lymphatic system, washes out the cerebrospinal fluid)

Energy saving?
Allows for dreaming?
Memory consolidation

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16
Q

Functions of dreaming hypotheses

A
Functions of dreaming: hypotheses
Deep psychological meaning ?
 Random activation of memory fragments ?
Role in consolidating memory (during REM sleep) ?
Protects us from waking ?
17
Q

Conscious

A

able to immediately respond to environment

18
Q

Unconscious

A

Sleep: able to be roused; complex pattern of brain states
Coma: unable to be roused; disordered brain state
Vegetative state; sleep cycles, but no return to consciousness

19
Q

Sleep

A

type of unconsicousness

Sleep: able to be roused; complex pattern of brain states

20
Q

Coma

A

type of unconsciousness

Coma: unable to be roused; disordered brain state

21
Q

Vegetative state

A

type of unconsciousness

Vegetative state; sleep cycles, but no return to consciousness

22
Q

Self-conscious vs automaton - key question of human existence? Mind=brain?

A

How brain activity produces it remains mysterious

Requires widespread brain function

23
Q

Disorders of consciousness example

A

schizophrenia

24
Q

Schizophrenia

A

Onset often in 20s, around this time that there is pruning and refining of neural circuitry

Disorder of thinking - psychosis
“Positive” symptoms: hallucinations, delusions, paranoia
“Negative” symptoms: social withdrawal, apathy, catatonia

25
Q

Schizophrenia and dopamine

A

Thought to be related to brain dopamine system

Drugs useful to treat usually decrease dopamine transmission
Increasing dopamine activity (amphetamines) can produce similar symptoms
Dopamine system is part of the reared system - likely reinforcing the patterns of thought that do not reflect their reality and shape their world view
Drugs can disorder thinking and give schizophrenia like symptoms

26
Q

Schizophrenia underlying cause

A

Underlying cause not known

Genetic predisposition, developmental + environmental factor(s)

27
Q

Schizophrenia and hallucinations

A

During auditory hallucinations in schizophrenia, areas of brain active that normally process auditory input
Activation due to internal brain activity interpreted as reflecting external auditory input, ‘voices’ (reliving memories etc.)
Schizophrenics are not able to determine that voices are being generated internally - internal voices would be a real person

28
Q

Disorders of mood examples

A
depression 
bipolar disorder (manic-depression)
29
Q

Neglect

A

Contralateral neglect
Lesion in the parietal lobe association cortex e.g. has a stroke here (it is behind the somatosensory cortex) - a right parietal lobe lesion
Patients copy of a drawing…
Miss half of the diagram that they are supposed to reproduce
They see it but they do not incorporate it into their awareness of the environment overall

30
Q

Depression

A

Changes our experience of the world

Persistent sadness, apathy, feelings of hopelessness, loss (or gain) of appetite, sleep disturbance
Endogenous: arises without apparent bad life-event; harder to treat
Reactive: in response to bad life event

31
Q

Depression and serotonin

A

Thought to be related to brain serotonin system

Drugs useful to treat usually increase serotonin (e.g. by blocking reuptake)

32
Q

Depression underlying cause

A

Underlying cause not known

Genetic predisposition + environmental factor(s)

33
Q

SADD

A

Type of depression

SADD Seasonal affective depressive disorder. Annual depression.
Treatment with light
Treatable, mood problem that runs on a very long cycle - sensitive to the day light resetting of the suprachiamatic nucleus clock
Long term fluctuation of mood that is to do with this dinural cycle that is to do with the nervous system

34
Q

Bipolar disorder is also called

A

manic depression

35
Q

Bipolar disorder

A

Depression alternates with mania
Mania = elevated mood, high energy, grandiosity, poor judgement, delusions (level of hyperactivity above normal)
Irregular cycle, rapidly cycle on a daily basis so there is some disturbance of biological rhythms within the nervous system
Mood problems are the primary indicator of bipolar disorder

36
Q

Bipolar underlying cause

A

Underlying cause not known
Genetic predisposition important ( there is a biological basis)
Strong genetic component and one of the strongest genetic markers is to do with the protein that locates the sodium channels at the initial segments of axons

Likely a network problem, involving communication links (nodes of Ranvier, axon initial segment (AIS)
Network problem - why we get swings of mood from one mood to another, network of interconnected regions of the brain that are responsible for generating our experience not just one part of the brain, it is more global
Protein at the nodes of ranvier and these are the ones that are affected

37
Q

Treatment of bipolar disorder

A

Best treatment = Lithium, anticonvulsants; may smooth out fluctuations in neuronal excitability.
Brain cannot tell the difference between Na+ and Li+. Li+ ions are able to enter neurons through Na+ channels during action potentials and interact with biochemistry within the cell as well as with other ion channels
Anticonvulsants - the most useful ones that blocks sodium channels

EEG tomography of deep brain structures, computed from multi electrode scalp recordings. Li+ treatment affects functional brain networks in healthy individuals