Lecture 17 - Higher function 1: Sleep and waking Flashcards
EEG
electroencephalogram
EEG measures
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
EEG is used to (clinically)
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
Magnetoreception in humans
Alpha wave decrease shows processing of stimulus
Can be used to determine when someone is paying attention to something
EEG reflects
states of consciousness
alpha and beta rhythms
Alpha rhythm
Relaxed with eyes closed
Neurons are synchronisly active
Beta rhythm
Alert
Open eyes and pay attention
Not less active but it is just more distributed in time
Desynchronised
Seizures
(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
Sleep stages
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
Sleep cycle
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
Control of sleep/waking cycle
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
Orexins
Hypothalamic neurons release proteins called orexins, needed to keep us awake. People with narcolepsy unexpectedly fall asleep, because of defective orexin neurons
Neurons in reticular formation
Neurons in reticular formation (brainstem) - active = awake, reduced activity = sleep
Mechanisms of wakefulness
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
Functions of sleep hypotheses
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
Functions of dreaming hypotheses
Functions of dreaming: hypotheses Deep psychological meaning ? Random activation of memory fragments ? Role in consolidating memory (during REM sleep) ? Protects us from waking ?
Conscious
able to immediately respond to environment
Unconscious
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
Sleep
type of unconsicousness
Sleep: able to be roused; complex pattern of brain states
Coma
type of unconsciousness
Coma: unable to be roused; disordered brain state
Vegetative state
type of unconsciousness
Vegetative state; sleep cycles, but no return to consciousness
Self-conscious vs automaton - key question of human existence? Mind=brain?
How brain activity produces it remains mysterious
Requires widespread brain function
Disorders of consciousness example
schizophrenia
Schizophrenia
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
Schizophrenia and dopamine
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
Schizophrenia underlying cause
Underlying cause not known
Genetic predisposition, developmental + environmental factor(s)
Schizophrenia and hallucinations
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
Disorders of mood examples
depression bipolar disorder (manic-depression)
Neglect
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
Depression
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
Depression and serotonin
Thought to be related to brain serotonin system
Drugs useful to treat usually increase serotonin (e.g. by blocking reuptake)
Depression underlying cause
Underlying cause not known
Genetic predisposition + environmental factor(s)
SADD
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
Bipolar disorder is also called
manic depression
Bipolar disorder
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
Bipolar underlying cause
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
Treatment of bipolar disorder
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
