Neuro pt 2 Flashcards
1
Q
Define learning
A
the acquisition of knowledge or skills through study, experience, or being taught.
2
Q
Define memory
A
storage of learned information
3
Q
Define recall
A
reacquisition of stored information
4
Q
Define the engram
A
physical embodiment of a memory
5
Q
Describe the forms of memory
A
- Nervous system performs different types of learning/memory
- Multiple separable memory systems
6
Q
Define independent memory systems
A
• Different forms of memory stored in different ways / regions / pathways.
– e.g. playing piano vs passing exams
• Procedural vs declarative memory
– Implicit and explicit
7
Q
Define procedural memory
A
• Skills and associations largely unavailable to conscious mind
8
Q
Define declarative memory
A
• Available to conscious mind. Can be encoded in symbols and language
9
Q
Examples of memory duration
A
• Immediate memory – few seconds
• Short-term memory – seconds or minutes
– Working memory
• Long-term memory – days, months, years
10
Q
importance of Pre-frontal cortex in memory
A
– working memory
11
Q
impotence of the hippocampus in memory
A
– Essential for converting short to long term memory.
– Declarative
12
Q
importance of Amygdala in memory
A
– Multiple, processed sensory inputs (smell)
– Implicit / emotional / learnt fear
13
Q
importance of Cerebellum in memory
A
– Procedural
– Sensorimotor
14
Q
What in the hippocampus can cause memory loss?
A
• Hippocampal lesions (elective or accidental) cause memory loss
15
Q
Structure of the hippocampus including its inputs and outputs
A
- Three - layered cortex
- Unusual development
- Inputs from entorhinal cortex and beyond
- Outputs to many regions via fornix
16
Q
Mechanisms of memory
A
• Long-term storage seems to be distributed
• Reverberating circuits
• The Hebbian synapse concept
– activity modifiable, plastic synapse
17
Q
memory and synaptic plasticity
A
• Synaptic strength changes
• Facilitation / depression Short-term
(mins / hours)
- Ca2+ availability / vesicle depletion
• Long-term facilitation / depression
- Long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus.
- Sustained (days / weeks+)
18
Q
where are studies of Long term potentiation normally carried out?
A
• LTP in hippocampal slices (and elsewhere)
19
Q
What is Long term potentiation
A
Long-term potentiation (LTP) is a persistent increase in synaptic strength following high-frequency stimulation of a chemical synapse
• Post – “tetanic” LTP
• High frequency burst
• LTP in specific pathway
20
Q
What is Post – “tetanic” LTP
A
- High frequency burst
* LTP in specific pathway
21
Q
What is Paired LTP
A
- Coincident stimulus and depolarization
* Associativity
22
Q
What animal has the Gill withdrawal reflex shown and what does it show?
A
Aplysia californica Shows: – Habituation – Short-term sensitisation – Long-term sensitisation – Classical (Pavlovian) and operant (Skinner) conditioning
23
Q
Short-term sensitisation
A
• Repeated gentle stimuli to siphon causes reduced gill withdrawal
– Habituation
• Pair single tail pinch (aversive) with siphon touch
– Re-establish siphon reflex
– Short-term ~60min+
Short-term sensitization lasts seconds to minutes and involves the modification of neuronal membrane properties and synaptic efficacy, often through the alteration of the phosphorylation state of existing proteins.
24
Q
Long-term sensitisation
A
• Repeated pairing of siphon touch and tail pinch
– Long-term, non-habituating siphon / gill reflex
Long-term sensitization lasts from days to weeks, depending on the training protocol. Unlike the short-term version, long-term sensitization requires synthesis of new macromolecules—the inhibition of either gene transcription into mRNA or translation of mRNA into protein blocks long-term sensitization. In its most persistent form, long-term sensitization involves morphological changes and neuronal growth.
25
LTP, LTD and Aplysia
* Require receptor activation (glutamate / serotonin)
* Altered synaptic responsivity
* Mediated by second messengers (Ca2+/cAMP)
* Require protein phosphorylation changes in early stages
* Require protein synthesis for late stages
* Involve biochemical and structural pre and post-synaptic changes
26
How does LTP occur?
* Evidence suggests often a post-synaptic event.
* Most indicates a critical role for Ca2+
* Involves trafficking of AMPA receptors to the postsynaptic membrane
27
KLÜVER-BUCY SYNDROME
```
• Amygdala lesions
• The Papez circuit
– Visual and tactile agnosia
– Hyperorality
– Hyper exploration
– Hyperphagia
– Hypersexuality
```
28
Diseases of the brain are traditionally divided into
* neurological (“physical”) signs + symptoms
* psychiatric (mental) disorders
Research has shown that the brain is also
functionally/anatomically abnormal in
psychiatric disorders- eg Schizophrenia
29
Neurological Assessment
State of consciousness- Glasgow Coma scale
• Mental state, attitude, insight
• Cognitive function
• Gait
• Co-ordination and fine movements
• Cranial nerves
• Motor system - (wasting, tremor, power, tone,
reflexes)
• Sensory system - (vibration, touch, pain, 2 point
discrimination)
30
Psychiatric Assessment
Appearance and general behaviour
• Mood and affect (affect = emotional responses)
• Speech- disorders of thought-(stream, form,
content)
• Insight
• Abnormal beliefs (e.g. delusions) and
perceptions (e.g. hallucinations)
• Cognitive state- (concentration, confusion,
memory)
31
What are the symptoms of Parkinson's?
Paucity of spontaneous movement – insufficiency of movement
Bradykinesia- very slow movements
Akinesia- no movements
Increased muscle tone- rigidity
Resting tremor- @4-5Hz- ‘pill rolling’
Shuffling gait and flexed posture, impaired balance
Mask-like expression
32
Parkinson’s disease is first example of a brain disorder resulting from what?
resulting from a deficiency of a single neurotransmitter
33
Where is 80% of the brains dopamine?
| What was found that Parkinson's sufferers were deficient of?
-80% brains dopamine in basal ganglia
Oleh Horynekiewicz found brains of Parkinson disease
sufferers were deficient in DA in striatum.
34
What is Parkinson's the result of and what causes it?
Parkinson disease shown to be result of degeneration
due to the loss of dopamine caused by the loss of dopaminergic cells of the substantia nigra
35
what the importance of L-DOPA and how long does its effects last?
- Was found that IV L-dihydroxyphenylalanine (L-DOPA- a dopamine precursor) provided a dramatic albeit brief reversal of symptoms!
- A gradual increases in oral L-DOPA provided significant and continuous benefits
- Beneficial effects of L-DOPA only last for ~ 5 yrs
side effects increase-motor response fluctuations and
drug related dyskinesias.
36
Describe the inhibitory pathway
- Indirect Pathway transiently active inhibitory neurones from the caudate and putamen which project to tonically active inhibitory neurones of the external
globus pallidus. DAergic input to this pathway is inhibitory.
- drive acts to oppose the disinhibitory action of the
direct pathway. In this way the indirect pathway modulates the effects of the
direct pathway
indirect pathway
- inhibits moto thalamus
- inhibits thalamo-cortex
- inhibits motor cortex
- inhibits movement
37
What causes Parkinson's symptoms?
Excessive output from internal pallidal segment cause parkinson's symptoms
38
What makes the symptoms of Parkinson's reduce/disappear
Lesions in internal segment- symptoms reduce/disappear
39
Describe direct pathway
Direct pathway
- disinhibits motor pathway
- Activates thalamo-cortex
- Activates motor cortex
- facilitates movement
40
What does processing of movement involve? and how does it do this?
the processing of movement in the basal ganglia involves a direct pathway and an indirect pathway.
The thalamus will receive signals from the two pathways and then decide – based on those signals – whether to send an excitatory or inhibitory message to the primary motor cortex, telling it what to do
41
How does the hypokinetic feature of Parkinson's appear?
1. loss of dopaminergic input from the substantia nigra to striatum
2. indirect pathway- increased activity
Direct pathway- decreased activity
3. increased activity in internal pallidal segment
4. increased inhibition of thalamocortical and midbrain tegmental neurons
5. Hypokinetic feature of Parkinson's
42
What's the importance of the gene huntingtin and how does it become abnormal?
- Associated with nuclear and cytoplasmic inclusions containing mutant huntingtin and other proteins
Huntingtin gene (HTT) expresses for protein ‘huntingtin’.
- This gene normally produces 6-35 ‘residues’ in the protein
- In the abnormal gene (those affected by the condition) it contains 36+ residues…sometimes hundreds.
- Normal function of the protein is unclear but something to do with neurones-binding proteins, transporting materials, inhibiting apoptosis, synaptic vesicle dynamics and transmitter release.
- Get deposited in nucleus and cytoplasm- huntingtin
- Protein becomes abnormal
43
What type of genetic condition is huntington's disease?
autosomal dominant genetic condition
44
During psychotic episode, one or more of the following groups of positive signs must be present:
Delusions-
eg. belief that one is being persecuted, or others control one’s thoughts and feelings
Prominent Hallucinations-
usually auditory-hearing voices commenting on one’s actions
Disordered Thoughts
incoherence, loss of association of ideas poverty of speech, lack of emotional expression
45
how do treatments work?
D1 and D5:
- expressed mainly in cortex and hippocampus. low affinity for antipsychotic drugs
D2 , D3, D4 :
- expressed in caudate nucleus, putamen, nucleus accumbens. high affinity for typical antipsychotics. Thought to be major site of theraputic action
D3 and D4:
- expressed in limbic system and cortex, weakly in basal ganglia. even higher affinity for atypical antipsychotics
positive signs only
46
Prodromal signs of Schizophrenia- what do they show? what do they include? what are the followed by?
First schizophrenic episode is often preceded by prodromal signs- (sign that condition is impending)
```
These include:
Social isolation and withdrawal
Impairment in normal fulfilment of expected roles
Odd behaviour and ideas
Neglect of personal hygiene
Blunted affect
```
Prodromal period then followed by one or more episodes of psychosis
47
What are the positive signs of schizophrenia? what causes them?
Positive signs:
- Loss of reality testing
- Memory disturbances
- Delusions
- Hallucinations
Positive signs are referred to as such because they reflect
the presence of distinctively abnormal behaviours
Positive- excess of dopamine
48
What are the negative signs of schizophrenia? what causes them?
```
The episodes separated with periods where the patient isn’t overtly psychotic but behaves:
Negative signs:
- Eccentrically
- Socially isolated
- Low levels of emotional arousal
- Impoverished social drive
- Poverty of speech
- Poor attention span
- Lack of motivation
```
Negative signs are chronic features
and are most difficult to manage
Negative signs are the absence of normal social and
interpersonal behaviours
Negative- loss of neurons
49
What happens during psychotic episodes?
During psychotic episodes, patients often exhibit unusual postures, mannerisms or rigidity.
50
What's the modern diagnosis of schizophrenia?
Must be continuously ill for at least six months, there must be one psychotic phase followed by a residual phase.
51
On basis of these criteria, schizophrenia is divided into sub-groups:
Paranoid Schizophrenia-usually men, systematic delusions of persecution predominate
Disorganised Schizophrenia (hebephrenia)-early age of onset, wide range of symptoms, profound deterioration of personality
Catatonic Schizophrenia-rare form-mutism, abnormal postures predominates.
52
Genetic predisposition
- Incidence is 1% uniformly around the world despite social and environmental factors varying dramatically!!!!
- But amongst parents, children and siblings of sufferers- 15%! Strong evidence that disease runs in families.
- In monozygotic twins (same genotype) incidence-45%
- Dizygotic twins (different genotype) incidence-15%
- Could still be acquired behaviour
53
Investigations into adopted twins found:
Higher incidence of schizophrenia in biological relatives of schizophrenic adoptees than among relatives of normal adoptees-10-15%!
Schizophrenia has strong genetic component,
rearing does not play a major role!!
(Kety et al. 1975)
Its NOT environmental but genetic
54
Anatomical Abnormalities in the Brains of Schizophrenics
- Some schizophrenics have one or more of four major anatomical abnormalities.
- Reduced blood flow to the globus pallidus suggestive of a disturbance in the system that connects the basal ganglia to the frontal lobes.
55
What changes of the morphology of the brain can be seen in patients with schizophrenia? what does this suggest?
Blood flow to the frontal lobes does not increase during tasks involving working memory (as in normal)
Cortex of the medial temporal lobe is thinner and anterior portion of the hippocampus is smaller than in normal (especially in the left side-consistent with memory defect)
Lateral and third ventricles are enlarged with a widening of the sulci, especially in the thinner temporal and frontal lobe-reduction in volume of frontal lobe.
Findings suggest that the hippocampus, globus pallidus and prefrontal cortex is part of a cognitive system impaired by schizophrenia
56
What do negative symptoms of schizophrenia involve? what did monkeys show?
The negative symptoms of schizophrenia involve activities that normally require the prefrontal cortex association areas.
Indeed, in monkeys, activation of these executive functions is correlated with increased metabolism in a distributed network that includes the anterior hippocampus, parietal lobe,
and the dorsolateral prefrontal cortex
57
Causes of schizophrenia
Genetics- 50% concordance in monozygotic twins
Environmental factors- 50% concordance with monozygotic twins
Development- infection in utero, poor diet, asphyxia
Social Factors – environment, stressful relationships
Drug abuse- cannabis and cocaine. Uncertain whether they are cause or effect
Dopamine hypothesis – excessive D2R receptor stimulation
58
Treatment for schizophrenia
Chlorpromazine or atypical antipsychotics such as clozapine, risperidone and olanzapine
Intense psychotherapy and social support
59
how do treatments work for schizophrenia?
D1 and D5:
- expressed mainly in cortex and hippocampus. low affinity for antipsychotic drugs
D2 , D3, D4 :
- expressed in caudate nucleus, putamen, nucleus accumbens. high affinity for typical antipsychotics. Thought to be major site of theraputic action
D3 and D4:
- expressed in limbic system and cortex, weakly in basal ganglia. even higher affinity for atypical antipsychotics
positive signs only
60
Symptoms of depression
* lowered mood
* anhedonia-inability to feel pleasure in normally pleasurable activities
* avolition-decrease in the motivation to initiate and perform self-directed purposeful activities.
* altered appetite
* Hyposomnia/hypersomnia
* worthlessness and guilt
* reduced ability to concentrate
* recurrent thoughts of death
* reduced life span
* 3-7% risk of suicide
61
Pathology of depression
* reduced hippocampal volume
* vascular lesions- lesions in the brain caused by blockages in blood supply
* reduced Brain Derived Neurotrophic Factor-stimulates nerve growth
62
Cerebrovascular Accident
- Neurological deficits cause by an interruption of the normal blood flow (ischaemia) to the brain that persists for more than 24hrs
- Brain requires a lots of blood flow (oxygen, nutrients and removal of metabolic waste products)
- Brain function ceases after 60-90 seconds of an ischaemic event this is irreversible of it lasts greater than 3hrs
- How the stroke presents itself depends upon which part of the brain is damaged.
63
What are the two types of cerebrovascular accident?
```
Ischaemic strokes:
•embolus (‘wandering’ clot)
•thrombus (‘locally’-formed clot)
•systemic hypoperfusion e.g. heart attack
•venous thrombosis
```
Haemorrhagic strokes:
•entry of blood into CNS via rupture of a blood vessel/sinus
or an aneurysm
64
what stages do body movements/twitches and arousals occur?
Body movements/twitches: between- 1&2, 2&3, 3&4
| Arousals: between- 1&2, 2&3, 3&4
65
what do Sleep and Wakefulness follow? what are circadian rhythms and how are they modulated?
follow circadian rhythm with periodicity of about 24hrs
Circadian rhythms are endogenous and persist without environmental cues
However, they are modulated by external timing cues- ‘zeitgebers’
These adapt the rhythm to the environment
66
what is the major internal clock? what does it regulate? what does lesioning of this internal clock cause?
Suprachiasmatic nucleus of anterior hypothalamus
Suprachiasmatic nucleus regulates timing of sleep.
Not responsible for sleep itself
Lesioning of the suprachiasmatic tract dampens down the circadian rhythm of sleep
67
What does sleep consist of? and how is it defined?
Sleep consists of cycles of non-REM and REM sleep (REM= rapid eye movement)
Sleep defined behaviourally as:
- Reduced motor activity
- Reduced response to stimulation
- Stereotypic postures (eye closed in humans)
- Relatively easily reversible
68
Physiological activity can be measured using what?
electrical recording
- Muscles movements with electromyography
- Eye movements with electro-oculography
- Brain activity with electroencephalography
69
what does the Electroencephalogram measure and how?
Measures the synchronous, electrical activity from large populations of neurones in the brain
Caused by cellular, ionic movement, which creates an electric field
Many millions of neurones, all of a similar ‘spatial orientation’
Electrodes placed on the surface of the scalp detect these electric fields
Linked to an electrical amplifier (they are tiny electric fields) and to a monitor
- Non invasive
- Easy to administer
- Data easily gathered
High temporal resolution (milliseconds)
Event generated potentials
Low spatial resolution
Electric fields follow an inverse square law so only cortical activity detectable
70
Non-REM sleep (four mains stages)
- Neuronal activity is low-not much action potential firing between neurones.
- Metabolic rate and brain temperature at their lowest.
- Heart rate and blood pressure decline- decreased sympathetic nervous system outflow
- Increase in parasympathetic outflow dominates non-REM sleep- constricted pupils
- Muscle tone and reflexes are intact
71
Stage one of sleep
Drowsiness
Awakened easily
Eye moves slowly and muscle activity slows
During this stage, many people experience sudden muscle contractions preceded by a sensation of falling
Transition from wakefulness to onset of sleep-lasts several minutes
Awake people show low voltage EEG activity (10-30μV@16-25Hz)
As they relax- sinusoidal (alpha) activity 20-40μV@10Hz
EOG- eye show slow, rolling movements
EMG- during stage 1 and all non-REM, some muscular activity
EEG characterised by low-voltage activity if mixed frequencies
72
what is EOG, EMG, EEG
EOG- Electrooculography
EMG- Electromyography
EEG- Electroencephalography
eachmeasured with a differential amplifier which registers the difference between two electrodes attached to the skin
73
Stage 2 of sleep
Light sleep
Eye movement stops and brain waves become slower with only an occasional burst of rapid brain waves
The body begins to prepare for deep sleep
Body temperature drops, heart rate slows
characterised by bursts of sinusoidal waves called 'sleep spindles' (12-14Hz) and biphasic waves called K complexes
K complexes occur episodically against background of continuing low-voltage EEG activity
74
Stage 3 of sleep
deep sleep
Extremely slow delta waves are interspersed with smaller, faster waves.
sleepwalking, night terrors, talking during one’s sleep, and bedwetting ‘parasomnia’. Occur during the transitions between non-REM and REM sleep.
high amplitude, slow delta waves (0.5-2Hz)
75
Stage 4 of sleep
very deep sleep
brain produces delta waves almost exclusively.
Disorientation for several minutes following arousal from stage 4
Slow wave activity increases and dominates the EEG record
Stages 3 & 4 in humans called SLOW WAVE SLEEP
Some animals, all non-REM is slow wave
76
Stage 5 of sleep
Rapid eye movement (REM) sleep
EEG mimics wakefulness! REM found in birds!
Closed eyes move rapidly from side-to-side,
Perhaps related to the intense dream and brain activity
77
EEG during human REM is similar to what?
is similar to stage 1/Awake
| low voltage mixed frequency
78
Paradoxical Sleep - explain
REM-neuronal firing very like in wakefulness!
Neurones in Pons, lateral geniculate nucleus and occipital cortex fire in more intense bursts during REM that in wakefulness!!!
This intense firing generates high-voltage spike potentials in EEG trace called ponto-geniculo-occipital spikes or PGO spikes
79
ponto-geniculo-occipital spikes (PGO spikes) - what is it?
intense firing generates high-voltage spike potentials
PGO spikes originate in the pontine reticular formation, propagate through the lateral geniculate nucleus and on to the occipital lobe.
PGO-type spikes can be produced in alert subjects by startling them with an abrupt stimuli like a load noise!
This suggests that the PGO of REM sleep may be activated by the same neural circuits that initiate the ‘startle response’
PGO’s are also correlated with bursts of eye movements in REM sleep
80
During REM sleep
Brain temperature and metabolic rate rise-
- consistent with increased neural activity
- In some areas-greater than in waking
All skeletal muscles are atonic- flaccid and paralysed
Muscles controlling movements of the eye, middle ear ossicles, and diaphragm remain active
So, you can breathe and hear any impending danger!
Penile erections in men
clitoral engorgement in women
Pupils highly constricted (miosis)
Respiration is unresponsive to changes on blood pCO2
Responses to heat and cold reduced or even absent- body temperature drifts toward ambient
81
What could be said about REM and non-REM sleep?
REM could be said to be a lighter sleep since arousal is easier than in stages 3-4
Non-REM could be said to be lighter sleep because body temp, muscle tone and reflexes are all maintained.
82
Normal sleeping pattern (humans)
REM and non-REM sleep alternative cyclically
After 70-80 minutes sleeper returns to stages 3 or even 2 before entering first REM phase of the night which lasts 8-10 minutes.
Time from first stage to end of REM = 90-110minutes
Repeated four or five times per night-during each repetition, stages 3 & 4 decrease in duration and REM increases
83
In young adults- how much time is spent in each stage during sleep?
Only 5% of sleep time spent in stage one
Largest amount of sleep time is spent in stage 2, 50-60% in stage 2
Stages 3 and 4 only constitute 15-20%
REM phases constitute only 20-25%
84
Dreaming
The functions of dreaming (and sleeping) are not known
Dreaming in particular is a mystery-there are some useful observations
Once thought that dreams occurred only in REM (from waking studies)
Recent work research suggests that as high as 70% occur in non-REM sleep!
85
Theories of dreaming
```
Strange imagery-brain not fully functioning
Exercises synapses when no
external activity
‘Circuit Testing’
‘Memory consolidation’
```
86
stimulation of the paraventricular nucleus due to high leptin levels...
acts to release TSH and ACTH from the anterior pituitary gland. Increases BMR
87
What is behaviour and what are the different types?
Behaviour - the response of an organism to a stimulus
Behaviours can be:
‘unconscious’, eg reflex movement from pain
‘conscious’ eg writing lecture notes-Higher-level voluntary or conscious behaviours require motivation (a driving force)
88
Explain the ‘WC’ model:
The water cistern fills up (increasing motivation) until it reaches its limit
Flushing releases the behaviour and the motivation is low
Gradually the motivation builds up again until there needs to be another release.
Works at a crude level for some behaviours but NOT all - has many flaws
89
what causes probability and direction of a behaviour to vary?
the driving force (‘motivation’)
Motivation may be required for a behaviour, but it does NOT guarantee it (social, cultural, personal influences)
Balance conflicting motivations (eg write this lecture or go for a coffee and cake)
The more basic (survival) behaviours can be explained to some extent
90
What is anabolism?
Building up macromolecules for energy storage
91
What is catabolism?
Breaking down macromolecules for energy usage
92
what did bilateral lesioning show in mice?
Many years ago, it was shown that bilateral lesioning of a rat’s lateral hypothalamus caused anorexia (weight loss).
In contrast, bilateral lesions of the venteromedial part of hypothalmus caused overeating and obesity.
93
Long term regulation of feeding
Kennedy (1953) proposed that the brain monitors body fat levels and acts to maintain them (‘lipostatic hypothesis’)
A signal from fat to the brain was hypothesised to tell the brain what the body’s fat levels are.
In the late 1960s Coleman proposed a ‘soluble substance’ in genetically predisposed obese mice (from the ob gene) ‘fooled’ the brain into thinking fat levels were normal, so the mouse continued to eat, despite not requiring extra food.
94
importance of Leptin- what is it released by? what's its function? what does it cause?
Leptin is released by fat cells to decrease eating behaviour and increase energy expenditure
In times of starvation leptin deficiency stimulates eating behaviour, reduces energy expenditure and reduces reproductive competence
High levels of leptin act on receptors on neurones in the arcuate nucleus (infundibular nucleus) of the hypothalamus (collection of a lot of different neurons)
The neurones that are activated contain the neurotransmitters alpha-MSH and CART (cocaine and amphetamine-regulated transcript)
Treating ob/ob obese mice with leptin reversed the eating disorder
95
Correlation between fat and leptin levels
More fat, higher the levels of leptin, the bigger the drive to stop you from eating.
Less fat, less leptin produced – get tired, reduces the drive for reproduction - less likely to get pregnant (need a lot of energy for this)
96
neurones in the arcuate nucleus send projections to
Lower brain stem and spinal cord
Paraventricular nucleus of the hypothalamus
Lateral hypothalamus
97
What mimics the effect of raised leptin levels?
injection of alpha-MSH and CART and can be called anorectic peptides (appetite suppressors)
98
Low levels of leptin (low fat) do what?
switch off the effects of alpha-MSH and CART
| Additionally, falling levels of leptin stimulate other neurones in the arcuate nucleus; these contain NPY and AgRP
99
NPY and AgRP (orexic peptides) -what do they do?
Inhibit TSH and ACTH secretion
Activate the parasympathetic nervous system
Stimulate feeding behaviour
100
Low levels of leptin (low fat) do what?
switch off the effects of alpha-MSH and CART
| Additionally, falling levels of leptin stimulate other neurones in the arcuate nucleus; these contain NPY and AgRP
101
what does Gherelin stimulate the release of?
stimulates NPY and AgRP release (stimulating feeding)
102
What do Orexic peptides do?
make you start feeding and reduce energy expenditure
103
Short term regulation of food intake
Short term factors also influence daily food intake (eg cultural pressures such as meal times, when we last ate, how much we last ate)
The motivation to continue eating a meal depends on what and how much we have already eaten - this can be overridden.
The long-term regulation of feeding (leptins etc) is modified by short term signals that are generated when we eat
104
Satiety signals
what these short-term signals of feeding are called
* Satiety signals are produced when we eat and during initial digestion (the prandial period)
* They terminate eating and inhibit future feeding
* When the satiety signals decline the orexigenic signals dominate and stimulate feeding
* Satiety factors terminate feeding- eg. distention of the stomach, cholecystokinin and insulin
105
Other aspects of feeding/eating
We can enjoy food/eating! (hedonistic motivation)
Mood and food - some foods produce changes in mood via serotonin
Post-absorption of food (especially carbohydrates) elevates serotonin levels
Typical to see carbohydrate-rich feeding during stress (eg exam stress)
Some drugs that elevate neural serotonin levels inhibit appetite.
Anorexia nervosa and bulimia nervosa can both be linked to mood and serotonin levels
Prozac and other serotonin-raising drugs can relieve depression and bulimia
106
The sexual brain-age related sex differences
Interstitial nucleus of the anterior
hypothalamus (INAH) 2.5 bigger in male-
responsible for male sexual behaviour.
Cells sensitive to androgens
Men lose brain tissue at earlier age and more of it-particularly in frontal
and temporal lobes mainly for personality
Causes irritability + personality changes
Complex mental tasks- male only use the hemisphere of brain most suited to task - ‘focused’ activation
107
Stimulation of sexual behaviour in males
Corticomedial amygdala receives positive inputs from medial preoptic area due to sexual stimulation- sends signals to medial preoptic area
Basolateral amygdala receives positive signals from medial preoptic- sends signals to medial preoptic area- leading to sexual behaviourr
these both lead to assertive/aggressive behaviour
108
Area of hypothalamus used in male sexual behaviour
Medial Preoptic area
- signals from preoptic area sent to cortex
- conscious excitement down to penis
- erection
109
Area of hypothalamus used in female sexual behaviour
Ventromedial nucleus
| - in animals stimulation in sexual context produces lordosis/genital display
110
The sexual brain-age related sex differences- male
Interstitial nucleus of the anterior
hypothalamus (INAH) 2.5 bigger in male-
responsible for male sexual behaviour.
Cells sensitive to androgens
Men lose brain tissue at earlier age and more of it-particularly in frontal
and temporal lobes mainly for personality
Causes irritability + personality changes
Complex mental tasks- male only use the hemisphere of brain most suited to task - ‘focused’ activation
111
The sexual brain-age related sex differences- women
Corpus callosum larger in women-more connections between hemispheres richer supply of axons
Anterior commissure larger- links subcortical areas of corpus callosum-transfer of emotional information larger in men than women
More tissue in massa intermedia (connects lobes of thalamus) route action potentials to correct place
Lose tissue in hippocampus and parietal areas- lose memory and visuo-spatial functions- ‘forget things and get lost!’
Complex mental tasks-women use both sides of brain- ‘broader view’
112
Male/female differences created exposure to hormones
pre-Nataly and modified by behaviour and environmental factors.
Underlying layout determined by genes.
Why do men have nipples? Because female body form is the default pattern- only exposure to hormone decide what to develop
Physical differences mirrored in behaviour.
Default setting is female
113
Male-typical sexual behaviour
More assertive-closely linked to aggression
Medial preoptic area is active in copulating male monkeys. When area electrically stimulated-fanatically interested in any female (if in oestrous). If preoptic area is removed-loss of interest in females, but not sex -continue to masturbate!
114
Female-typical sexual behaviour
Mediated by ventromedial nucleus of hypothalamus (same area controls hunger)
Rich in oestrogen-sensitive neurones
when in oestrous = lordosis (animals)
In humans, lordosis is completely under conscious control
But still displayed in erotic dance moves, clothing
Female hormones dictate type of sexual behaviour
but not strength of sex drive, no correlation to hormone, don’t understand why
some women have a higher sexual drive than others
115
In both sexes, sex drive controlled by?
adrenaline and testosterone-affect many different areas of brain
116
In sexual behaviour in humans, cortex does what?
‘pushes’ sexually stimulating info gathered from environment down into limbic system- limbic system readies the system for sex! (animals only have sex when female ready to reproduce)
117
sex involves all area of brain- what happens if damaged?
from high level cognition-romantic love to vision down to bodily function
damages to any area may produce some sort of sexual dysfunction
118
what disease can cause sexual disinhibition in people?
sex has infiltrated the frontal lobes thus entangled with deepest notions of morality
hence sexual obscenity and disinhibition are characteristic of people with type of frontal lobe damage that causes destruction of higher function
dementia, picks disease
