Warrens Neuroscience

  • Created by: Sarah
  • Created on: 15-05-17 07:42
who discovered leptin?
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what gene made rats obese as it fools the brain into thinking fats normal so you should eat?
Ob gene
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what is the name for the theory that said the brain monitors fat levels in the body and acts to maintain them
lipostatic mechanism
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what is the driving force behind behaviour?
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who found there a soluble factor, substance released by fat cells tells you whether to eat?
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what is catabolism?
breaking down molecules
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a lesion of the lateral hypothalamus causes what?
anorexia (breaks on switch)
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what are some positive (enhanced) symptoms of scizophrenia?
delusions, hallucinations, disorded thought and speech
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a reduced function of what causes schizophrenia?
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what is the dopamine hypothesis in schizophrenia?
there is excessive D2R stimulation, dopamine hyperstimulated
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they found a 50% concordance rate in monozygotic twins in schizophrenia which gene was this associated with?
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what are the 3 patholgies of depression?
1) reduced BDNF 2) vascular lesions 3) reduced hippocampal volume
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2 types of stroke?
1) ischaemic strokes 2) haemorrhagic strokes
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what can ischaemic strokes be caused by?
embolus (wandering clot), thromus (locally formed clot), venous thrombosis, systemic hypoperfusion (heart attack)
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what is a stroke?
neurological feficit of cerbrovascualar cause that persists beyond 24 hours or is interrupted by death within 24 hours
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what is like a stroke but distinguished from one where you get stroke like symptoms that resolve within 24 hours?
transient ischaemic attack
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causes of depression?
genetic 5-HT transporter abnormalities, monamine hypothesis- depletion in monamine, psychological:self/others/future, social: abuse, poverty and stress
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what are some selective serotonin reuptake inhibitors used to treat depression?
fuoxetine (prozac) and paroxetine (paxil)
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what is the monoamine hypothesis of depression?
depletion in the levels of serotonin, noradrenaline and dopamine in the cns
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what are the tricyclic antiepressants used to treat depression?
imipramine and amitriptyline
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4 classifications of haeatomas affeing the brain?
1)epidural 2) subdural 3) subarachnoid 4) intracerebral
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what is a subdural hameotoma caused by?
rapid movement of the head resulting in tearing of the cerebral vein as it enters a dural venous sinus
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what kind of memory loss do you get in alzeheimers?
short term
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what are the causes of alzeheimers?
genetics but early onset eg ApoE4 gene variant, trauma, environmental factors?, high bp/hypercholesterimia
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treatment for alzeheimers symptoms?
acetyl cholinesterase inhibitros, NMDA receptor antagonist mematine
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what are the risks associated with alzeheimers?
NSAIDS and caffeine, intellectual stimulation, diet and exercise
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what is childhood absence epilepsy characterized by?
4-12yrs of age, chaacteristic 2Hz spike wave discharge, resolves without pathology in puberty, mutations in low threshold voltage dep- calcum channels
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causes of stroke?
ischaemic cascade, ATP production red -> ion pumps fail, glutamate levels rise, NMDA recs activated, calcium enters neurons- ROS/free radicals produced -> cll death -> inflammatory response and pressure
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what is the 2nd leading cause of death?
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how many deaths does stroke produce worldwide?
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what is an epidural haematoma caused by?
traumatic damage to a meningeal artery or dural venous sinus caused by blow to head
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antipsychotics (typicla and atypical) more effective in trating what syptoms of schizophrenia?
positive symptoms
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what developmentl causes can cause schiazophrenia?
infection in utero, asphyxia during birth
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what percent of the population world wide has schizophrenia?
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when is the peak onset of scizophrenia?
early 20s
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what is the pathology of schizophrenic?
increased levels of dopamine in the mesolimbic pathway
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what is the WC model for behaviour?
water cistern fills up increasing motivation untillimit is reached, flushing releases the behaviour and motivation is low, gradually behaviour moivation build up and is not all
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what does the hypothalamus develop from?
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what is the ventromedial hypothalamus know as?
satiety centre
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who proposed lipostatic hypothesis?
kennedy in 1953
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what does leptin being reduced do to the body?
reduce energy expenditure, stiulates eating behaviour, reduces reproducive competence
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where does leptin act?
arcuate nucleus (hypothalamus) receptors on neurones here in
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what do arcuate nucleus neurones contain? (high leptin)
NTs alpha MSG and CART
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where do the arcutae nucleus neurones send projections to (high leptin)?
1) lower brain stem + SC 2) paraventricular nucleus 3) ateral hypothalamus (on sich)
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what does stimulation of the paraventricular nucleus by MSG apha and CART do?
relese TSH and ACTH from the anterior pituitary gland
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what do TSH and ACTH do?
act on thyroid gland and adrenal gland to increase basal metabolic rate
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what does stimulation of the lower brainstem + SC do in response to aructae nucleus?
increases sympa, raised body temp -> increases basal metabolic rate
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what are anorectic peptides?
alpha-MSH and CART = apeptite supressors- released when high levels of leptin
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what happens to alpha MSG and CART when theyres low levels of leptin?
switch off effects of hrem
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low levels of leptin stimulate the arcuate nucleus to release what?
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what do NPY and AgRP do? (power saving mode)
inhibit TSH and ACTH secretion, activate parasympa, stimulate feeding behavioru
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what are NPY and AgRP also called?
orexegenic peptides
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what stimulates NPY and AgRP being released?
gherlin rellease from an empty stomach
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what do satieryty signals do?
terminate eating and inhibit future feeding
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what dominates as satiety signals decline?
orexigenic signals-GPYY and AgRP
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when are satiety signals produced?
when we eat and duringintial digestion (prandial period)
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what satiety factors terminate feeding?
stretching of stomach receptors, cholecyst
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what is hedonistc motivation in eating beh?
we can enjoy food/eating
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what does post-absorption of food (esp carbs) elevate?
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some drugs that elevate serotonin levels inhibit what?
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what can anorexia and bulia nervosa both be linked to?
mood and serotonin levels
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what can relieve depression and bulmia?
prozac and other serotonin raising drugs
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pathology of huntingtons?
cytoplasmic and nuclear inclusions with hungtindin protein, (neurodegeneraton) Gpe stiato neurons die first the Gpi then widespread degen
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what kind of disease is hungtingtons disease?
autosomal dominant
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how many CAG repeats do you have to have over in the polyglutamine tract to have hungtintons?
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what exon is the CAG (cytosine, adenine, guanine) repeats in hungtindons?
exon 1
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what is the hungtindin protein for?
synaptic vesicle dynamics and NT release
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incidence rate of hungtindons?
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what are 21st century treatments for parkinsons?
1) stimulation- smart stimulators and optiogenetics 2) protection- calcium voltage channel blockers, glial neutrophic factors (amgen) 3) regeneration (Stem cells+transplant)
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what is the problem with calcium channels in parkinsons?
abnormal stimulation of Ca channels, hyperstimulation and cell loss
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what is degenerated in parkinsons?
substantia nigra -> pigmented neuron loss, these contain dopamine =lack of dopamine neurons
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treatment of parkinsons?
increase L-dopa but become habituated. stem cells produce dopamine -> but tumours
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where is the most effective site for deep brain stimulation?
subthalamic nucleus
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what is the suggestion of why deep brain stimulation works?
prevent lows frequency rhythm generation and de synchronous extrastraiatal basal ganglia snd cortex
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genetic forms of parkinsons are associated with mutations in wat?
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4 reasons substantia nigra neurones die in parkinsons?
1) environmental (mito function pesticides) 2) genetic mutation of -- 3) most idiopathic 4) abberant proteostasis (alpha-synuclein) or mito func (PINK!,DJ-1, parkin) 5) dopamine kills neurones
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substantia nigra dopamine neurons express what?
low voltage dependent calcium channels
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what may be particularly high in dopaine neurones in the substantia nira?
energy burden for calciumhomeostasis
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what dopamine expressing neurons are relatively reistant?
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what do animal models suggest is the main trigger for huntingtons?
cortical dysfunction
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what happens in the direct pathway?
motor cortex excites striatum (CP-caudate+putmaten)-> inhibits the Gpi+SNr - Gpi+Snr usually inhibit thalamus, striatum removes inhibition inhibits it -> thalamus sigs to cortex
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what happens in the indirect pathway?
cortex activates striatum -> striatum inhibits Gpe -> Gpe usually normally inhibits subthalamic nucelus -> subthalamic not inhibited so stimulated Gpi -> Gpi inhibits thalamus-> prevents movement
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what dopamine receptors are in the direct pathway?
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where do the D1 receptors project to?
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where does the D2 receptors project to in the indirect pathway?
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what does globus pallidus externa usually do?
inhibits subthalamic nucleus
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what dos globus pallidus interna usually do?
inhibits thalamus
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what does the subthalamic nucleus exert on the Gpi and SNr?
excitatroy influence
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which nucleus does the gpi/SNr inhibit in the thalamus?
ventral lateral nuclues of the thalamus
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dopamine is released from what neurons?
the nigrostriatal neurons
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what does dopamine do to the direct pathway?
actvates it
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what inhibits the indirect pathway?
dopamine from nigrostriatal
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what happens in parkinsons disease?
decreased striatal dopamine causes increased inhibitory output from the Gpi/SNr
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what protein is in lewy bodies in parknsons in neurons?
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what is the pathology of parkinsons?
accumulation of a protein alpga-synucleininto inclusions called lewy bodies into neurons 2) insufficient formation+activity of dopamine produced in certain neurons in the midbrain (substantia nigra)
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what pathway is supressed in parkinsons?
inhibition of thalamocortical pathway
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decreased striatal dopamine stimulation causes what?
decreased inhibition of Gpi/SNr so the thalamus is not stimulated as inhibition not removed
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decreased dopamine inhibition in the direct pathway causes what?
increased inhibition of GPe resulting in no inhibition of Subthalamic nucleus output increases Gpi/SNr output to thalamus
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what are the anorexic peptides?
Alpha MSH and CART
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what modifies long term regulation (leptin) of eating?
short term satiety signals
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what are some satiety factors?
insulin, cholecytokinin and distension of the stomach
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what is the on switch for feeding?
lateral hypothalamus
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if lesions in the lateral hypothalamus what did rats become?
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leptin deficiency in times of stravation does what?
stimulates eating behaviour, reduces reproductive competence and reduces energy expenditure (energy saving mode)
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what part of the ANS do orexigenic peptides stimulte?
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what are orexigenic peptides when are they prevalent?
AgRP and NPY, activated when leptin levels are low
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what is another way of thinking of anorectic peptides?
they are appetite supressors when you're full, Alpha MSH and CART
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what does stimulation of the brainstem and SC by ALPHA MSH and CART do?
stimulate sympathetic NS and increase temp (and BMR)
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what is the word for enjoying food?
hedonistic motivation
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what is usually elevated after post absorption of food (esp carbs)?
serotonin levels
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what can anorexia and bullimia nervosa be linked to?
mood and serotonin level
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what drugs can relieve depression and bulimia?
serotonin elevating drugs like prozac
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what can be be a bad thing about drugs that elevate serotonin level?
they can inhibit apeptite
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when are satiety sigs produced?
during eating and initial digestion (prandial period)
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what are the three things AgRP and NPY do?
1) increase parasympa stimulation 2) stimulate feeding behaviour 3) inhibit TSH and ACTH secretion
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what does the motivation to coninue eating a meal depend on?
how much we've already eaten
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what is the simple definition of behaviour?
the respnse of anorganism to a stimulus
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what 2 things can behaviour be?
conscious or unconscious
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what is testosterone?
an androgen- male hormone
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features of Testosterone?
it is linked to aggression, levels vary during the day, it can form oestodiol
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how can testosterone form oestodiol?
by aromitisation
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what is the stages in masters and johnsons human sexual response?
excitement, plateau, ****** and resolution
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what is the 4 things sexual reproduction is and an explanation of each?
1) complicated- beh rituals, sigs, seqs 2) expensive- metabolic costs of pregnancy, raising a child, even unsucesful repro is costly to the F 3) Dangerous- risks of pregnancy, predation (F eat M) 4) confusing- mistake signals
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do men and women have each type of sex steroid (T,prog, oest)?
yes but in different proporitons
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what is polyandry?
one female mates with many males, rare in mammals
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whatpercentage of mammilian species and primates have monogamy?
3% mamilian species 12% primates
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what is monogamy?
1 male and 1 femlae form an exclusive relationship
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what is polygyny?
one male mates with many females, very common in mammals
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what is the sexual dimorphism with Onufs nucleus in the human brain?
more neurones in the Onufs nucleus of Ms because bulbocavernosus (BC) muscle is bigger, motor neurones that control the BC lie in Onufs nucleus in the sacral SC
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the sexually dimorphic nucleus of the pre-optic area of the hypothalamus is larger in what gender?
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where is the sexually dimorphic nucleus?
in the pre-optic area of the hypothalamus
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3 things bigger in males?
1) the brain 2) Onuf nucleus more neurones 3) sexually dimorphic nucleus
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in these regions what is there differences in?
testosterone receptors and aromatase activity
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what are some differences in cognition between men and women?
after pubety women seem to have better verbal ability (verbal memory) cos mature earlier? how raised?
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when do women exibit better performance in spatial reasoning tests?
when oestrogen levels are lowest
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what kind of examplea re there for mammals including women showing behavioural changes throughout the reproductive cycle?
more initiation of sexual acts increasing prior to ovulation, area of flesh exposed changes throughout the cycle
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in some species what changes throughot the oestrus cycle?
sexual attractiveness
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synaptic density in the hipocampus has been related to what? effect?
levels of oestrogen, synapses are more sensitive to excitatory synaptic input
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what causes congenital adrenal hyperplasia?
a genetic female (**) adrenals secrete high levels of androgen in early life
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what are the consequences of cogenial adrenal hyperplasia?
ovaries are normal but external genetilia often indistict (intermediate between ******** and penis)
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what disease shows an intermediate between ******** and penis?
congenital adrenal hyperplasia
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what area women with congenital adrenal hyperplasia usually described as? possible reason?
aggressive and masculine, possible masculinisation of the brain
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what are sex hrmones?
steroids based on cholesterol molecules
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what does progesterone do?
prepares endometrium
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what inhibits prolactin?
dopamine from hypothalamus
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where is prolactin relased from?
anterior pituitary gland
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which bit of the pituitary gland is vasopressin and oxytonin released form?
posterior pituirary gland
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what can be important in an ******?
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what happens in the sex response?
genital response (erection+lubrication) hairs stand up, heart rate increases, diff blood flow (ncreased to labia and ********), temp, resp rate
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what helps excitement and plateau?
DAO- desire, arousal, ******
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what causes an ****** in a boy?
smooth muscle contraction
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parts that make up mind-body interactions in sexual arousal?
sexual response (genital response+other syst excite eg resp sys), peripheral arousal syst (stimuli, SC reflexes) cognitive info processining (imagery sexual meanings), emitions+how they're experienced
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what is a mismatch in terms of sex?
secondary sex characteristic (breasts, hair, genitals) by sex hormones do not match genetic sex seen in congenital adrenal hyperplasia
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what is a freemartin how does this happen?
cow with a M+F twin results in a F calf exposed to T in utero, F behaves as a bull+is infertile known as a freemartin
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what does treating F rats with T reducing F sexual behaviour do?
normal rats exhibit lordosis (curved spine) prior to maitng, exposure to T for a few days at birth prevents lordosis = critical period in dev
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what haemotoma affects the dural venous sinus or meningeal artery by a blow to the head?
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what does subdural haemotoma caused by rapid movement of the head cause
tearing of Cerebral Vein as it enters a Dural Venous Sinus
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what is a subdural haemotoma caused by?
rapid movement of head, tearing of cerebral vein as it enters DVS
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how many strokes happen to over 45's?
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what percent of deaths worldwide does strokes cause?
10% 2nd leading cause of death
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risk factors for strokes
high bp, high cholsesterol, diet, physical inactivity, drugs of abuse (alcohol, cirgarates, exctsasy cociaine)
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what are the mechanisms htat cause a stokre?
ischaemic cascade, ATP peoduction reduced-> ion pump fails -> glutamate rises -> NMDA recs activated -> Ca enters neurons -? ros/free radicals produced -> cell death -> inflammatory response or pressure
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what are the neurofibrilliary tangles in alzeheimers?
phosphorylated tau
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what is the most common epilepsy in adults?
temporal lobe epilepsy
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where is the epilogenetic focus in epilepsy?
hippocampus/amygdala/parahippocampal gyrus (recurrent excitatory circuits)
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temporal lobe epilepsy, complex seizures are preeced by aura, what is aura?
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what is childhood absence epilepsy characterised by?
3Hz spike-wave discharge, absence seizures/petit mal, mutations in low threshold Ca channels, resolves without pathology during puberty
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what is the overall effect of the causes of epipelsy?
an imbalnce in excitation and inhibition in the NS
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what are the causes of epilepsy?
2/3s idiopathic, reflex seizures-flashing lights, genetic-mutations in Na channels, cerbovascular disease, tumours, alcohol/drugs, trauma/hypoxa, infection, dev/degenerative/metabolic disorder, pathological synaptic plasticity
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what are the acute tratments for epilepsy?
generalized/complex partial- recovery position, simple patial- reassurance, maintain seafe env, benzodiazepenes
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tratments of chronic epilepsy?
surgical- remove tumour, AVM or epileptogenic issue, electrical-deep brain stimulation, vangal, avoid triggers, pharmological ethosuximide + cabamazepine
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how does ethasuximide treat chronic eplepsy?
block/modulates Ca + Na channels
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what does carbamazepine do to treat chronic epilepsy?
modulates Na channels potentiates GABA receptors
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what gene made rats obese as it fools the brain into thinking fats normal so you should eat?


Ob gene

Card 3


what is the name for the theory that said the brain monitors fat levels in the body and acts to maintain them


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Card 4


what is the driving force behind behaviour?


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who found there a soluble factor, substance released by fat cells tells you whether to eat?


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