biological Flashcards
(162 cards)
1
Q
what kind of communication happens within cells and between cells
A
within - electric
between - chemical
2
Q
why do actions potentials not lose strength
A
are actively generated and newly triggered at synapses -> so do not lose power when they split
3
Q
features of a synapse
A
presynaptic terminal -> releases NTs across cleft
postsynaptic density -> protein receptor molecules
4
Q
features of neurotransmitters
A
become EPSP or IPSPs (excitatory/inhibitory postsynaptic potentials) when they bind and diffuse in synaptic cleft
have local action - purely at synapse
different to hormaones -> bloodstream and global action
5
Q
what molecule is both a hormone and neurotransmitter
A
noradrenaline
6
Q
what are all the sex organs
A
gonads -> testes or ovaries
internal sex organs -> mullerian (precusor of female) and wolfian (masculine)
external genitalia
7
Q
which chromosome determines sex, what do the chromosomes and appearance this look like
A
Y
X = looks female
XXY = looks male
gene SRY on Y -> absence = ovary
8
Q
what do the early testis produce and do
A
anti mullerian - defeminizing
when anti mullerian hormone bind to mullerian system it begins to deteriorate
androgens - masculinising
maintains wolfian system (mostly vas deferens, seminal vesicle and epididymis)
9
Q
how does external anatomy become differentiated
A
7-8th week, testis or ovary is androgen sensitve -> specifically to DHT (dihydrotestosterone)
which turns into external anatomy
female anatomy develops when DHT isn’t present or does not bind
10
Q
explain turner syndrome
A
is X
no gonads - so no testes/ovary
female anatomy does not come from ovaries, just lack of dht
no periods, need supplemental estrogen for puberty
11
Q
what are organisational and activational roles of hormones
A
O - effect stays after hormone is removed, occurs in sensitive period - castrated baby boy stays male
A - effect is reversible depending on presence (estrogen/testosterone)
12
Q
androgen sensitivity syndrome vs persistent mullerian duct syndrome
A
ASS - external genitalia is female - androgens can’t bind
PMDS - male external genitalia, testes, male and female internal genitalia
13
Q
puberty organisational vs activational
A
activational
pubic and auxillery hair are androgen sensitive in both males and females
organisational - castration pre puberty = boys voice wouldn’t drop
14
Q
GnRH pre puberty
A
there are gnrh and kndy neurons but are not released
the neurons that stimulate them are inhibited by GABA and NPY
15
Q
when is GnRH released (hypothalamus)
A
in puberty
kisspeptin neurons are activated, GABA is inhibited
kisspeptin stimulate GnRH neurons to make GnRH
happens in pulses in the hypothalamua, makes testis make testosterone and estrogen
16
Q
GnRH in the pituitary portal system
A
when stimulated by kisspeptin
around pituitary gland but moves to anterior portion, surrounding neurons make gonadotrophins
17
Q
what do gonadotrophins do
A
males -> FSH (follicle stimulating hormones) create sperm, (LH) luteinising hormone creates testosterone
females -> FSH causes follicles to ripen, LH induces ovulation and formation of corpus luteum
18
Q
what is the HPG axis for men - hypothalamo-pituitary-gonadal
A
negative feedback to keep testosterone optimal
hypothalamus releases gonadotropin release factors, and anterior pituitary releases gonadotrophins to gonads to release male hormones
behaviour is influenced by gonadal hormones acting on the brain
19
Q
what happens to the HPG axis when men take anabolic steroids
A
mimics testosterone so less testosterone made, hypothalamus makes less GnRH and testes shrink
20
Q
explain role of hormones in menstrual cycle (FSH, LH, estrogens, progesterone)
A
day 5 - FSH increases, so follicles grow around ova
day 10 estradoil increases, follicle reseases estrogens
day 15 - LH increases, estrogens stimulate hypothalamus to increase release of LH and FSH from anterior pituitary
LH makes a follicle rupture and release ovum -> develops into corpus luteam
progesterone makes uterine lining
progesterone and estradial falls when not fertilised
21
Q
explain androgen insensitivity syndrome
A
gonads = tests
non working androgen receptors
testosterone can’t work normally
xy develops phenotypically female
22
Q
5a reductase deficiency
A
5a reductase turns testosterone into DHT (needed to for external genitalia dev)
puberty - high levels of testosterone mimic DHT, therefore develop male genitalia
23
Q
explain congenital adrenal hyperplasia
A
21 hydroxylase deficiency - prevents cortisol being made in adrenal gland
side effect - precursors to cortisol will be made into testosterone
cause high androgen levels (shouldn’t be any in typically developing females)
primary sex characteristics = male
46xx- prenatal testosterone in girls = ambiguous genitalia
24
Q
what happens to 46xy individuals with 5a reductase deficiency
A
high testosterone levels interact with DHT
25
how can you separate the effects of gonadal and sex effects in mice
moving the sry gene in mice makes 4 core genotypes
XY no SRY = no testes and no testosterone
XY SRY - normal males, normal T
XX no SRY - normal females, no testes or T
XX SRY = female but testes and T
sex diffs are T based organisational
26
how can you separate the effects of gonadal and sex effects in humans
cogentical adrenal hyperplasia in 46XX - high levels of adrogens lead to male or ambiguous genitalia
androgen sensitivity 46XY -> male chromosomes but develop female bc testosterone can't work
hormonal treatment in transgender individuals - estrogren and testosterone create activational effects, changing voice, phenotype etc
27
sex differences - toys
early T exposure and cogenital adrenal hyperplasia: 46XX preferred masculine toys, but no other accompanying masculinisation like activity or aggression
androgen sensitivity and 36XY = more feminine toy preferences
28
behavioural sex differences
- men tend to be faster in mental rotation
- Cogenital Adrenal Hyperplasia 46 xx perform better than normal women
- androgen sensitivity 46xy are the same as women
- suggests role of testosterone in spatial mental rotation
29
sex differences and brain structure
female cortex is thicker with more brain matter
males have larger white matter volume and subcortical structures
however - is on average
30
sexual orientation differences
androphile (attracted to men: larger SCN, larger commissure smaller nucleus in hypothalamus
cognitive: androphile men are better at verbal abilities and worse at visuospatial performance
gynepile women at better at spatial rotation
31
activational hormonal sex interest differences
T effects sex interest, not orientation
sex interest varies with menstual cycle
32
when is prenatal testosterone higher in boys
week 8 - when external genitalia develops
week 24 - causes brain differentiation
33
sex and orientation differences finger length
males have larger 2d/4d fingertip length difference
butch lesbians has more masculine 2d/4d
34
genetic mapping
higher sex orientation concordance in MZ, and women
androphillic men often have androphillic maternal uncle which suggests and x-chromosome inheritance pattern
birth order -> more older brother = more likely to be androphillic which is related to mothers immune response to a protein
35
trangender - pre transition brain differences
- Brain volumes are in line with natal sex
- MtF individuals show more feminine cortical thickness and white matter in some brain areas
- FtM individuals show more masculine basal ganglia and some white matter tracts
- Some aspects of brain anatomy are different from both cis males and cis females
36
when do we not feel pain
if the signal does not reach the brain
37
free nerve endings and action potentials
free nerve endings are in the periphery and bring info from the branching
must depolarise membrane potential (resting = -70mv -> +40mv)
free nerve endings experience high pressure in pain, detected by nociceptors in dorsal root ganglion and cause gated na+ channels to open
once 0 is reached - voltage gated na+ open and cell depolarises
38
action potential movement
after depolarisation, domino effect across the axon, APs run across nodes of ranviar
39
direction of pain signals travelling to the brain
free nerve endings
nociceptors in dorsal root ganglion (swelling on dorsal root)
enters spinal cord
into brain
exists ventral paths
40
how does pain info travel from dorsal root to spine
end of axon - AP triggers voltage gated CA2+ channels at presynaptic neuron
releases vesicles containing NTs at synaptic cleft
substance p and glutamate co released and bind to receptors of post synaptic sit
trigger ligand gated sodium channels which delivers APs up to the brain
41
outline of descending analgesia circuit
pain travels up the brain
brain sends signals to stop this
endogenous opioids released to make brain inhibition
inhibition spreads to prevent further brain signals
42
role of endogenous opioids
EO released by pain stimuli (drugs stimulate opulate receptors in periaqueductal GM)
EO reach dorsal horn of spinal cord grey matter
interneurons inhibit neurons that transmit pain messages to the brain
these axons contain opiate receptors which inhibit pain and travel along pain pathway to brain and cell body in dorsal root ganglia and pain receptor
stops pain in brain and origin
43
descending analgesia circuit - Peri-aqueductal grey area
PAG - projection neurons triggered when endogenous opioids released
this inhibits GABA -> no GABA binds to projection neuron which causes depolarisation of the projection neurons
APs run down PAG neuron which makes synapses to raphe magnus nuclei
44
descending analgesia circuit - raphe magnus nuclei
glutamate is excited by RMN and releases ca2+ and binds across the synaptic cleft and nuclei depolarises
RMN makes axon to dorsal horn of spinal cord and this travels to all vertebrae and floods with inhibition
45
descending analgesia circuit - inhibition
when spinal cord inhibition floods
serotonin and noradrenaline is released (can be excitatory or inhibitory)
first order neuron - enkephalin is a neurotransmitter and causes cells to hyperpolarise and become more negative
if enkephalin and serotonin hyperpolarise enough - no glutamate can depolarise membrane - brain does not know pain
46
appetitive vs consummatory behaviour
A - trying to find and obtain sexual partner
C - behaviour of sex act
47
what is the vomeronasal organ and who has it
detects pheremones, in the nose/mouth cavity and different to normal smelling
mammals and well established in rodents, debate about humans
48
role of androstadienone in sexual behaviour
in mens sweat
triggers good mood and arousal in women - opposite for men
more arousal when on top lip
49
testosterone and sexual interest in men and women
men: suppression of T reduces interest but not performance
anticipation of encounter increases T
women: long distance 30% increase in T the day before reunion
highest T around ovulation
50
GnRH and sexual interest
GnRH antagonists (no FSH or LH to inhibit production of sex hormones)
given to men
within two weeks there was a decrease in sexual activity and interest
51
estradoil and sexual interest
sexual initiations by lesbians and women peak in middle of cycle - when highest
androgens do no stimulate sexual interest, but boost estradoil effect
52
medial preoptic area and male sexual behaviour
most important for men
stimulation increases sex behaviour - and sex behaviour increases cell firing
MPA receives input from vomeronasal, genitals, central tegmentum and medial amygdala
53
sexually dimorphic nucleus size differences
larger in men
54
what are the 4 stages of arousal
excitement
plateau
orgasm
recovery
55
explain excitement and plateau
parasympathetic. preganglion activated by interneuron in spinal cord - info from excitatory or inhibitory brain, and stimulation from dorsal horn/genitals
pregang neurons fire APs and release acetycholine (at nicotinic receptors) to post-ganglionic receptors
releases acetyl for muscarinic receptors -> physiological arousal
erections and blood flow
smooth muscle relaxation
56
explain the role of the smooth muscle in sex
signalling of nitric oxide increases cyclic GMP
cannot be voluntarily controlled
post ganglionic neurons relax SM
comes from stimulation
57
how does viagra work
inhibits breakdown of cyclic GMP by PDE5 to keep smooth muscle relaxed
replaces the need for nitric oxide from excitement
58
how does an orgasm work
series of smooth muscle contractions by pelvic floor
stimulation causes pre-gang neurons release acetyl onto post-gang
post-gang release noradrenaline
= rhymic contractions
also needs disinhibition of CNS: nPGi in the medulla usually inhibits orgasm via serotonergic pathways.
to disinhibit - hypothalamus inhibits the Peri-Aqueductal Grey, which normally excites the nPGi, allowing orgasm
59
how do SSRIs impact orgasm
increases serotonin in lumbar spinal cord - therefore it is harder to inhibit the nPGi area and the CNS
is an antagonist
60
what does recovery after sex do
release oxytocin for pair bonding
release prolactin to suppress further sexual motivation
61
actions of agonists
precursor
stimulates release
stimulate post synaptic receptors
block autoreceptors
block reuptake
inactivates acetycholinesterase
62
actions of antagonists
prevents neurotransmitter storage in vesicles
inhibits NT release
block postsynaptic receptors
stops NT production
stimulates autoreceptors
63
autoreceptors and the negative feedback loop
autoreceptors are at the pre synaptic terminal and membrane which detect when enough neurotransmitter has been released and inhibits production
64
what does an antagonist do at a presynaptic receptor
blocks receptor
NTs can't bind
NTs increase in the membrane and more are released because they are not regulated by negative feedback
65
distribution of drugs across the body
water soluble - pass through blood easily - don't pass cell membranes
lip-soluble - need carriers to transport through blood, pass cell membranes. diffuse through blood-brain barrier easy
66
metabolic vs functional tolerance
more metabolic = faster elimination
functional = change in receptor numbers, sensitivity and intra-cellular cascades - these increase tolerance
67
reinforcement and psychological dependence
operant
positive reinforcements by good effect
neg reinforcements by fear of withdrawal
dopamine action also means drug addicts can crave drugs even when they don't like the effects
68
major brain subdivisions
forebrain - split into telencephalon (cortex and basal ganglia) and diencephalon (thalamus and hypothalamus)
midbrain collectively can be called mesencephalon
tegmentum is where the Peri-aqueductal-grey area is
69
brain areas most important for reward and behaviour
nucleus accumbens
ventral tegmental areas
this is part of the mesotelencephalic dopamine system
70
dopamine in reward
rats had medial forebrain bundle stimulated-
this normally induces rewarding behaviour
When they infused dopamine receptor blockers, the animals stopped responding to the stimulation.
dopamine is necessary for the reinforcing effects of brain stimulation, supporting the idea that the mesotelencephalic dopamine system (including the VTA and nucleus accumbens) is central to reward not just pleasure.
71
dopamine in novel information
male rat nucleus accumbens -> dopamine when females are introduced, peaks when they meet and decreases when she leaves
not about enjoyment but exploring potential pleasure
can cause compulsion when not pleasurable
72
cocaine and the mesotelencephalic dopamine system
will make you do it more
drives exploration
73
where does cocaine work and what kind of synapses are they
mono-amine
serotonin, dopamine, noradrenaline and adrenaline
74
what does cocaine do to receptors and reuptake
block reuptake - no recycling
no effect on autoreceptors so no new are produced
75
long term effects of coke
act in sympathetic ns -> activity at noradrenergic supresses arousal and plataeu
monoamine removal on comedown = depression
vasoconstriction breaks down nose
serotonin and schizophrenia like symptoms -> schizo serotonin hypoth
may be vulnerable to convulsiveness, stereotyped behaviour and addiction
76
compare addictiveness of cocaine, amphetamines, caffience, alcohol and nicotine
Coke: dopamine in nucleus accumbens and prefrontal cortex = repetition. psych addiction
amphetamines: similar effects
caffeine: headaches - vasodilation/constriction. psych from dopamine release in nucleus accumbens
nicotine: fast tolerance, physical dependence, strong dopamine in NA
alcohol: tolerance from day dot, fatal withdrawal (GABA-A, GABA overactivation) dopamine in nucleus accumbens
77
short term effects of amphetamines - good and bad
similar to cocaine
Euphoria, Energy, Confidence, Talkativeness, Activity etc
too much use
Dehydration, Exhaustion, Muscle breakdown, Overheating, Convulsions
78
amphetamines at mono aminergic synapses
do not need APs - push neurotransmitters out of the receptor channels
block reuptake
79
what is ritaline
blocks reuptake
slower and more gradual effect than cocaine
effective from ADHD
80
physiological action of caffeine
blocks adenosine receptors -> to stop sleep and vasodilation
stimulates release from adrenal medulla
81
short term effects of nicotine
affects brainstem for nausea
reduces muscle tone and relaxes
increases heartrate and blood pressure
82
physiological action of nicotine
binds to nicotinic acetyl receptors
nicotinic receptors in the brain and sympathetic NS
releases adrenaline
both symp and para NS, stronger in sympathetic - hr, dry mouth
83
short term effects alcohol
water and lipid soluble for blood stream and brain barrier
euphoria, anxiolytic, less inhibition, slower reflexes
vasodilation - feel warmer lose temo
diuretic - wee
84
physiological action of alcohol (important)
GABA-A agonist - mimics/increases GABA - increase inhibition of NS
NMDA antagonist - memory formation blocked
85
inflammatory response when the skin is damaged
body makes prostaglandins
vasodilation - blood to surface
sensitize free nerve endings so more likely to fire APs
86
types of nociceptors
A delta fibres - mechanical pain, cuts and bruises. highly myelinated
C delta - unmyelinated, vague, late pain and more split free nerve endings
87
what is capsaicin
causes and treats pain
C fibre nociceptor react to cap pain (hot)
treats pain by depleting substance P
88
explain the somatosensory pathway of pain
info from nociceptor which sit in dorsal root ganglion
synapse to dorsal horn in spinal cord
glutamate and substance P (more = stronger) released at synapse
dorsal horn's long axon crosses spine and runs to thalamus
synapse to primary somatosensory - map pain
89
what is the dual brain mechanism of pain
physical pain from somatosensory
pleasantness from anterior cingulate cortex
90
how do we know the anterior cingulate cortex is involved in pain
hypnosis induced analgesia
pain from 47degree water
PET scan - pain mapped and also in ACC
pain reduction hypnosis - somatosensory the same but less ACC activity
91
how is pain suppressed
descending analgesia circuit inhibits pain by inhibiting the pain signal entering the synapse at the first synapse
stop APs reaching the brain
stimulating the peri-aqueductal grey with adrenaline inhibits pain - not noticed
92
using placebos and acupucture to hijack the descending analgesia circuit
placebo - human, p cream activates the dorsolateral pfc which activates the PAG, then the circuit can be activated. doesn't work in other animals
acupuncture - activates circuit in rabbits and humans using naloxone - opioid receptor blocker. therefore, endogenous opiates can't bind to receptors
93
how does NSAIDS/ibruprofen work
acts peripherally - poor bbb crossing
inhibits COX1 + COX2 to reduce prostaglandin production
COX1 = blood clotting, bad for stomach acid
94
how does paracetamol work
reacts with endogenous molecules to form AM404 -> agonist of PRPV1 and Cb1 cannabinoid receptors
cb1 receptors found on peripheral pain circuits and DEC - to reduce inhibition
95
opiate side effects
pain relief
coughing diarrhoea, hyperthermia, sleep, pleasure, reduce breathing rate (overdose)
96
how do opiates and their receptors work
mimic action of endogenous opioids/endorphins
bind to opioid receptors
receptors -> delta, kappa, mu - contribute to side effects- ventral tegmental and nucleus accumbens for reward
inhibit DAC by hijacking inhibitory neurons
97
heroin withdrawal and how to counteract
restless, watery nose/eyes, chills, nausea, tremors
counteract with methadone - gradually reduce dosage over time
98
how does addictiveness work in the mesotelencephalic dopamine systen
in the ventral tegamental area
Opiates inhibit GABA-ergic interneurons
releases inhibition from neurons which project to Nucleus Accumbens
= More dopamine release
Nucleus Accumbens: effects independent from but similar to Dopamine from VTA
99
medical uses of cannabis (not pain)
reduce nausea and increase appetite
dilate bronchioles
blocks seizures (cannot use alone)
decreases glaucoma severity - reduce pressure on optic nerve
100
cannabis and pain
debated
yes: can treat chronic pain - better potency but many side effects
CB1 and CB2 receptor activation modulates nociceptive signals at the spinal cord, peripheral nerves, DAC and ACC
however - often low quality studies with non standardised ingestion
101
physiological action of THC and CBD
THC - more active effects, partial agonist on cb1 and cb2 receptors
CBD - antagonist on CB1, interacts with many pain receptors
102
explain endocannabinoids and how they work
endo = made by the body
primary function may be to maintain homeostasis (of pain, sleep, memory etc)
ECBs are released from POST synaptic side of synapse when depolarised and bind on PRE synaptic side
to supress pre-synaptic release
supresses GABA release - supresses inhibition
103
cannabis at a glutamate primary pain afferent
decreased pain signal
by interfering with DAC
no glutamate to work with substance P to release at dorsal horn and reach thalamus
104
how did the woman feel no pain
breakdown in FAAH enzyme which breaks down anandamide
endogenous anandamide + no 2ag (not broken down by FAAH) = no signals
105
cannabis and IQ
adolescents who used cannabis exhibited greater neuropsychological decline - iq decrease - compared to their non-using twins.
cannabis use during adolescence may have a direct effect on cognitive functioning, independent of familial or genetic influence
106
cannabis addictiveness
physical dependence -> tolerance, not withdrawals
psych - THC acts on nucleus accumbens to increase dopamine release from ventral tegmental terminals
107
which analgesics work in the CNS vs PNS
CNS
- opiates
- cannabis and cannabinoids
- paracetamol
PNS
- capsaicin
108
describe the stages of sleep
1: transition, theta waves, 10mins ish
2: k-complexes and sleep spindles start,
3: delta waves and synchrony (4 too)
4: deep sleep - REM
109
describe REM sleep
active brain - theta and beta
paralysis, boners and wetness
dreams
110
which 5 neurotransmitters are involved in arousal (sleep)
acetylcholine
noradrenaline
serotonin
histamine
hypocretin
111
acetylcholine in sleep
2 groups - one is telencephalon/basal forebrain, one in the pons/RAS - metencephalon
neurons have long reaching axons over the brain to influence brain state
acetyl released when awake, little for sleep EXCEPT REM - wake like sleep - causes EEG pattern
112
noradrenaline in sleep
from locus coeruleus in pons - long axons to work with acetyl
about vigilance -
need NONE for REM sleep
decreases as part of sleep transition
113
what is the RAS
reticular activating system - groups of nuclei running through the medulla pons and tegmentum
114
serotonin in sleep
from raphe nuclei
same pattern as noradrenaline
NONE for REM
influences locomotion and cortical arousal, not sensitive to external stimuli
115
why is serotonin and noradrenaline not enough for sleep?
about internal and external
116
histamine action in sleep
tuberomammillary nucleus in the hypothalamus
high when waking - low in sleep
anti histamines = sleep
117
how do anti-histamines work
in the periphery
ease inflammation
when crosses the blood brain barrier - affects wakefulness and become sleepy
118
hypocretin in sleep
lateral hypothalamus
excitatory connections to locus coeruleus, raphe, tuberomammillary nucleus, dorsal pons, basal forebrain and cerebral cortex
excites all areas - may manage other NTs in sleep
119
how does the vlPOA regulate sleep
actively in the hypothalamus
vlPOA connects through (inhibitory) GABA-ergic synapses to inhibit
basal forebrain and acetylcholinergic area
tuberomamilary nucleus and histamine
raphe nucleus - serotonin
locus coeruleus - noradrenaline
lateral hypothalamus - hypocretin
inhibited areas release their NTs back onto the vlPOA to flip flop
120
explain REM ON and REM OFF
ON - region in the sublaterodorsal nucleus of dorsal pons, initiates and maintains cortical activity, eye movement and paralysis
OFF - region in ventral lateral PAG (vlPAG) and lateral pontine tegmentum (LPT). suppresses REM by inhibiting the SLDin wakefulness and non-REM
121
how does the REM flip flop work
when REM off is active - inhibits REM ON. also inhibited by locus coeruleus and raphe nucleus
to change - clPOA inhibits REM OFF so ON can take over
when REM ON is active - responsible for all of REM and inhibits OFF
LH hypocretinergic neurons in lateral hypothalamus excite REM OFF
122
what do REM ON neurons effect
acetylcholinergic neurons in basal forebrain and the pons
ons activates erections, and lateral geniculate nucleus, and mesencephalon for eye movement
123
how does paralysis work in REM sleep
magnocellular nucleus is activated by REM ON
ventral horn of the magno inhibits spinal motor neurons to stop muscle tone and cause paralysis
124
activation synthesis hypothesis of dreams
idea that the brain synthesis a story from random electrical activity in REM sleep that is sent from the pons across the cortex.
cerebral cortex tries to make sense of meaningless symbols by weaving a story
125
what is the sleep wake flip flop influenced by
homeostatic control - working system
allostatic control - override in case of danger
circadian control
126
homeostatic control of sleep - why does adenosine make us sleepy
adenosine makes us tired the longer we are awake, because it is produced by astrocytes which use glycogen stores through the day
adenosine inhibits neurons to stop firing
127
explain the two hypotheses of adenosine action
1. disinhibition of vlPOA - adenosine builds and inhibit the neurons in basal forebrain that inhibits vlPOA, activates vlPOA and waking mechanisms are inhibited
2. inhibition of hypocretin-ergic neurons . they have adenosine receptors, break down into enzyme based on diff genotypes
128
how does the brain recover in slow wave sleep
slow wave sleep affected by brain temp = more brain used = more sleep needed
breakdown products are cleared in SWS
regulated by adenosine the signalling mechanisms
129
how does hunger in allostatic control influence sleep - 2 hormones and hypocretin
hypocretin-ergic neurons are inhibited by leptin, which signals full fat reserves
hypocretin-ergic neurons are stimulated by ghrelin -> why we fall asleep on a fall stomach
130
allostatic control and stress - waking up
we wake up when stress in activated immediately
sensory stimulation activates hypocretin and noradrenaline neurons
Mpfc has excitatory synapses on these neurons
central extended amygdala also activates
131
what is our body clock
SCN - suprachiasmic nucleus
nearly 24hrs
132
explain how the SCN works - clock, bmal1, cry and per
CLOCK and BMAL1mproteins activate PER and CRY gene expression in the nucleus -> are transcribed into MRNA which leaves into cytoplasm
MNRA is translated into crytochrome proteins with one or more PERs.
They re-enter the nucleus back into the clock/bmal protein complex and inhibits it to stop transcription of its own MRNA
is a negative feedback loop which takes 12hrs to grow and 12hrs to fall
133
how does the SCN fire
more RNA = more activity which peaks in the middle of the day
gene expression and membrane potential interacts which causes firing
less negative membrane potentials cause more spontaneous APs
134
how does the SCN influence the flip flop
daytime = SCN excites vSPZ through signals
causing vSPZ to send APs to excite to dorsomedial nucleus of hypothalamus (DMH)
DMH inhibits vlPOA and excites lateral hypothalamus at hypocretin-ergic synapses
135
lights' effect on the circadian rhythm - jet lag
light early in the day sets the clock back (still day stay awake)
light late at night sets clock forward (wake sooner)
RNA goes up more quickly, peaks sooner (RNA inhibits clock and bmal) and heads towards night sooner
136
action of molecules when resetting the biological clock
ganglion cells perceive the light and project to SCN using glutamate onto NMDA receptors
calcium enters SCN neurons to increase trancription for MRNA and clock genes are unregulated
= inducing more per and cry for more day
137
SCN and the pineal gland - melatonin
pineal releases melatonin during subjective night
sympathetic activity releases noradrenaline onto pineal which triggers synthesis of melatonin to release onto blood stream
melatonin keeps the body synchronised with the circadian rhythm
138
how can light shift the body clock
light increases the amount of RNA levels in the SCN
by retinal ganglion cells
-> optic nerve branch to SCN and make glutamate
binds to NMNDA receptors and releases calcium
ca2+ independently adds and releases PER and CRY to make RNA
139
explain narcolepsy
deficit of hypnocretinergic neurons -> which influence the other NTs in sleep -> histamine, serotonin, noradrenaline, and acetylcholine
140
how does melatonin affect the SCN and how it can be used for jet lag
melatonin is higher in subjective night which inhibits neuronal firing
when SCN is firing during the day melatonin would suppress the SCN and tell it that it is night time
why it helps in jet lag → when you travel east - gonna act like its day time when it is already dark
when you take melatonin at your new night time - it shuts the SCN up and shifts the biological clock forward
141
using light for jet lag
light in the middle of day does not affect SCN - because RNA is already up
but if you show earlier - RNA goes up more quickly, peaks sooner (RNA inhibits clock and bmal) and heads towards night sooner
142
activational vs organisational changes by studying trans people
- if they transition after puberty know activational if it appears in trans men and disappears in trans women
- organisational if it appears in trans men and doesn’t disappear if trans women
- and vice versa
143
neurotransmitter action in insomnia
over-active arousal NTs -> dopamine for alert, norepinephrine for vigilance, cortisol activates stress and wakefullness, histamine blocks action of antihistamines
low activity of inhibition -> less GABA, melatonin and adenosine (can't inhibit arousal)
144
what does stress do to the sympathetic and parasympathetic NS
stimulates sympathetic
inhibits parasympathetic
145
what is the neurotransmitter used by the sympathetic nervous system, and which is used by the parasympathetic
(ganglionic neurons)
sym = noradrenaline, used by post ganglionic neurons
para = acetylcholine post ganglionic but also pre ganglionic in both
146
what does the adrenal medulla and adrenal cortex
medulla: releases adrenaline and noradrenaline - fast
cortex: releases cortisol when stimulated by ACTH from anterior pituitary (consequence of HPA axis) - slow and longer
147
how does the amygdala activate the stress response -> 2 nuclei
central nucleus - in response to homeostatic challenges
medial - responds to psychogenic challenges (social and anvironment assessment)
148
how does the subgenual ACC activate the stress response
activates indirectly by activating the sympathetic NS which activates the HPA axis
149
explain the HPA axis negative feedback loop
regulates cortisol
stresser activates the amygdala which sends info to the hippocampus which has two types of corticoid receptors from everyday and dramatic stressors
hypothalamus and pituitary gland make cortisol be released into bloodstream - when detected by corticoid receptors this stops
150
dorsal ACC in the stress response loop
has many gluco-corticoid receptors that instantly feedback and decrease stress response but can be damaged over time
151
explain chronic stress as a positive feedback loop
amygdala stimulates the HPA axis normally, which activates corticoids to activate locus coeruleus
LC project noradrenaline to amygdala for cortisol
chronic stress reinforces cortical release and spirals out of control
152
how does chronic stress reduce negative feedback loops
repeated stimulation by corticoid receptors reduce its sensitivity in the hippocampus so feedback doesn't work as well
high corticoid action also damages to hippocampus to stop stress being kept under control
153
what does congenital adrenal hyperplasia do - sex and stress
reduces stress response due to lack of cortisol -less negative feedback over stimulates adrenal gland causing excess androgens
overproduce androgens for male external genitalia
154
depression and REM sleep
too much and too soon, antidepressants can also suppress REM because of serotonin (serotonin must be low for rem sleep)
155
monoamine effects of chronic stress
depletion of noradrenaline from locus coeruleus -> which has been stimulating cortisol release by activating amygdala
depletion of serotonin from raphe - pain pathway
depletion of dopamine from ventral tegmental to nucleus accumbens and pfc
156
monomine action in depression
serotonin is reduced in depressed people, because when recovered people take tryptophan to stop making serotonin they are depressed again
157
explain how SSRIS affect depression
in raphe nuclei
SSRIs block reuptake so there is more recycling and less negative feedback
however - autoreceptors still work, so it takes several weeks to allow more serotonin over time and be less sensitive. can help repair damage of HPA axis
158
antidepressants and neurogenesis
increase neurogenesis
159
how does ketamine work as an antidepressant
is an NMDA-R antagonist
works through new synapse formation in ACC
also damaged memory because NMDR receptors are blocked and blocks calcium entry into post-synaptic neurons
160
how do benzodiazepines work
facilitate GABA for more inhibitory processes and efficiency
is a sedative, relaxes so reduces anxiety
hippocampus = amnesia
spinal cord = relaxant
amygdala and ofc = anxiolytic
161
if you take benzodiazepines, what other processes might it affect?
sleep = GABA initiates by inhibiting histamines
alcohol withdrawal - both work on GABA-A receptors
162
write out the pain circuit - up and down
use photo for points
