neurobiology Flashcards
what does the hippocampus do?
formation of memories
pituitary gland
production and release of hormones
hypothalamus
homeostatic regulation
wide laminar 4
sensory input
wide laminar 5
motor output
basket cells
inhibitory- innervate different layers or are confined to a single layer
functional scan
detects changes in blood flow and metabolism
lesion in parietal association cortex
lead to deficits in attention
contralateral neglect syndrome- cannot perceive objects or body parts in space
temporal association cortex
recognition of objects and memory
frontal association cortex
planning
whats in the diencephalon?
epithalamus, hypothalamus and thalamus
rubrospinal pathway
from red nucleus to spinal cord- magnocellular
from red nucleus to cerebellum- parvocellular
mesencephalic locomotor region
important in regulating speeding pattern of motion
epithalamus
circadian rhythms
reticular nucleus
GABAergic input to thalamus
sub thalamic nucleus
basal ganglia, motor control
deep brain electrode stimulation
which layer is the lateral horn in
thoracic
what does an alpha motor neurone do
innervates muscle
wallenbergs syndrome
medullary
thrombosis of vertebral artery, wide ranging of sensory and motor deficits
- Ipsilateral loss from face- trigeminal system- taste
- Contralateral loss- pain/ temperature sensitivity
Dysphagia- glossopharyngeal and cranial
brainstem glioma
account for approximately 10-20% of all childhood brain tumours.
double vision, weakness, unsteady gait, difficulty in swallowing, drowsiness, nausea, and vomiting. Rarely, behavioural changes or seizures may be seen.
functions of reticular nucleus
ascending- control arousal- sleep, attention + awareness
descending- form reticule-spinal tract- posture
contribute to HR and respiration
what does medullary nuclei of raphe nuclei do?
project to spinal cord and modulate pain transmission, movement and autonomic control
what does rostral nuclei of raphe nuclei do?
project to diverse higher brain areas- modulate pain, mood and sleep-wake cycles
axo-dendritc
excitatory- glutamate
axo-somatic
inhibitory- GABA
ago-axonic
modulatory and control transmitter release
what is presynaptic inhibition used for?
endogenous pain pathways- whether or not pain reaches CNS
1- C is inhibitory so depresses calcium current
2- reduction in transmitter released
3- synaptic potential reduced
neural integration
decision making
occurs at axon hillock
convergence and divergence
orthodromic direction
direction AP travels, from axon hillock to terminal
events at a chemical synapse
1- AP arrives at presynaptic terminal causing depolarisation
2-voltage gated calcium channels open
3-calcium rushes into the cell
4- calcium ions trigger neurotransmitter release
5-calcium influx can influence the shape of the action potential
where are neuropeptides manufactured?
in the cell body using protein manufacturing- rough ER and golgi apparatus
where are amines and amino acids manufactured?
in the synaptic terminal using synthesising enzymes that are transported from the soma
what is co-existence?
single neurone released more than one NT
3 ways to remove a NT
1- enzymatic break down- acetylcholinesterase
2-diffusion of neurotransmitter
3- reuptake of neurotransmitter
disinhibition
arrangement of inhibitory and excitatory cells in a circuit the generates excitation by transiently inhibiting a tonically active neurone
synaptotagmin
calcium sensor
synaptobrevin
binds to SNAP-25 to form a complex- moves vesicle into juxtaposed position with the membrane
3 integral membrane proteins
snaptobrevin
SNAP-25
snaptotagmin
ionotropic receptors
ion channels- action potentials
fast response
metabotropic receptors
coupled to intracellular proteins that transduce signal
slow response
how many subunits does GABA have
5
how many subunits does glutamate have
4
NMDA receptor
excitatory
needs to bind both glutamate and glycine
coincidence detector
allows sodium and calcium through- calcium acts as a secondary messenger for synaptic plasticity
noradrenaline on beta receptors
Gs- adenyl cyclase- cAMP- PKA- protein phosphorylation
metabotropic glutamate on mGLuR1
mGLuR1- Gq- phospholipase C- produces 2 secondary messengers
1- diacylglycerol- protein kinase C
2- IP3- Ca2+ release
increases protein phosphorylation and activate calcium binding proteins
dopamine
D2
Gi
decrease in adenyl cyclase- decrease in cAMP, PKA and protein phosphorylation
what happens when glutamate binds to mGLuR2
it is linked to Gi- decrease in adneyl cyclase and cAMP
hemicolinium
blocks reuptake of choline so decreases Ach signalling
vesamicol
inhibits Ach uptake- decreasing signal
botulinum
prevents release of Ach- muscle paralysis
nicotine
enhances activity of Ach
scopolamine
decreases activity of Ach
sarin
enhances activity of Ach
AchE is an unreliable thing to stain
1- it might be located postsynaptically
2- it could be serving other cellular functions
3- missing from cholinergic neurones
enzyme that catalyses glutamine to glutamate
glutaminase
enzyme that catalyses glutamate to glutamine
glutamine synthase
Nisl staining
number of neurone
stains the cell body
Golgi staining
whole neurone
stains dendrites and cell soma
layer 2 and 3 in the brain
small pyramidal cells
excitatory neurones
layer 4 in the brain
stellate cells
massive dendritic aborisations
from the thalamus
layer 5 in the brain
large pyramidal cells
output
layer 6 in the brain
pyramidal cells that project to the thalamus
what is an EEG
electrodes are placed on the head and the frequency is measured
frequency varies depending on the state of activity