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Summary Introduction to Neuroscience
- Instelling
- Universiteit Leiden (UL)
Extensive summary of all exam material of the course Introduction to Neuroscience (Minor Brain and Cognition).
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Summary Introduction to NeuroscienceLecture 1 – Neuropharmacology
Basic information of synaptic transmission:
Synaptic transmission:
- 1. Neurotransmitter molecules are synthesized and packaged in vesicles
- 2. An action potential arrives at the presynaptic terminal
- 3. Voltage-gated Ca2+ channels open. Ca2+ enters.
- 4. A rise in Ca2+ triggers fusion of synaptic vesicles with the presynaptic membrane
- 5. Transmitter molecules diffuse across the synaptic cleft and bind to specific
receptors on the postsynaptic cell
- 6. Bound receptors activate the postsynaptic cell
- 7. A neurotransmitter breaks down, is taken up by the presynaptic terminal or other
cells, or diffuses away from the synapse
Neuron always overshoots and takes back, in order to see the end of a signal
Cannabinoids: We have cannabis-like neurotransmitters (opioids: endorphins) that bind
to the same receptors as cannabis itself
Neurons’ trick:
- The neuron has a way to excite membrane
- Neurotransmitters cause small changes in postsynaptic membrane potential (PSP)
- Size of change depends on type of transmitter
Excitatory Post Synaptic Potential (EPSP)
Glutamate, Glycine, Acetylcholine, (Nor)epinephrine, Serotonin
Inhibitory Post Synaptic Potential (IPSP)
Gamma-aminobutyric acid, Dopamine
- Textbook neuron: Can stop any decision of the dendrite/cell body by blocking its
axon terminals
- Signaling molecules can affect neuron activity at different areas
Dendrites, Soma and Axon
- Receptors:
One synapse has many receptors (in cell membrane)
Neurotransmitter binds to receptor
Ion channels or channel blocker (beta blocker)
Neurotransmitters:
- Serotonin: Nuclei raphes (only place where serotonin is made)
- Diffuse neuromodulatory system: One compound can affect whole brain
- Transmitter binds > receptor becomes active
Channel opens up OR it blocks the channel
- Neurotransmitters have different effects on different receptors (genes/(sub)types)
(Avoiding) contradiction
There are differences in sensitivity of receptors
- Global vs. local synthesis:
1. Dopamine: 5 receptor genes
2. GABA: 3 types + many subtypes
Most prominent inhibitory transmitter
3. Serotonin: 15 receptor genes
, 4. Glutamate: 4 types + subtypes
Most prominent excitatory transmitter
Impossible to say where GABA and glutamate are for, as they are
involved in literally anything
5. Acetylcholine: 2 types + many subtypes
- Receptor type influences the response of the receptor
E.g. serotonin can make something more active but could also make something
less active
E.g. adrenalin has 2 types of receptors: Some vasoconstrict (higher blood-
pressure = more energy for muscles) and some dilate (around the face to lose heat)
Neuropeptides:
- E.g. Vasopressin, Oxytocin, Substance P, Endorphin etc.
- Linked to specific behavioral effects
- Almost direct response
General neuropharmacology:
Knowledge of neuropharmacology:
- How do neurotransmitters act at receptors (and what of other neuroactive
molecules?)
- How can we use this with drugs we choose to deliver to people and other animals?
Pharmacology = dynamics & kinetics
- Dynamics: What does a drug do to the body?
Consequences of receptor activation
- Kinetics: What does the body do to a drug?
Absorption, distribution, elimination
Receptors:
- Human cellular targets
Proteins: Receptors, enzymes, ion channels
- Four receptor classes:
1. Ion channels (milliseconds): Direct effect on firing
Change the charge of a neuron (positive ions go in; negative go out)
which causes it to fire
Ligand-gated ion channels
Glutamate, GABA, Acetylcholine, Serotonin
2. G-protein coupled receptors (seconds): “Domino effect” with certain
outcome that gets kicked in place (open and close)
They sit in a membrane (stick out of a cell to probe the external
environment; “antenna”) and they kick proteins towards places
Many transmitters (and peptides)
Effect mechanism = G-protein
Stimulate or inhibit (opposite physiological effects)
3. Receptor Tyrosine Kinases (minutes)
Also stick out of the membrane of the cell; These are often related
to growth (insulin); Important for development of the NS
Growth factors: Nerve Growth Factor & BDNF
Cognition (learning/memory)
4. Nuclear receptor (hours)
, They are behind the membrane, so it does not probe at all; The
hormone has to enter the cell by itself; They are relatively rare
Effector mechanism = mRNA synthesis
Long-term effects (changes cell and response of cell to other stimuli)
- Targets other than actual (signaling) receptors:
Enzymes (e.g. aspirine/paracetamol)
Pumps (e.g. antidepressant targets)
DNA (e.g. chemotherapy)
Structural proteins (e.g. antibiotics > bind to bacterial cell wall)
Early “pharmaca”:
- Exogenous:
Natural products: Natural resources used medicinally
Phytotherapy (“forever”) & Purified (opium; 1805)
Synthetic drugs: Reproducing natural resources (e.g. aspirin from willow
bark)
Aspirin & Penicillin
- Endogenous:
Neurotransmitters (networks > local effects)
Hormones from other human/mammal products (blood > global effects)
Testis extract (1848) & Neurotransmitters (Vagusstoff (1921))
Drug action: From molecule to “population”:
- Agonists & antagonists:
Agonists: Activate receptors (not necessarily the tissue!)
Stimulate the nerve to the heart (n. vagus) > heart rate gets lower >
acetylcholine is released > binds to its receptor (GPCR) > delays contraction
Add acetylcholine-R agonist > heart beats slower
Like the endogenous transmitter; it activates the receptor
Then add acetylcholine-R antagonist > heart beats faster
Blocks the agonist effect by binding to the same receptors (= channel
blocker)
Agonists have higher affinity > harder for antagonist to have an effect
, Lecture 2 – Introduction & History
History
(Not exam material)
Methodologies
Hans Berger (1873-1941): Electroencephalogram (EEG)
Rontgen (1845-1923)
- Skull X-ray
Ventriculography
Angiography
Computed (Axial) Tomography
- Hounsfield (1959): EMIDEC 1100 > first large all transistor computer
- Cormack (1963): Mathematical equations for axial tomography
- Hounsfield (1971): First CAT scanner (head only)
Magnetic Resonance Imaging (MRI) in medicine
- Edward Purcell + Paul Lauterbur + Raymond Damadian + Peter Mansfield
- Series of inventions starting in 40’s
- Culminating in medical MRI in 70’s
- Lawrence Minkoff (1970): First human MRI (heart + ribcage)
- MRI Scanner:
Harmless
Many possibilities: Morphology + Functional imaging + Arterial spin labelling
+ Spectroscopy + Diffusion Tensor Imaging (movement of water) + Tract
tracing + Blood flow
- Resolution still improving!
- Saturation imaging: Active brain tissue uses oxygen
- fMRI (functional): Medicine + Moods + Disorders
- Many questions regarding cognitive functioning of our brain will be resolved in near
future using (f)MRI!
LUMC
Leiden Institute for Brain and Cognition: Interdisciplinary + State of the art
Gorter Institute: 7T MRI scanner + Highest field in Netherlands
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