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– Multiple per cell forming arbors, non/spiny; clustered near soma; highly plastic
– Organise, respond, synthesise inputs to neuron
nucleus contains the DNA (DNA the same in every nucleus).. Chromatin determines cell expression ie. what gene is what
Process of DNA –> protein
DNA transcribed to mRNA
mRNA moves to cytoplasm
in the ribosome –> aminio acids
in the rough ER –.> protein
cell membrane
phospholipid bilayer (impermeable to water)

transmembrane spanning proteins allow for communication

Hydrophilic messengers cannot cross the cell membrane.

The Synapse
• Electrical to chemical to electrical signalling

(if only electrical will just be excited – epilepsy)

• Conversion of AP to Ca2+ influx
-Calcium leaks in –> fusion of vesicles to membrane –> exocytosis

• Colocalisation of neurotransmitters (Dale’s law)

Selected neurotransmitters
• Biogenic amines
– Acetylcholine, adrenaline, dopamine,
histamine, noradrenaline, serotonin
• Amino acids
– Excitatory: glutamate, aspartate
– Inhibitory: GABA, glycine
• Purines
– ATP, adenosine
– Opioids: 20 peptides
• Endorphins from pre-proopiomelanocortin
• Enkephalins from pre-proenkephalin A
• Dynorphins from pre-prodynorphin

• Oxytocin, vasopressin
– Pituitary releasing hormones
• CRF, TRF, Somatostatin, GHRF
– Others – Substance P, CCK, VIP, NPY
• Fast (ionotropic)
– Milliseconds, ion channels, transmission of the
mediated by glutamate and GABA
magnesium blocks pore, when things bind – change shape and Mg displaced

Influx of NA = depolarisation = AP = excitatory (glutamate)

GABA –> Cl- –> hypopolarises

• Slow (metabotropic)
– 10-1 to 101 seconds, intracellular messengers
• Long-term (gene expression, protein
– Minutes to weeks
Initiation and adaptation
A drug or stimulus acts on a given target protein and causes an acute drug effect, with repeated administration perturbations in the target protein occur

Overtime and with continue administration adaptive changes in the neurons containing the target protein occurs
Adaptive changes in these neurons leads to changes in their neuronal circuitry that are stable and having lasting effects
Fundamentally psychotropic drugs bring about their effects by interfering with neurotransmission

Repeated agonist exposure……………. receptors
Repeated antagonist exposure…………..receptors
Repeated agonist exposure desensitises receptors
Repeated antagonist exposure sensitises receptors
GABAA receptor
5 subunits (pentamic ) usually comprising of 2α ,2β, 1γ

BZD binds to α and γ

G protein coupled receptors
They constitute a large family of receptors from many hormones and slow transmitters

They are membrane receptors that are coupled to intracellular effector systems via a G-protein which is attached to the cytoplasmic side of the membrane and functions like a switch

They are made or a single poly peptide chain threaded back and forth resulting in 7 transmembrane α helices (4 extracellular and 3 intracellular domains)

The N terminal domain is intracellular whereas the C- terminal domain is extracellular (false = opposite)

GPTase activity is associated with the α subunit of the G-protein.

G proteins can activate / deactivate ion channels

second messenger source
second messenger
target protein
1. Adenylate cyclase
2. cyclic AMP
3. Protein kinase A –> into cell nucleus and can turn on or off gene expression through chromatic. CREB —> transcription

nb. lithium increases IP3

Dale’s law
One neuron one neurotransmitter (exception rather than the rule)
Tyrosine Kinase
eg. BDNF
tyrosine kinase becomes phosphorylated – come together
Drugs work through..
adaptation and chronic changes
drug actions
dual serotonin and norepinephrine reuptake inhibition (venlafaxine);
serotonin-2 antagonism/reuptake inhibition (nefazodone);
a2 antagonism plus serotonin-2 and -3 antagonism (mirtazapine).
The selective norepinephrine and dopamine reuptake inhibitor bupropion defines a novel class of antidepressant that has no direct actions on the serotonin system.”
Categories: Neurochemistry