The Synapses
Neurons are simple computing devices
Brain functions (including cognitive functions) rely on the activity of
networks of interacting neurons
Interactions = synapses
Synaptic Morphology
 Pre/post synaptic sites
 Types of synapses
 Synaptic vesicles
 Neurotransmitter
 Axonal Transport
o Stuff moves along axon microtubules (axoplasmic
transport)
 How things move on the axon
 A synapse: the parts (figure 2.23)
o Synaptic vesicles are filled with neurotransmitter
molecules
o Soma A/B
o Mitochondrion
o Synaptic cleft
o Presynaptic membrane
o Postsynaptic membrane
o Microtubule
o Synaptic vesicletransported from soma
 3 kinds of synapse locations (figure 2.22)
o Axo-Dendritic synapse
o Axo-Somatic
o Axo-Axonic
Synaptic Physiology
 Synapse is the place where 2 neurons ‘talk’ to each other
 Neurotransmitter release (Figure 2.24)
o AP  vesicle fusion  neurotransmitter release in cleft
 Vesicles fuse with presynaptic membrane in Soma
A
 Molecules of neurotransmitter begin to leave
terminal button
 Transmitters flow into synaptic cleft and received
by postsynaptic membrane of soma B in 2 kinds
of neurotransmitter-dependent ion channels
 Ionotropic Receptors (Figure 2.25)
o Ionotropic: let ions go through
o Fast and local actions
o Transmitter binds  activates receptors  open ion
channels
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Metabotropic Receptor (figure 2.26)
o Mediate the influence of hormones and drugs, statedependent information processing
 If in distress vs. happy you’ll process information
differently
o Second messengers: molecules that link receptors to
ion channels
o Transmitter binds  activates receptors  activates
second messengers  open ion channels, intracellular
effect
o Slow and Diffuse action
IPSPs and EPSPs (figure 2.27)
o Excitatory/Inhibitory PostSynaptic Potential
o Adding Na+ to cell  excite cell, depolarize
o Taking K+ out of the cell  inhibit cell,
hyperpolarization
o Adding Cl- to the cell  inhibit, hyperpolarization
o Add Ca++ to cell  excite cell, depolarization
o Hyperpolarize  inhibitory (IPSP)
o Depolarize  Excitatory (EPSP)
o One given neuron releases the same neurotransmitter
at all of its synapses
Regulation of Release:
o Re-uptake (Figure 2.28)
 Recycling of molecules
 Help with fast, efficient neurotransmission (low
signal-to-noise)
o Autoreceptors, Enzymatic Deactivation
 Autoreceptors
 On the presynaptic membrane
 Regulate synthesis and release of
neurotransmitter
 Mostly metabotropic
 Enzymatic deactivation
 Acetylcholine (ACh)
 Acetylcholine esterase (AChE)
o Axo-Axonic Synapses (Figure 2.30)
 Presynaptic inhibition/facilitation
 The AB synapse helps (or interferes with) the BC
synapse
 The AB synapse exerts a presynaptic
facilitation (or inhibition) of the BC synapse
Nonsynaptic Communication
o Some neurotransmitters are released diffusely (leak
out): neuromodulators
 They have slow and diffuse actions (peptides)
 Influence many postsynaptic targets
 Involved in attention, emotions, pain sensitivity
o Most hormones are produced by endocrine glands in the
body (adrenal glands, stomach, liver, etc.)
 Some neurons produce hormones rather than
neurotransmitters
 Some neurons have hormone receptors (target
cells)
 Communication between nervous system
and body
 Sex hormones and aggression, stress
 AP  vesicle fusion  neurotransmitter release  receptor
opening  ion flow  postsynaptic potentials
o Neural integration
 In space
 In time
 Spatial summation
o Post synaptic potentials from different synapses sum up
at the soma
 Temporal Summation
o Post synaptic potentials from the same synapse (but
different action potentials) sum up
 Spatio-Temporal Summation (Figure 2.29)
o Sum up to maybe an AP generated if big enough
When Synaptic Transmission goes wrong
 Not enough neurotransmitter binding: ACh and Myasthenia
gravis treated by inhibition of enzymatic deactivation
 Not enough neurotransmitter binding: Depression and SSRI
 Weakness of postsynaptic receptors: Dopamine and drug
addiction
 Too much binding: dopamine and Schizophrenia
 Death of presynaptic neurons that produce a specific
neurotransmitter: dopamine and Parkinson’s disease
 Change in number/sensitivity of postsynaptic receptors:
Glutamate and learning and memory
Seven steps of neurotransmission
 1. Neurotransmitter molecules are synthesize dform
precursors under influence of enzymes
 2. Neurotransmitter molecules are stored in vesicles
 3. Neurotransmitter molecules that leak from their vesicles
are destroyed by enzymes
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4. Action potentials cause vesicles to fuse with the
presynaptic membrane and release their neurotransmitter
molecules into the synapse
5. Released neurotransmitter molecules bind with
Autoreceptors and inhibit subsequent neurotransmitter
release
6. Released neurotransmitter molecules bind to postsynaptic
receptors
7. Released neurotransmitter molecules are deactivated either
by reuptake or enzymatic degradation