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What is a synapse?
A junction where a neuron communicates with another cell to transmit electrical or chemical signals
What is synaptic transmission?
Communication between two neurons (or neuron and muscle) via neurotransmitters across a synapse
What are the two types of chemical synapses in the CNS?
Excitatory (EPSPs, depolarisation) and Inhibitory (IPSPs, hyperpolarisation)
What neurotransmitters are used in excitatory synapses?
Glutamate and Acetylcholine
What ions are involved in EPSPs?
Na⁺ (dominant), K⁺, sometimes Ca²⁺
What neurotransmitters are used in inhibitory synapses?
GABA and Glycine
What ions are involved in IPSPs?
K⁺ (out) or Cl⁻ (in) → hyperpolarisation
How is neurotransmitter released from a presynaptic neuron?
AP arrives → Ca²⁺ channels open → Ca²⁺ influx triggers vesicle fusion and exocytosis of neurotransmitters
What happens when neurotransmitters reach the postsynaptic cell?
They bind to ligand-gated ion channels → ion flow → EPSP or IPSP
What is an example of a synapse at the neuromuscular junction?
Uses ACh; always suprathreshold → always triggers AP in muscle
What condition is linked to impaired neuromuscular junctions?
Myasthenia Gravis – autoimmune breakdown in ACh signalling → muscle weakness
What are the main classes of neurotransmitters in the CNS?
Amino acids: Glutamate, GABA, Glycine
ACh (Acetylcholine)
Amines: Dopamine, Serotonin (5-HT), Noradrenaline
Neuropeptides: Substance P, Enkephalin, Neuropeptide Y
What’s the difference between classic and peptide neurotransmitters?
Classic: fast, direct (milliseconds); Peptides: slow, modulatory (seconds–minutes)
What is Long-Term Potentiation (LTP)?
Long-lasting strengthening of synapses from high-frequency stimulation → ↑Ca²⁺, ↑AMPA receptors
What is Long-Term Depression (LTD)?
Long-lasting weakening of synapses from low-frequency stimulation → ↓Ca²⁺, ↓AMPA receptors
Why is neurotransmitter inactivation important?
Prevents continuous activation of the postsynaptic neuron
What are the methods of neurotransmitter inactivation?
Diffusion from cleft
Enzymatic degradation (e.g. ACh by ACh-esterase)
Reuptake by presynaptic cell (e.g. dopamine/serotonin transporters)
What’s an example of multiple receptors for the same neurotransmitter?
Glutamate → NMDA, AMPA, kainate receptors (different responses in different cells)
What is excitotoxicity?
Excess glutamate causes overactivation of receptors → Ca²⁺ overload → neuron death
What conditions are linked to excitotoxicity?
Stroke, epilepsy, neurodegenerative diseases
What is temporal summation?
Multiple EPSPs from one synapse in rapid succession
What is spatial summation?
Multiple EPSPs from different synapses at the same time
How many mV does a single EPSP/IPSP contribute?
~0.1 mV at axon hillock
What happens if a neuron lacks GABA receptors?
No IPSPs → more excitable → potential seizures or overfiring