Lect 15 - CNS (Neurotransmitters) Flashcards
Channel Linked vs Ligand Gateed
Channel Linked (Ionotropic)
Fast acting
Ligand-Gated
When neurotransmitter leaves channel closes
G-Protein-Coupled Receptors (Metabotropic)
Slow acting
Ionotropic
Receptors is an Ion Channel
Directly Gated
Fast Response
Ex. Change in charge distribution
Metabotropic
Receptor acts through a G Protein
Ex. G-protein causes direct coupling and opens an ion channel
Steps in Synaptic Communication
- Action Potential Initiated
- Voltage-Gated Ca2+ Channels Open
- Ca2+ enters and triggers vesicle docking and secretion into synaptic cleft
- Neurotransmitter diffuse and binds to receptor on postsynaptic neuron
- Response in Cell, can lead to further messengers and amplification of signal
- Degradation by enzyme (Happens in multiple locations)
- Neurotransmitter is reuptake into presynaptic terminal by transported
Can be degraded or recycled - Diffusion out of synaptic cleft
Acetylcholine (Found Where)
PNS and CNS
Most abundant neurotransmitter in PNS
Acetylcholine (Synthesis)
Acetyl CoA + Choline –> Acetylcholine + CoA
Synthesized in axon terminal (presynaptic)
Acetylcholine (Enzyme for Synthesis)
Choline Acetyl Transferase (CAT)
Acetylcholine (Breakdown)
Acetylcholine –> Acetate + Choline
Occurs in synaptic cleft
Acetylcholinesterase (AChE)
Acetylcholine Synaptic Communication Path
- Synthesized in terminal
Choline + Acetyl Coenzyme A by Choline Acetyl Transferase (CAT) - Stored in synaptic vesicles
- Vesicles dock and secreted ACh into synaptic cleft
- ACh can bind with Cholinergic Receptors on postsynaptic cell
- ACh can be degraded by AChe into choline and acetate
- Choline is actively transported (reuptake) back into presynaptic terminal and reused
ACh (Classification)
Cholinergic Neurons
Can be excitatory or inhibitory
ACh (Receptor Types)
Nicotinic (Ionotropic)
Muscarinic (Metabotropic)
ACh (CNS Effects)
Few cholinergic nuclei, widespread projection of efferents
Cognition, Behaviour, Memory, Attention, Learning
ACh (nAChR)
Reward and Anti-anxiety pathway
ACh (PNS)
ACh is mostly in PNS, acts on:
Neuromuscular Junction
ANS
Alzheimer (Cause)
Degeneration of cholinergic neurons at basal forebrain, which projects to the hippocampus (memory)
Alzheimer (Physiology)
Loss of cholinergic input from the basal forebrain, unable to project properly to hippocampus (memory)
Loss of postsynaptic cells
Loss of frontal/temporal mass
Alzheimer (Histological Signs)
Beta-amyloid Plagues
Neurofibrillary Tangle
Alzheimer (Symptomology)
Memory loss
Deficits in language/perception
Confusion
Advanced: Motor Deficits
Myasthenia Gravis (Cause and Effects)
Autoimmune destruction of nAChR receptors at the motor endplate
–> Less receptors = Less total depolarization
–> Insufficient for AP resulting in reduced transmission
Causes Simpler junctional folds and Weakness of Muscles
Myasthenia Gravis (AChE)
Prevents breakdown of ACh meaning that it stays in synaptic cleft longer
ACh can have prolonged effects and may generate AP