Synapses and Synaptic Transmission Flashcards
A disease that involves dysfunction of ion channels = ?
Synapses and Synaptic Transmission
Channelopathy:
- Is a disease that involves dysfunction of ion channels
Disorders of Synaptic Function
Electrical signals carry information within a single neuron, communication between neurons is a _ process = ?
Synapses and Synaptic Transmission
Electrical signals carry information within a single neuron, communication between neurons is a chemical process.
Three components/structure of the synapse = ?
Synapses and Synaptic Transmission
Components & Structure of the Synapse:
- Presynaptic terminal
- Synaptic cleft
- Postsynaptic terminal (which can be another neuron, muscle cell, gland or any cell of an organ)
Types of Synapses
Synaptic transmission can occur on = ?
Synapses and Synaptic Transmission
Types of Synapses
(a) Synaptic communications between neurons (synaptic transmission) can occur on:
- cell body (axosomatic synapse)
- dendrites (axodendritic)
- axon (axoaxonic)
11 steps in synaptic transmission = ?
Synapses and Synaptic Transmission
Synaptic Transmission - Steps:
What role does Ca2+ play in vesicle fusion = ?
Synapses and Synaptic Transmission
Critical role of Ca2+ in Vesicle Fusion:
- Depolarization of the presynaptic membrane = Opens voltage-gated Ca++ channels.
- Notes:
- Influx of Ca++ is necessary and sufficient for vesicle fusion and neurotransmitter release.
- The amount of neurotransmitter released is very sensitive to the exact amount of Ca++ that enters.
Electrical Potentials at Synapses
Local changes in ion concentration across the postsynaptic membrane can be either = ?
Synapses and Synaptic Transmission
Electrical Potentials at Synapses - Postsynaptic Potentials:
“Local changes in ion concentration across the postsynaptic membrane” and can be either:
(-) Excitatory (from a local depolarization)
- Excitatory Postsynaptic potential (EPSP)
(-) Inhibitory (from a local hyperpolarization)
- Inhibitory Postsynaptic Potential (IPSP)
Electrical Potentials at Synapses
Presynaptic effects can be either = ?
Synapses and Synaptic Transmission
Electrical Potentials at Synapses:
(-) Presynaptic effects =
- Facilitation
- Inhibition
(-) Notes:
(-) Postsynaptic potentials:
“Local changes in ion concentration across the postsynaptic membrane” and can be either:
- Excitatory (from a local depolarization) =
- Excitatory Post Synaptic Potential (EPSP)
- Inhibitory (from a local hyperpolarization) =
- Inhibitory PostSynaptic Potential (IPSP)
Summation of Postsynaptic Potentials
Action potential triggered when = ?
Synapses and Synaptic Transmission
Summation of Postsynaptic Potentials:
(a) Only if the overall summation (both EPSPs and IPSPs) is sufficient to depolarize the cell to threshold at the axon hillock, is an action potential triggered.
Neurotransmitters, Neuromodulators, and Synaptic Receptors
Chemicals that convey information among neurons:
- Neurotransmitters are released by a = ?
- Neuromodulators are released into = ?
Synapses and Synaptic Transmission
Chemicals that convey information among neurons:
(a) Neurotransmitters:
- Released by a presynaptic neuron into the synaptic cleft (e.g., glutamate)
- Acts directly on postsynaptic ion channels or activates proteins inside the postsynaptic neuron.
(b) Neuromodulators:
- Released into extracellular fluid and adjust the activity of many neurons.
- Alter neural function by acting at a distance away from the synaptic cleft.
- Effects manifest more slowly and usually last longer than those of neurotransmitters, which happen in seconds; the effects last from minutes to days.
Neurotransmitters and Synaptic Receptors
The same molecule can act as neurotransmitter or neuromodulator depending on = ?
Synapses and Synaptic Transmission
Neurotransmitters and Synaptic Receptors:
(-) May excite or inhibit the postsynaptic neuron, depending on:
- The molecules released (e.g., ACh, Dopamine, GABA), and
- The receptors they interact with
Notes
(-) The same molecule can act as neurotransmitter or neuromodulator depending on whether molecule is released at the synapse or the extracellular fluid.
(-) Synaptic receptors are typically named for the transmitter/modulator to which they bind (e.g., glutamate and GABA receptors)
Common Neurotransmitter and Modulators
Synapses and Synaptic Transmission
Common Neurotransmitter and Modulators:
Neurotransmitter
- Agonists are drugs that = ?
- Antagonists are drugs that = ?
Synapses and Synaptic Transmission
Neurotransmitter - Agonists and Antagonists:
(a) Agonists:
- Drugs that bind to the receptor and mimic the effects of naturally occurring neurotransmitters (e.g., dopamine agonist).
(b) Antagonists:
- Drugs that prevent the release of neurotransmitters or bind to the receptor and impede the effects of a naturally occurring transmitter (e.g., botulinum toxin (BOTOX).
Acetylcholine
- Excitatory or Inhibitory = ?
- Site of action = ?
- Transmitter binding causes = ?
- Clinical application = ?
Synapses and Synaptic Transmission
Acetylcholine:
(-) Excitatory
(-) Site of action:
- PNS: Excititory at all neuromuscular junctions.
(-) Transmitter binding causes:
- Initiation of skeletal muscle contraction.
- Slowing of heart rate
- Increased digestive secretions and smooth muscle contractions
- Eye - Pupil constriction
(-) Clinical application:
- Myathsthenia gravis, disease destroys ACh receptors
- Botulinum toxin inhibits ACh release
- Nerve and organophosphate insecticides (prolong ACh effect, causing tetanic muscle contractions)
- Curare blocks nicitinic ACh receptors, causing skeletal muscle paralysis
Norepinephrine
- Excitatory or Inhibitory = ?
- Transmitter binding causes = ?
- Clinical application = ?
Synapses and Synaptic Transmission
Norepinephrine:
(-) Excitatory/Inhibitory
(-) Transmitter binding causes:
- Increased HR
- Control of mood; increased attention to sensory information
(c) Clinical application:
- Propranol blocks B-receptors preventing heart disease
Dopamine
- Excitatory or Inhibitory = ?
- Transmitter binding causes = ?
- Clinical application = ?
Synapses and Synaptic Transmission
Dopamine:
(-) Excitatory/Inhibitory
(-) Transmitter binding causes:
- Feelings of pleasure; reinforcement of behaviors, including behaviors associated with drug use.
- Decision making and goal-orientated bahvior (caudate head); control of movement (putamen).
(-) Clinical application:
- Parkinson’s disease (movement and cognitive disorders): DA levels in caudate and putamen are inadequete.
- L-DOPA = A drug used to treat Parkinson’s disease, is converted to DA in the brain.
- Drugs for Parkinson’s to increase dopamine can induce involuntary movements.
Serotonin
- Site of action = ?
- Transmitter binding causes = ?
- Clinical application = ?
Synapses and Synaptic Transmission
Serotonin:
(-) Site of action:
- Throughout the gray matter in spinal cord and brain.
(-) Transmitter binding causes:
- Regulation of sleep, appetite, arousal, mood.
(-) Clinical application:
- Low levels of 5-HT are associated with depression and anxiety.
- Serotonin reuptake inhibitors (including Prozac) treat depression and anxiety.
- High levels of 5-HT assciated with OCD and with some symptoms of schizophrenia.
GABA
- Excitatory or Inhibitory = ?
- Transmitter binding causes = ?
- Clinical application = ?
Synapses and Synaptic Transmission
GABA: Main inhibitory neurotransmitter
(-) Inhibitory
(-) Transmitter binding causes:
- Sedation
- Anti-anxiety
- Anti-seizure
- Sleep inducing
(-) Clinical application:
- Benzodiazepines (including Valium) enhance action of GABA.
- In epilepsy, drugs that increase GABA levels can decrease the excessive neural activity.
Glutamate
- Excitatory or Inhibitory = ?
- Transmitter binding causes = ?
- Clinical application = ?
Synapses and Synaptic Transmission
Glutamate
(-) Excitatory
(-) Transmitter binding causes:
- Learning and memory
(-) Clinical application:
- Excessive glutamate levels can cause epileptic seizures.
- Excessive release of glutamate by dying neurons causes excitotoxicity; death of neurons due to overstimulation.
Endorphins
- Excitatory or Inhibitory = ?
- Transmitter binding causes = ?
Synapses and Synaptic Transmission
Endorphins:
(-) Usually Inhibitory
(-) Transmitter binding causes:
- Inhibiting of pain signaling
Substance P
- Excitatory or Inhibitory = ?
- Transmitter binding causes = ?
Synapses and Synaptic Transmission
Substance P:
(-) Usually excitatory
(-) Transmitter binding causes:
- Sensation of Pain
- Respiratory and cardiovascular control
- Mood regulation; signals interpreted as pain
Overview of Treatment
Neuropharmacological therapies are based on drugs that affect = ?
Synapses and Synaptic Transmission
Overview of Treatment:
- Many neuropharmacological therapies are based on drugs that affect neurotransmitters , their receptors , and/or the transporters responsible for removal of neurotransmitters from the synaptic cleft.
Describe this picture
nothing on back right now
Synapses and Synaptic Transmission
Lambert-Eaton syndrome = ?
Synapses and Synaptic Transmission
Disease affecting the NM junction: Signaling between efferent nerve terminals and muscle cells can be disrupted by disease
(b) Lambert-Eaton syndrome:
- Cause: autoimmune disorder
- Disease in which antibodies destroy voltage-gated Ca++ channels in the presynaptic terminal
- Decreased release of neurotransmitter
- ” “ Excitation of neurotransmitter and muscle
- Weakness
- Trouble walking
- Fatigue
Myasthenia gravis = ?
Synapses and Synaptic Transmission
Disorders of Synaptic Function:
(a) Myasthenia gravis:
- Disease in which antibodies attack and destroy acetylcholine receptors on muscle cells.
- Normal amount of ACh is released into the cleft; but few receptors are available for binding.
- Affecting the neuromuscular junction
Myasthenia Gravis
- What is it = ?
- Clinical features = ?
Synapses and Synaptic Transmission
Myasthenia Gravis = Disorder of Synaptic Function.
- Autoimmune attack on postsynaptic acetylcholine (ACh) receptors (AChRs) that disrupts synaptic transmission
(-) Clinical features:
- Repetitive use of muscle leads to increased weakness.
- Usually affects eye movements or eyelids first (dropping of eyelid).
- Facial expression, proximal limb muscles and swallowing is also affected, difficulty speaking, weakness of breathing muscles.
Myasthenia Gravis - Clinical Features
- W = ?
- E = ?
- A = ?
- K = ?
- N = ?
- E = ?
- S = ?
- S = ?
Synapses and Synaptic Transmission
Myasthenia gravis - Clinical Features:
- W = weakness of neck, face, eyes, arms, legs
- E = Eyelid dropping: Ptosis
- A = Appearance (not a lot of expressions)
- K = Keep choking, gaging while eating
- N = No energy
- E = extraocular muscle weakness, diplopia (double vision)
- S = slurred speech, hoarse voice
- S = shortness of breath
Myasthenia Gravis
Treatment = ?
Synapses and Synaptic Transmission
Myasthenia Gravis - Treatment:
(-) Drugs that inhibit the breakdown of ACh receptors usually improve function.
- They increase the amount of time available to bind with remaining receptors.
- Neostigmine (cholinesterase inhibitor).
(-) Removal of thymus gland, an immune organ
(-) Immunosuppressive drugs
(-) Plasmapheresis : Process of removing blood from the body, separating plasma and cells, returning blood cells and replacing plasma with plasma substitute.
