Lecture 21- Communication Between Nerve Cells Flashcards
What is synaptic plasticity?
-Is a form of neuromodulation
-Defined as the activity-dependent modification of the strength (or efficacy) of synaptic transmission
Is synaptic plasticity as a form of neuromodulation short or long lasting?
Short or long-lasting
What processes does synaptic plasticity underly?
Underpins learning and memory
What are the two ways which we can study learning and memory? What are they each ideal for?
-in vitro= molecular and cellular events
-in vivo= behaviour
What are some examples of in vitro techniques?
- Cells in culture
- Acute brain slices
e.g. hippocampal slices (only last a few hours)
Organotypic brain slices (last a lot longer than hippocampal) - others
What are some examples of in vivo techniques?
- Simple invertebrate models
- Vertebrate rodent models
- Others
- Cellular events too
What are some advantages and disadvantages of in vitro techniques?
-Advantage= easy to apply drugs and see effect
-Disadvantage= true circuitry isn’t actually actually being reflected
What are two examples of Invertebrate models?
- Drosophila melanogaster
- Aplysia californica
What are the advantages associated with the Drosophila melanogaster invertebrate model?
Small genome and rapid life cycle
* Drosophila is good for genetics
* Small nervous system
* ~135,000 neurons
* Easy to identify and circuits
What are the advantages associated with the Aplysia californica invertebrate model?
- Small nervous system
- ~1,000 neurons
- Large neurons
- Easy to impale and record from
- Easy to identify individual neurons and
circuits
What is the Aplysia californica method for learning and memory?
Siphon-gill-withdrawal reflex:
* Tactile stimulus to siphon causes gill withdrawal
* This reflex undergoes habituation or sensitization (a simple form of learning)
when a noxious stimulus is applied.
What are the two types of Nonassociative learning than result in behavioural responses? Draw what neural activity looks like in these processes on a graph…
Habituation: learning to ignore a stimulus that lacks
meaning
vs.
Sensitization: Stimuli results in increased sensitivity
Graphs shown in slides (12)
What pattern of receptors/ what is happening at the neural level in the siphon-gill-withdrawal reflex?
-Touch activates sensory
neurons in the siphon skin
-Relayed to motor neuron
(L7) in abdominal ganglion
-Stimulates gill muscles and
thus gill withdrawal
What neural changes happen when habituation occurs?
-weakened neurotransmission
-decreased neurotransmitter release from sensory neuron
-fewer vesicles released per action potential
How is Sensitization demonstrated in the Aplysia?
When the siphon of Aplysia is gently touched, the animal withdraws its gill for
a brief period.
* But, if the “touch” is preceded by an electrical shock to its tail, the same gentle
touch to the siphon will elicit a longer period of withdrawal.
* If the Aplysia is given multiple shocks its subsequent response to a gentle
touch on the siphon is much larger and is retained longer.
What does Sensitization to a noxious stimulus delivered to the Aphysia’s tail require neurally?
- a sensory neuron that picks up the stimulus from the tail connecting to
- interneurons that terminate on the sensory neuron in the siphon-gill pathway.
What does Sensitization require?
Sensitization depends on increased synaptic activity, this process is called facilitation
What is presynaptic facilitation? (within the context of the gill withdrawal response)
- Stimuli results in increased sensitivity of the gill withdrawal response
- Noxious stimuli activate interneuron
- This enhances neurotransmitter release
from the sensory neuron presynaptic terminal
and - alters gene expression
What happens at the neuron/ molecule level in presynaptic facilitation as a result of a single tail shock to the Aphysia?
- L29 releases 5HT (serotonin)
- 5-HT (5-hydroxytryptamine receptors), serotonin
- activates 5HT receptors on presynaptic
nerve terminal - stimulates formation of cAMP
- activates protein kinase A (PKA)
!Release of neurotransmitter
What does PKA do in the context of presynaptic facilitation?
PKA increases phosphorylation of K+ channels:
-Phosphorylated K+ channels close
-K+ does not exit terminal as rapidly
-Prolonging the Action potential (limits repolarisation)
-Ca2+-channels increase their opening
What happens in presynaptic facilitation with regards to synaptic vesicles?
Increased mobilisation of synaptic vesicles
-via PKC
What does PKA do to calcium channels? and what is the result of this for the Aphysia?
PKA increases phosphorylation of Ca2+ channels
-voltage-sensitive Ca2+-channels open
-greater Ca2+ influx increases release of neurotransmitter
-stronger signal to motor neuron
-enhanced gill-withdrawal
What happens during presynaptic facillitation where the Aphysia receives multiple tail shocks as opposed to just one?
- L29 releases 5HT (serotonin)
- 5-HT (5-hydroxytryptamine receptors), serotonin
- activates 5HT receptors on presynaptic
nerve terminal - Higher levels of cAMP
- Activates protein kinase A (PKA) which
now moves to the nucleus
-Altered gene expression
-new proteins stimulate synapse growth
In vertebrate models what is long term potentiation?
-Long-lasting activity dependent increase in
synaptic responses
-Brought about by brief patterned high frequency stimulation to excitatory
pathways of hippocampus
