Learning in the Aplysia Californica

basic functioning of the aplysia californica

SN = sensory neuron
MN = Motor neuron
Exc = excitatory node
Inh = inhibitory node
TSN = tail sensory neuron

the gill is essential for survival
but when the gill is closed too long, it cannot breathe
if you touch the area around the gill (siphon), the gill retracts inward

There are two ways to activate the MN. One fast one and a delayed one via the Exc. In case one fails, there is still the other.
After a delay, the Inh is also activated, which will, after a delay, deactivate the Exc branch.

Also, when the tail receives a shock, it makes the SN, MN and Exc more excitable. But it does not cause the gill to retract; it’s not enough for that.
The input merely enhances the strength of the signalling when the siphon is being touched.

Learning

When the tail is shocked, TSN releases Serotonin (triggering cAMP) into SN increasing the amount of neurotransmitter to activate MN for about a minute.
When the siphon is touched now, the gill will retract for twice as long.

When the tail is shocked 4 times in a row, there is more stuff released into SN. That much serotonin activates a Genee on the 031 🧬DNA that produces a Protein that stabilizes the Neurotransmitter so that it is resistant to degradation. → the neurotransmitter stays around for longer
⇒ leads to a retraction of the gill for 3 times as long

What if the tail is shocked with intensive shocks for a few days in a row?
→ activates a whole range of genes
⇒ creating a new synapse
-⇒ retracting the gill for 10 times as long

now it takes weeks to months for the synapse to reconstruct to all things getting back to normal

Transclude of Habituation#habituation-in-aplysia-californica

Why do the voltage-gated calcium channels release less calcium into the SN after repeated touches of the siphon (habituation)?

chatbot
The decreased responsiveness of voltage-gated calcium channels during habituation in Aplysia is due to synaptic plasticity, specifically changes in the properties of the presynaptic terminal in response to repeated, non-threatening stimulation. Several mechanisms contribute to this reduction in calcium channel activity:

1. Inactivation of Calcium Channels

One of the primary reasons voltage-gated calcium channels become less responsive is through a process called channel inactivation. After repeated siphon stimulation, these channels may enter a state where they are less likely to open in response to depolarization of the presynaptic membrane. This is a protective mechanism seen in many types of ion channels that prevents over-activation or excessive calcium influx, which can be damaging to neurons.

Over time, with repeated siphon touches, calcium channels enter a state of partial inactivation, reducing the amount of calcium that enters the neuron during each action potential. This reduction in calcium influx directly leads to less neurotransmitter release.

2. Decreased Sensory Neuron Excitability

Another factor contributing to decreased calcium channel responsiveness is a decrease in the excitability of the sensory neurons. With repeated stimulation, the sensory neuron membrane can become more resistant to depolarization. This is often due to a reduction in sodium or potassium channel activity that affects the overall excitability of the neuron. If the neuron depolarizes less effectively, the voltage change is not strong enough to fully activate the calcium channels, leading to a reduced calcium influx.

3. Modulatory Effects of Intracellular Signaling Pathways

Repeated stimulation can also activate intracellular signaling pathways that modulate the function of voltage-gated calcium channels. For example, a reduction in calcium channel responsiveness can be driven by:

Activation of second messenger systems (e.g., cAMP or cGMP): Repeated non-threatening stimulation can activate signaling molecules that reduce the activity of calcium channels through phosphorylation or other modifications.
Involvement of protein kinases: Enzymes like protein kinase C (PKC) or protein kinase A (PKA) may become activated and phosphorylate calcium channels or associated proteins, leading to a reduction in their activity or a decrease in the likelihood that they open in response to membrane depolarization.

4. Reduction in Synaptic Vesicle Cycling

Another factor contributing to the reduced calcium influx is synaptic fatigue or a reduction in the availability of synaptic vesicles. With repeated stimulation, fewer synaptic vesicles may be available for release, which could trigger feedback mechanisms that reduce calcium channel responsiveness to avoid excessive calcium entry when it is not needed.

5. Negative Feedback Mechanisms

Neurons often have negative feedback mechanisms to prevent excessive calcium influx, which can be toxic to the cell. Calcium-sensitive proteins in the neuron may detect high intracellular calcium levels after repeated siphon stimulation and actively reduce the sensitivity of the calcium channels to protect the neuron from calcium overload. This feedback ensures that, over time, the neuron becomes less responsive to repeated, non-threatening stimuli.

Summary:

Voltage-gated calcium channels in Aplysia become less responsive with repeated siphon touches due to several mechanisms:

Inactivation of the calcium channels themselves.
Reduced excitability of the sensory neuron membrane, making it harder to depolarize.
Modulatory intracellular signaling pathways that alter channel function.
Negative feedback mechanisms to prevent excessive calcium influx. These changes are adaptive and represent the cellular basis for habituation, reducing the strength of the gill withdrawal reflex in response to harmless stimuli.

Sensitization in Aplysia californica

Sensitivity and Learning: In the context of learning processes like habituation and sensitization in Aplysia, the role of calcium influx becomes particularly interesting. For example, during habituation (a decrease in response to a repeated, harmless stimulus), repeated stimulation leads to a decrease in calcium influx into the sensory neurons. This results in less neurotransmitter being released and, therefore, a reduced response in the connecting neurons over time.

In contrast, during sensitization (an increased response to a stimulus following a noxious or strong stimulus), there is an enhanced calcium influx in response to stimuli, leading to more neurotransmitter release and a stronger response. This can be mediated by modulatory neurons that release serotonin or other neuromodulators, which increase the sensitivity of the sensory neuron to calcium influx, thereby amplifying the response.

Due to the greater activation of the sensory neuron, another interneuron is activated also releasing Serotonin enhance the signalling between the sensory and the motor neuron. This is done by a prolonged Action Potential, therefore allowing more calcium to enter the sensory neuron. Therefore there is a longer retraction of the gill.

Neuronal Correlates of Learning in Aplysia

Klassische Konditionierung des Kiemenrückzugreflexes findet nur statt, wenn der
Berührungs-CS etwa ½ Sekunde vor der elektrischen Reizung des Schwanzeserfolgt.

Paradigm	Associative	Stimulus specific	Mechanisms	short term (s), long term (l)
Habituation	no	yes	presynaptic Decrease of Glutamate levels	s: cellular
Sensitivierung	no	no	Serotonin-induced increase of Glutamate levels	s: cellular
Classical Conditioning	yes	yes	1. presynaptic: activity-depending enhancement of Glutamate release at sensory neuron; 2. postsynaptic change: in Receptor of the motor neuron (LTP - long term potentiation works); 3. cascade of intrazellulär molecular events: activate Genes in the cell nucleus → increase of synapses from sensory to motor neuron, long term	s : cellular and l: structural

Source

Chapter 12 The Ancient Gear within Us How Does Change Happen?

Created: 14-09-24 14:32

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Learning in the Aplysia Californica