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Trace conditioning in insects-keep the trace!

Dylla KV, Galili DS, Szyszka P, Lüdke A - Front Physiol (2013)

Bottom Line: It is still unknown how the brain encodes CS traces and how they are associated with a US in trace conditioning.In this review we summarize the recent progress in insect trace conditioning on the behavioral and physiological level and emphasize similarities and differences compared to delay conditioning.Moreover, we examine proposed molecular and computational models and reassess different experimental approaches used for trace conditioning.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Neurobiology, University of Konstanz Konstanz, Germany.

ABSTRACT
Trace conditioning is a form of associative learning that can be induced by presenting a conditioned stimulus (CS) and an unconditioned stimulus (US) following each other, but separated by a temporal gap. This gap distinguishes trace conditioning from classical delay conditioning, where the CS and US overlap. To bridge the temporal gap between both stimuli and to form an association between CS and US in trace conditioning, the brain must keep a neural representation of the CS after its termination-a stimulus trace. Behavioral and physiological studies on trace and delay conditioning revealed similarities between the two forms of learning, like similar memory decay and similar odor identity perception in invertebrates. On the other hand differences were reported also, like the requirement of distinct brain structures in vertebrates or disparities in molecular mechanisms in both vertebrates and invertebrates. For example, in commonly used vertebrate conditioning paradigms the hippocampus is necessary for trace but not for delay conditioning, and Drosophila delay conditioning requires the Rutabaga adenylyl cyclase (Rut-AC), which is dispensable in trace conditioning. It is still unknown how the brain encodes CS traces and how they are associated with a US in trace conditioning. Insects serve as powerful models to address the mechanisms underlying trace conditioning, due to their simple brain anatomy, behavioral accessibility and established methods of genetic interference. In this review we summarize the recent progress in insect trace conditioning on the behavioral and physiological level and emphasize similarities and differences compared to delay conditioning. Moreover, we examine proposed molecular and computational models and reassess different experimental approaches used for trace conditioning.

No MeSH data available.


Related in: MedlinePlus

Models relying on spike timing dependent plasticity (STDP) or biochemical processes can account for trace processes. (Ai) In the model by Izhikevich (2007), the coincident firing of a pre- and then a postsynaptic neuron (within 10 ms; marked by a rectangle) elicits a synaptic eligibility trace c(t) in the corresponding synapse. This eligibility trace decays exponentially to zero. Reinforcement d(t), here a dopamine (DA) release delayed by 1–3 s in combination with the residual eligibility trace, increases the synaptic strength s(t) [s(t) = c × d] of the particular synapse. (Aii) Repeated reinforcement of such a pre–post firing event increasingly strengthens the particular synapse. This in turn increases the probability of coincident firings of this synapse. Adapted from Izhikevich (2007), with permission. (B) Lingering Ca2+ and coincidence detection by an adenylyl cyclase (AC) might account for trace conditioning in the model by Yarali et al. (2012). (Bi) Ca2+ influx and Gα activation (induced by CS and US, respectively) synergistically act on the AC, leading to increased cAMP production and strengthening of the synaptic output. (Bii) In this model Ca2+ is supposed to transiently accelerate both the formation and dissociation rates (kA and kD) of the AC*/Gα* complex to the same extent. When the system is in equilibrium (kA and kD are the same), Ca2+ has no effect on the cAMP level. But when Ca2+ influx shortly precedes the transmitter induced activation of Gα*, the formation (kA) of AC*/Gα* is at this time point the dominant reaction. This leads to a rise in AC*/Gα* concentration and thus, enhanced cAMP production. When Ca2+ influx follows Gα*, the dissociation of AC*/Gα* is promoted, leading to decreased cAMP production. (Biii) This model can account for trace conditioning by changing the Ca2+ decay time constants (different decay time constants chosen are 0.1, 1 and 10 s). The larger decay constants (e.g., 10 s) cause a long tail of Ca2+ transient (upper row). This allows for associations of stimuli over longer interstimulus intervals (ISIs; bottom row) and is critical for reproducing the behavioral measurements of trace conditioning. The longer the Ca2+ decay time is, the larger the negative “associative” effect is in the simulation. This reveals that lingering Ca2+ in KCs might contribute to bridge the temporal gap between CS and US. Note that in this model the US onset is set to 0 and the CS onset shifts to the left for increasing ISIs (CS–US intervals). The negative associative effects correspond to the learned odor avoidance in olfactory aversive delay and trace conditioning. The Ca2+ influx is always constant (rising to a Ca2+ concentration peak of 6 × 10-4 mol/L within 40 ms). Adapted from Yarali et al. (2012).
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Figure 4: Models relying on spike timing dependent plasticity (STDP) or biochemical processes can account for trace processes. (Ai) In the model by Izhikevich (2007), the coincident firing of a pre- and then a postsynaptic neuron (within 10 ms; marked by a rectangle) elicits a synaptic eligibility trace c(t) in the corresponding synapse. This eligibility trace decays exponentially to zero. Reinforcement d(t), here a dopamine (DA) release delayed by 1–3 s in combination with the residual eligibility trace, increases the synaptic strength s(t) [s(t) = c × d] of the particular synapse. (Aii) Repeated reinforcement of such a pre–post firing event increasingly strengthens the particular synapse. This in turn increases the probability of coincident firings of this synapse. Adapted from Izhikevich (2007), with permission. (B) Lingering Ca2+ and coincidence detection by an adenylyl cyclase (AC) might account for trace conditioning in the model by Yarali et al. (2012). (Bi) Ca2+ influx and Gα activation (induced by CS and US, respectively) synergistically act on the AC, leading to increased cAMP production and strengthening of the synaptic output. (Bii) In this model Ca2+ is supposed to transiently accelerate both the formation and dissociation rates (kA and kD) of the AC*/Gα* complex to the same extent. When the system is in equilibrium (kA and kD are the same), Ca2+ has no effect on the cAMP level. But when Ca2+ influx shortly precedes the transmitter induced activation of Gα*, the formation (kA) of AC*/Gα* is at this time point the dominant reaction. This leads to a rise in AC*/Gα* concentration and thus, enhanced cAMP production. When Ca2+ influx follows Gα*, the dissociation of AC*/Gα* is promoted, leading to decreased cAMP production. (Biii) This model can account for trace conditioning by changing the Ca2+ decay time constants (different decay time constants chosen are 0.1, 1 and 10 s). The larger decay constants (e.g., 10 s) cause a long tail of Ca2+ transient (upper row). This allows for associations of stimuli over longer interstimulus intervals (ISIs; bottom row) and is critical for reproducing the behavioral measurements of trace conditioning. The longer the Ca2+ decay time is, the larger the negative “associative” effect is in the simulation. This reveals that lingering Ca2+ in KCs might contribute to bridge the temporal gap between CS and US. Note that in this model the US onset is set to 0 and the CS onset shifts to the left for increasing ISIs (CS–US intervals). The negative associative effects correspond to the learned odor avoidance in olfactory aversive delay and trace conditioning. The Ca2+ influx is always constant (rising to a Ca2+ concentration peak of 6 × 10-4 mol/L within 40 ms). Adapted from Yarali et al. (2012).

Mentions: Other models suggested that the combination of STDP and neuromodulators might solve the timescale discrepancy and explain coincidence detection in trace conditioning. Izhikevich (2007) suggested a network where transient synaptic changes, induced by coincident pre- and postsynaptic spiking (following the STDP rule), were enhanced by a DA reinforcement (Figure 4Ai). These transient synaptic changes—acting as synaptic eligibility traces—could be the activation of an enzyme with slow kinetics, important for synaptic plasticity. In the model, these eligibility traces were exponentially decaying over several seconds. During this decay, the synapse got reinforced by a global DA release (1–3 s after the STDP; Figure 4Ai) leading to a reinforcement of the synaptic eligibility trace and strengthening of the synapse. Other synapses in the network that also elicited coincident firing which was not linked to the reward, were not strengthened. Repetition of reinforcing each such pre–post firing event increasingly strengthened the particular synapse. This in turn increased the probability of coincident firings at this synapse, leading to even more reinforcement (Figure 4Aii). The model shows how STDP might also contribute to insect trace learning when the fast STDP mechanism is combined with slower biochemical processes and subsequently mediated by neuromodulators.


Trace conditioning in insects-keep the trace!

Dylla KV, Galili DS, Szyszka P, Lüdke A - Front Physiol (2013)

Models relying on spike timing dependent plasticity (STDP) or biochemical processes can account for trace processes. (Ai) In the model by Izhikevich (2007), the coincident firing of a pre- and then a postsynaptic neuron (within 10 ms; marked by a rectangle) elicits a synaptic eligibility trace c(t) in the corresponding synapse. This eligibility trace decays exponentially to zero. Reinforcement d(t), here a dopamine (DA) release delayed by 1–3 s in combination with the residual eligibility trace, increases the synaptic strength s(t) [s(t) = c × d] of the particular synapse. (Aii) Repeated reinforcement of such a pre–post firing event increasingly strengthens the particular synapse. This in turn increases the probability of coincident firings of this synapse. Adapted from Izhikevich (2007), with permission. (B) Lingering Ca2+ and coincidence detection by an adenylyl cyclase (AC) might account for trace conditioning in the model by Yarali et al. (2012). (Bi) Ca2+ influx and Gα activation (induced by CS and US, respectively) synergistically act on the AC, leading to increased cAMP production and strengthening of the synaptic output. (Bii) In this model Ca2+ is supposed to transiently accelerate both the formation and dissociation rates (kA and kD) of the AC*/Gα* complex to the same extent. When the system is in equilibrium (kA and kD are the same), Ca2+ has no effect on the cAMP level. But when Ca2+ influx shortly precedes the transmitter induced activation of Gα*, the formation (kA) of AC*/Gα* is at this time point the dominant reaction. This leads to a rise in AC*/Gα* concentration and thus, enhanced cAMP production. When Ca2+ influx follows Gα*, the dissociation of AC*/Gα* is promoted, leading to decreased cAMP production. (Biii) This model can account for trace conditioning by changing the Ca2+ decay time constants (different decay time constants chosen are 0.1, 1 and 10 s). The larger decay constants (e.g., 10 s) cause a long tail of Ca2+ transient (upper row). This allows for associations of stimuli over longer interstimulus intervals (ISIs; bottom row) and is critical for reproducing the behavioral measurements of trace conditioning. The longer the Ca2+ decay time is, the larger the negative “associative” effect is in the simulation. This reveals that lingering Ca2+ in KCs might contribute to bridge the temporal gap between CS and US. Note that in this model the US onset is set to 0 and the CS onset shifts to the left for increasing ISIs (CS–US intervals). The negative associative effects correspond to the learned odor avoidance in olfactory aversive delay and trace conditioning. The Ca2+ influx is always constant (rising to a Ca2+ concentration peak of 6 × 10-4 mol/L within 40 ms). Adapted from Yarali et al. (2012).
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Related In: Results  -  Collection

License
Show All Figures
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Figure 4: Models relying on spike timing dependent plasticity (STDP) or biochemical processes can account for trace processes. (Ai) In the model by Izhikevich (2007), the coincident firing of a pre- and then a postsynaptic neuron (within 10 ms; marked by a rectangle) elicits a synaptic eligibility trace c(t) in the corresponding synapse. This eligibility trace decays exponentially to zero. Reinforcement d(t), here a dopamine (DA) release delayed by 1–3 s in combination with the residual eligibility trace, increases the synaptic strength s(t) [s(t) = c × d] of the particular synapse. (Aii) Repeated reinforcement of such a pre–post firing event increasingly strengthens the particular synapse. This in turn increases the probability of coincident firings of this synapse. Adapted from Izhikevich (2007), with permission. (B) Lingering Ca2+ and coincidence detection by an adenylyl cyclase (AC) might account for trace conditioning in the model by Yarali et al. (2012). (Bi) Ca2+ influx and Gα activation (induced by CS and US, respectively) synergistically act on the AC, leading to increased cAMP production and strengthening of the synaptic output. (Bii) In this model Ca2+ is supposed to transiently accelerate both the formation and dissociation rates (kA and kD) of the AC*/Gα* complex to the same extent. When the system is in equilibrium (kA and kD are the same), Ca2+ has no effect on the cAMP level. But when Ca2+ influx shortly precedes the transmitter induced activation of Gα*, the formation (kA) of AC*/Gα* is at this time point the dominant reaction. This leads to a rise in AC*/Gα* concentration and thus, enhanced cAMP production. When Ca2+ influx follows Gα*, the dissociation of AC*/Gα* is promoted, leading to decreased cAMP production. (Biii) This model can account for trace conditioning by changing the Ca2+ decay time constants (different decay time constants chosen are 0.1, 1 and 10 s). The larger decay constants (e.g., 10 s) cause a long tail of Ca2+ transient (upper row). This allows for associations of stimuli over longer interstimulus intervals (ISIs; bottom row) and is critical for reproducing the behavioral measurements of trace conditioning. The longer the Ca2+ decay time is, the larger the negative “associative” effect is in the simulation. This reveals that lingering Ca2+ in KCs might contribute to bridge the temporal gap between CS and US. Note that in this model the US onset is set to 0 and the CS onset shifts to the left for increasing ISIs (CS–US intervals). The negative associative effects correspond to the learned odor avoidance in olfactory aversive delay and trace conditioning. The Ca2+ influx is always constant (rising to a Ca2+ concentration peak of 6 × 10-4 mol/L within 40 ms). Adapted from Yarali et al. (2012).
Mentions: Other models suggested that the combination of STDP and neuromodulators might solve the timescale discrepancy and explain coincidence detection in trace conditioning. Izhikevich (2007) suggested a network where transient synaptic changes, induced by coincident pre- and postsynaptic spiking (following the STDP rule), were enhanced by a DA reinforcement (Figure 4Ai). These transient synaptic changes—acting as synaptic eligibility traces—could be the activation of an enzyme with slow kinetics, important for synaptic plasticity. In the model, these eligibility traces were exponentially decaying over several seconds. During this decay, the synapse got reinforced by a global DA release (1–3 s after the STDP; Figure 4Ai) leading to a reinforcement of the synaptic eligibility trace and strengthening of the synapse. Other synapses in the network that also elicited coincident firing which was not linked to the reward, were not strengthened. Repetition of reinforcing each such pre–post firing event increasingly strengthened the particular synapse. This in turn increased the probability of coincident firings at this synapse, leading to even more reinforcement (Figure 4Aii). The model shows how STDP might also contribute to insect trace learning when the fast STDP mechanism is combined with slower biochemical processes and subsequently mediated by neuromodulators.

Bottom Line: It is still unknown how the brain encodes CS traces and how they are associated with a US in trace conditioning.In this review we summarize the recent progress in insect trace conditioning on the behavioral and physiological level and emphasize similarities and differences compared to delay conditioning.Moreover, we examine proposed molecular and computational models and reassess different experimental approaches used for trace conditioning.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Neurobiology, University of Konstanz Konstanz, Germany.

ABSTRACT
Trace conditioning is a form of associative learning that can be induced by presenting a conditioned stimulus (CS) and an unconditioned stimulus (US) following each other, but separated by a temporal gap. This gap distinguishes trace conditioning from classical delay conditioning, where the CS and US overlap. To bridge the temporal gap between both stimuli and to form an association between CS and US in trace conditioning, the brain must keep a neural representation of the CS after its termination-a stimulus trace. Behavioral and physiological studies on trace and delay conditioning revealed similarities between the two forms of learning, like similar memory decay and similar odor identity perception in invertebrates. On the other hand differences were reported also, like the requirement of distinct brain structures in vertebrates or disparities in molecular mechanisms in both vertebrates and invertebrates. For example, in commonly used vertebrate conditioning paradigms the hippocampus is necessary for trace but not for delay conditioning, and Drosophila delay conditioning requires the Rutabaga adenylyl cyclase (Rut-AC), which is dispensable in trace conditioning. It is still unknown how the brain encodes CS traces and how they are associated with a US in trace conditioning. Insects serve as powerful models to address the mechanisms underlying trace conditioning, due to their simple brain anatomy, behavioral accessibility and established methods of genetic interference. In this review we summarize the recent progress in insect trace conditioning on the behavioral and physiological level and emphasize similarities and differences compared to delay conditioning. Moreover, we examine proposed molecular and computational models and reassess different experimental approaches used for trace conditioning.

No MeSH data available.


Related in: MedlinePlus