Event Timing in Associative Learning: From Biochemical Reaction Dynamics to Behavioural Observations

Yarali, Ayse; Nehrkorn, Johannes; Tanimoto, Hiromu; Herz, Andreas V. M.

doi:10.1371/journal.pone.0032885

Cited by 24 publications

(32 citation statements)

References 63 publications

(118 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This was explored in a computational study by Yarali et al (2012). In their model, upon the application of shock-alone, all Kenyon cells receive a shock-induced neuromodulatory signal, which triggers G-protein signaling, consequently activating the adenylate cyclase.…”

Section: Possible Mechanisms Underlying Relief-learningmentioning

confidence: 99%

“…In any event, both Drew and Abbott's (2006) STDP-based model and the adenylate cyclase-based model by Yarali et al (2012) follow the "canonical" view of short-term mnemonic odor coding in the mushroom body, holding that odors are coded combinatorially across the full array of g-lobe Kenyon cells (regarding longer-term memory, this has recently been challenged by Perisse et al 2013, suggesting that the a/b set of Kenyon cells responsible for 3-h memory may be internally "multiplexed" by valence and/or memory strength). That is, punishment and relief-learning rely on the same olfactory representation such that both kinds of learning modify the same Kenyon cell output synapses onto the same downstream circuit (depicted in Fig.…”

Section: Possible Mechanisms Underlying Relief-learningmentioning

confidence: 99%

See 1 more Smart Citation

Pain-relief learning in flies, rats, and man: basic research and applied perspectives

et al. 2014

Self Cite

View full text Add to dashboard Cite

Memories relating to a painful, negative event are adaptive and can be stored for a lifetime to support preemptive avoidance, escape, or attack behavior. However, under unfavorable circumstances such memories can become overwhelmingly powerful. They may trigger excessively negative psychological states and uncontrollable avoidance of locations, objects, or social interactions. It is therefore obvious that any process to counteract such effects will be of value. In this context, we stress from a basic-research perspective that painful, negative events are "Janus-faced" in the sense that there are actually two aspects about them that are worth remembering: What made them happen and what made them cease. We review published findings from fruit flies, rats, and man showing that both aspects, respectively related to the onset and the offset of the negative event, induce distinct and oppositely valenced memories: Stimuli experienced before an electric shock acquire negative valence as they signal upcoming punishment, whereas stimuli experienced after an electric shock acquire positive valence because of their association with the relieving cessation of pain. We discuss how memories for such punishment-and relief-learning are organized, how this organization fits into the threat-imminence model of defensive behavior, and what perspectives these considerations offer for applied psychology in the context of trauma, panic, and nonsuicidal self-injury.The acknowledged "negative" mnemonic effects of adverse experiences mostly relate to what happens before the onset of an aversive, painful event. However, there is a less widely acknowledged type of memory that relates to what happens after the offset of or after escape from such a painful event, at the moment of "relief" (Fig. 1) (we use "relief" to refer specifically to the acute effects of punishment offset; an equally legitimate yet broader use of the word in, e.g., "fear relief," encompasses any process that eases fear [Riebe et al. 2012]). Indeed, in experimental settings, it turns out that stimuli experienced before and during a punishing episode are later avoided as they signal upcoming punishment, whereas stimuli experienced after a painful episode can subsequently prompt approach behavior, arguably (Box 1) because of their association with the relieving cessation of pain (Konorski 1948;Smith and Buchanan 1954;Wolpe and Lazarus 1966;Zanna et al. 1970;Solomon and Corbit 1974;Schull 1979;Solomon 1980;Wagner 1981;Walasek et al. 1995;Tanimoto et al. 2004;Yarali et al. 2008Yarali et al. , 2009bAndreatta et al. 2010Andreatta et al. , 2012Yarali and Gerber 2010;Ilango et al. 2012;Navratilova et al. 2012;Diegelmann et al. 2013b); for a corresponding finding in the appetitive domain, see Hellstern et al. (1998) andFelsenberg et al. (2013). Such relief can both support the learning of the cues associated with the disappearance of the threat and reinforce those behaviors that helped to escape it. Obviously, the positive conditioned valence of and ensuing learned approach behavi...

show abstract

Section: Possible Mechanisms Underlying Relief-learningmentioning

confidence: 99%

Section: Possible Mechanisms Underlying Relief-learningmentioning

confidence: 99%

Pain-relief learning in flies, rats, and man: basic research and applied perspectives

et al. 2014

Self Cite

View full text Add to dashboard Cite

show abstract

“…Several modeling approaches aiming at the neural circuits and/or molecular mechanisms of associative learning might help to understand trace conditioning (Desmond and Moore, 1988; Drew and Abbott, 2006; Izhikevich, 2007; Yarali et al, 2012). The models are based on the mechanism of synaptic plasticity: strengthening the synapses where stimuli coincide.…”

Section: Computational Models Reveal Potential Mechanisms For Trace Lmentioning

confidence: 99%

“…Adapted from Izhikevich (2007), with permission. (B) Lingering Ca 2+ and coincidence detection by an adenylyl cyclase (AC) might account for trace conditioning in the model by Yarali et al (2012). (Bi) Ca 2+ 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.…”

Section: Computational Models Reveal Potential Mechanisms For Trace Lmentioning

confidence: 99%

See 1 more Smart Citation

Trace conditioning in insects—keep the trace!

Dylla¹,

Galili²,

Szyszka³

et al. 2013

Front. Physiol.

View full text Add to dashboard Cite

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.

show abstract