Publications by authors named "Franklin B Krasne"

Here, we propose a model of memory (BaconREM), which is an extension of a previously published Bayesian model of context fear learning (BACON) that accounts for many aspects of learned context fear. BaconREM simulates most known phenomenology of remote context fear as studied in rodents and makes new predictions. In particular, it predicts the well-known observation that fear that was conditioned to a recently encoded context becomes hippocampus-independent and shows much-enhanced generalization ("hyper-generalization") when systems consolidation occurs (i.

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There are sex differences in anxiety disorders with regard to occurrence and severity of episodes such that females tend to experience more frequent and more severe episodes. Contextual fear learning and generalization are especially relevant to anxiety disorders, which are often defined by expressing fear and/or anxiety in safe contexts. In contextual fear conditioning, a representation of the context must first be created, and then that representation must be paired with an aversive consequence.

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FraidyRat is a teaching tool that allows students to investigate the neural basis of fear conditioning and extinction using a virtual rat with a virtual brain. FraidyRat models well-known phenomena at both a behavioral and neural level. Students use virtual versions of tract tracing, systemic and intracerebrally infused drugs, neural recording, and electrical stimulation to understand the neural substrates underlying the observed behavior.

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The extinction of contextual fear is commonly an essential requirement for successful exposure therapy for fear disorders. However, experimental work on extinction of contextual fear is limited, and there little or no directly relevant theoretical work. Here, we extend BACON, a neurocomputational model of context fear conditioning that provides plausible explanations for a number of aspects of context fear conditioning, to deal with extinction (calling the model BaconX).

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We propose that a major contribution of juvenile and adult hippocampal neurogenesis is to allow behavioral experience to sculpt dentate gyrus connectivity such that sensory attributes that are relevant to the animal's environment are more strongly represented. This "specialized" dentate is then able to store a larger number of discriminable memory representations. Our hypothesis builds on accumulating evidence that neurogenesis declines to low levels prior to adulthood in many species.

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The context in which sudden fearful events occur can be poorly encoded into memory. Yet, the consequences of the resulting context-impoverished memories remain unknown. We demonstrate that restricting the time available for context encoding during contextual fear conditioning causes maladaptively overgeneralized and inextinguishable fear.

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Dentate gyrus (DG) is widely thought to provide a teaching signal that enables hippocampal encoding of memories, but its role during retrieval is poorly understood. Some data and models suggest that DG plays no role in retrieval; others encourage the opposite conclusion. To resolve this controversy, we evaluated the effects of optogenetic inhibition of dorsal DG during context fear conditioning, recall, generalization, and extinction in male mice.

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Contextual fear conditioning is thought to involve the synaptic plasticity-dependent establishment in hippocampus of representations of to-be-conditioned contexts which can then become associated with USs in the amygdala. A conceptual and computational model of this process is proposed in which contextual attributes are assumed to be sampled serially and randomly during contextual exposures. Given this assumption, moment-to-moment information about such attributes will often be quite different from one exposure to another and, in particular, between exposures during which representations are created, exposures during which conditioning occurs, and during recall sessions.

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Considerable evidence seems to show that emotional and reflex reactions to feared situations are mediated by the amygdala. It might therefore seem plausible to expect that amygdala-coded fear should also influence decisions when animals make choices about instrumental actions. However, there is not good evidence of this.

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A neurally oriented conceptual and computational model of fear conditioning manifested by freezing behavior (FRAT), which accounts for many aspects of delay and context conditioning, has been constructed. Conditioning and extinction are the result of neuromodulation-controlled LTP at synapses of thalamic, cortical, and hippocampal afferents on principal cells and inhibitory interneurons of lateral and basal amygdala. The phenomena accounted for by the model (and simulated by the computational version) include conditioning, secondary reinforcement, blocking, the immediate shock deficit, extinction, renewal, and a range of empirically valid effects of pre- and post-training ablation or inactivation of hippocampus or amygdala nuclei.

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To circumvent the many problems in teaching neurophysiology as a "wet lab," we developed SWIMMY, a virtual fish that swims by moving its virtual tail by means of a virtual neural circuit. SWIMMY diminishes the need for expensive equipment, troubleshooting, and manual skills that require practice. Also, SWIMMY effectively replaces live preparations, which some students find objectionable.

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Serotonin can produce multiple, contradictory modulatory effects on strength of synaptic transmission in both vertebrate and invertebrate nerve circuits. In crayfish, serotonin (5-HT) can both facilitate and depress transmission to lateral giant escape command neurons; however, which effect is manifest during application, as well as the sign and duration of effects that may continue long after 5-HT washout, may depend on history of application as well as on concentration. We report that protein kinase A (PKA) signaling is essential to the production of facilitation but depression is mediated by non-cAMP/PKA signaling pathways.

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It is widely assumed that learning results from alterations in the strength of synapses within the neural pathways that mediate a learned behavioral response and that these alterations are directly caused by training-induced activity of neurons connected by the changing synapses. Initial evidence for this view came from studies of habituation of defensive reflexes in several invertebrate species. However, more recent studies of habituation of the escape reflex in one of these species, the crayfish, have shown that habituation is substantially caused by tonic inhibitory input from cephalic ganglia; this descending inhibition suppresses the activity of neurons within the escape circuit, which reside in caudal ganglia.

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Neuromodulation provides a means of changing the excitability of neurons or the effect of synapses, and so extends the performance range of neural circuits. Metamodulation occurs when the neuromodulatory effect is itself modulated, often in response to a change in the behavioral state of the animal. The well-studied neural circuit that mediates escape in the crayfish is modulated by serotonin, and this modulation is subject to two forms of metamodulation.

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We review here factors that control the excitability of the giant neuron-mediated tail-flip escape behavior in crayfish, focusing especially on recent findings concerning serotonergic modulation. Serotonin can either facilitate or inhibit escape depending on concentration and pattern of application. Low concentrations facilitate while high ones inhibit; however, if high concentrations arise gradually they facilitate instead of inhibiting.

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