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The hosted weather change looks wrong values: ' proletariat; '. Your poem were an several website. Intrinsic OB circuits display functional plasticity similar to other regions of the brain, including long-term synaptic potentiation Gao and Strowbridge, and adult neurogenesis Lledo et al. Established behavioral paradigms enable insight into the changing form as well as the persistence of odor representations over time, and physiological studies enable measurements of direct correspondence between environmental changes, behavioral performance, and the synaptic and molecular changes that occur in neural circuitry Abraham et al.
In particular, odor learning exhibits varying memory durations that are related to behavioral task parameters and depend on evolving physiological substrates for short-term memory Figure 4 ; McNamara et al. Figure 4. Olfactory generalization gradients measured at various latencies after conditioning. A Progressive decay of a newly learned olfactory generalization gradient over an STM timescale. Mice received 12 massed training trials in which they dug in a dish of sand scented with a 1. Separate cohorts of conditioned mice then were tested at different latencies for their perseverative responses digging times to the odor CS, a highly similar odorant S1, a moderately similar odorant S2, and a structurally and perceptually different odorant D.
Responses declined and generalization gradients flattened with greater training-testing latencies. Methodology follows that of Cleland et al. Four of six latencies tested are depicted for clarity. B Lin-log plot of digging time in the CS during testing at all six latencies tested 2, 10, 30, 60, , min. Figure 5. Learning curves for an odor discrimination task. A Mice received 20 trials of discrimination training Cleland et al.
Twenty-four hours later, the discrimination training was repeated Day 2. The correct trials were scored and averaged across animals. Trials are grouped into 4 blocks of 5 consecutive trials for display and analysis.
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A steady improvement across trials on Day 1 is remembered 1 day later. B Data from trial blocks 1 and 4 replotted for comparison. Comparable findings have been observed by Schellinck et al. In this non-associative olfactory learning paradigm, animals first are habituated to an odorant, responding to repeated presentations with progressively lower investigation times. Some time after habituation, they are presented again with that odorant, or with a series of structurally and perceptually similar odorants cross-habituation , also referred to as spontaneous discrimination.
Perceptually distinct odors elicit normal, non-habituated investigation times, but odorants similar to the habituated odorant elicit reduced, partially-habituated responses depending on the degree of similarity between the habituated and test odorants. A generalization gradient therefore can be constructed by presenting a battery of similar odorants to habituated animals and measuring the pattern of cross-habituation among odorants Cleland et al.
Interestingly, memory for odorant habituation acquired on short timescales tens of seconds is predominantly mediated within piriform cortex Wilson, , whereas habituation on the minutes timescale is localized within OB McNamara et al. Habituation and cross-habituation memory persistence is sensitive to the degree of habituation, declining over a 10—20 min period in standard protocols Freedman et al. Both the extent and persistence of cross-habituation memory are regulated by neuromodulatory and hormonal effects in the OB as well as task parameters and state variables Mandairon et al.
Generalization gradients also can be measured in response to odorants that are conditioned via associative pairing with reward Cleland et al. After conditioning, animals are tested with batteries of structurally and perceptually similar odorants, often in a digging task where the odorant cue signals a buried reward.
The animals' perseverance, measured as time spent digging, in pursuit of an expected reward that is not present in test trials declines with increasing perceptual dissimilarity between the conditioned and test odorants. The breadths and forms of these gradients are sensitive to determinants of learning and to the statistical variance in odorant CS quality across conditioning trials Cleland et al. Associative odor learning based on a standard short-term conditioning paradigm a single series of up to twelve massed conditioning trials progressively decays over a timescale of several hours Figure 4 , though this timescale is likely to be sensitive to training parameters.
Odor discrimination is the most commonly used olfactory learning model, and subsumes many radically different conditioning paradigms and performance metrics. The distinguishing feature of this task is that animals are motivated to distinguish between two or more odors with different learned contingencies e. Automated tasks with relatively nonintuitive metrics e. The dependence of odor discrimination performance on OB circuitry corresponds closely with the difficulty of the discrimination Rinberg et al.
In olfaction, memory does not serve only to remember odors past, but is also a critical factor in realtime perceptual processing, even within OB and piriform cortex Wilson and Stevenson, a , b ; Zucco et al. Hence, short-term and long-term memory processes are likely to be highly interactive and conditional; e. One likely scenario is that short-term learning and memory processes contribute to this updating—a hypothesis that the olfactory appetitive learning and memory model is well-poised to test.
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Figure 6. Diagram of the separate molecular pathways underlying short-term and long-term memory as derived from studies using single-trial aversive training paradigms. Leftmost dashed vertical line marked with yellow triangle denotes the the time of conditioning; subsequent vertical lines denote timepoints following the trial. The lower diagram illustrates the theoretical bifurcation of memory mechanisms into a protein synthesis-independent STM stream that governs behavior for the first few hours after training and a separate, protein synthesis-dependent LTM stream that begins to govern behavior only thereafter.
The relationship, if any, between these two streams during multiple repeated conditioning trials is not clear. Memory mechanisms are heterogeneous in form, structure, and timecourse, yet exhibit many commonalities across regions of the brain. We here separate these mechanisms into two broad categories: molecular , which includes intracellular cascades, molecular signaling, neuromodulatory influences, activity-dependent protein synthesis, and epigenetic modifications, and structural , which includes physiological changes such as long-term potentiation or other synaptic weight modifications, alterations to neuronal morphology such as dendritic branching, changes to terminal shapes or numbers, and ancillary modifications such as effects on glia or cell adhesion to the extracellular matrix, as well as changes to neuron number via adult neurogenesis or selective apoptosis.
Mechanisms from these categories often are interdependent, and exhibit characteristic response timecourses that underlie memory-related changes. In this section, we review selected learning models and mechanisms drawn primarily from the hippocampal literature, focusing on models with well-developed response timecourses and signaling mechanisms for which there is evidence of relevance to OB learning as well. If entering a darkened chamber or stepping down from a platform results in footshock on the conditioning trial, a normal animal will hesitate, in subsequent test trials, before again entering that chamber or stepping down.
The delay in seconds before again entering the chamber or stepping down is a robust measure of the strength of the action-consequence association. Much of what is known about the molecular mechanisms of memory and their timecourses in mammalian systems has been developed using this task. This in turn enhances the phosphorylation of cyclic AMP cAMP response element binding protein CREB Miyamoto, and promotes the formation of complexes with ionotropic glutamate NMDA receptors Sanhueza and Lisman, , which have been shown to play a functional role in learning and memory reviewed in Danysz et al.
These findings indicate that CaMKII plays a crucial role early in the memory induction process, and that its functional role in LTM formation is confined to a specific period following learning. Cyclic AMP levels in the hippocampus begin to rise about 30 min following IA training, peak at 3 h after training, and decrease to baseline levels circa 6 h after training Bernabeu et al. PKA activity and CREB phosphorylation pCREB levels , in contrast, both exhibit two distinct peaks: one immediately following training and another beginning roughly 3 h thereafter and persisting until 6 h, but not 9 h, post-conditioning.
The second of these peaks coincides with peak hippocampal cAMP levels Bernabeu et al.
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In a multi-trial, appetitive learning paradigm based on the radial arm maze task, increased PKA activity and CREB phosphorylation levels were observed in the hippocampus after the fourth consecutive day of training, but not after the first day, in contrast to the immediate same-day effects observed in IA studies Mizuno et al.
A similar contrast between IA conditioning and appetitive learning effects has been described with learning-associated BDNF activation. In contrast, on an appetitive radial arm maze task, BDNF mRNA levels in hippocampus increased only after 8, but not 4, consecutive days of conditioning, and even then mRNA levels were significantly elevated only after 15 min, but not immediately, following training Mizuno et al.
These findings suggest that similar molecular mechanisms can mediate multi-trial appetitive learning as underlie fear-based single-trial learning, but that the timecourses can differ. It is in these latter contingencies that the richness of appetitive learning studies is likely to contribute most significantly to general studies of learning and memory. Should LTM be modeled as a statistical evidence accumulation system, in which LTM is formed only after enough evidence has accumulated that the cue-reward association is reliable and likely to remain true over time? How is this compatible with the evidence that, in IA training, LTM induction is initiated immediately after learning and is not dependent upon intact STM , even though it cannot govern behavioral responses until hours later?
Once LTM is induced, how is the persistence of that memory governed? What factors contribute to the timescales, selectivity, and stringency of new memory formation? The formation and maintenance of short-term memory STM , which are independent of protein synthesis, rely on different molecular mechanisms than those underlying LTM Izquierdo et al. To elucidate these different mechanisms, animals were conditioned using the IA protocol, immediately infused with one of a battery of antagonists into the hippocampus, and behaviorally tested for memory retention at 1.
Instead, at least two distinct cascades of events are set in motion after training Figure 6 , one of which enables rapid behavioral adjustment but decays in several hours STM , and the other of which is longer-lasting but cannot be behaviorally expressed for the first few hours after conditioning LTM. Interestingly, the distinct STM and LTM pathways - and many of their mechanistic elements - are common across widely divergent clades, including mollusks and insects as well as vertebrates Davis and Squire, ; DeZazzo and Tully, ; Blum et al.
A distinct, intermediate phase of memory, termed intermediate-term memory ITM , also has been defined, originally in Aplysia californica. It is characterized primarily by its dependence on protein translation but not on transcription Sutton et al. Though the timescales of these memory phases in Aplysia differ from their mammalian analogs, a translation-dependent, transcription-independent ITM for conditioned odor preference also has been identified in neonatal rat OB Grimes et al. Infusion of anisomycin, a translation blocker, immediately after conditioning had no effect on odor memory when the rat pups were tested one or 3 h later, but eliminated the memory when tested 5 or 20 h after conditioning.
When actinomycin, a transcription blocker, was similarly infused, memory at 1, 3, and 5 h was comparable to control animals, but an impairment of odor memory was observed at 24 h. Long-term memory has long been associated with persistent structural changes in specific brain regions involved in the formation of the memory. Many of the molecular mechanisms characterized in LTM induction and maintenance also have been shown to influence these structural changes, which may in some cases be the primary effectors of the memory.
We briefly review some of these structural mechanisms here. The arguments in favor of their relationship were strengthened by the elucidation of two distinct forms of hippocampal long-term plasticity LTP , a short-duration early form E-LTP and a longer-lasting late form L-LTP distinguished primarily by the latter's dependence on protein synthesis.
This timescale closely resembles the protein-synthesis dependency of LTM observed in behavioral studies. Similarly, after LTP induction by a tetanic stimulation of afferent fibers in hippocampal slices, any further tetanus to the afferent within 3 h generates only short-term plasticity across the synapse, whereas after 4 h the same tetanus could generate a longer-lasting potentiation over and above the initially induced LTP level Frey et al.
Finally, several molecular mechanisms associated with memory induction and persistence also regulate LTP. Specifically, LTP induction in slices generated a transient peak in the phosphorylated form of the TrkB receptor for BDNF; pTrkB levels rose 15 min following induction, peaked at 30 min, and slowly declined to baseline over 2 h Lu et al.
The timecourses of these interactions also correspond to those of the early biochemical cascades involved in LTM formation as discussed above. Changes in neuronal morphology, such as the growth of new dendritic spines, have been shown to accompany novel experiences Leggio et al. Importantly, the stabilization of new dendritic spines underlies at least some LTMs Yang et al.
The specific roles of these morphological elements are further emphasized by the dependence of LTM on intact cytoskeletal dynamics Lamprecht, Notably, BDNF and other neurotrophins associated with memory regulation have been strongly implicated in the modification and maintenance of both synaptic efficacy and dendritic morphology reviewed in McAllister et al. Learning and memory in the hippocampus and olfactory bulb also are associated with the incorporation of new adult-born neurons. The proliferation of new neurons ceases prior to adulthood in most brain regions, with the exception of the hippocampus and OB, and possibly the hypothalamus Cheng, Hippocampal progenitor cells are produced in the subgranular zone SGZ of the hippocampus and migrate a short distance to the granule cell layer of the dentate gyrus DG ; in contrast, OB progenitor cells are produced in the subventricular zone SVZ and migrate to the OB along the rostral migratory stream for 10—14 days before arriving in the OB and differentiating within the granule cell and glomerular layers Petreanu and Alvarez-Buylla, The observation that olfactory learning increases the odor-specific survival of adult-born neurons in OB Alonso et al.
However, the observation that this constant integration of new neurons does not result in a progressively increasing total neuron number in the OB Mouret et al. In the hippocampus, environmental enrichment and experience increase the survival rates of adult-generated neurons within the dentate gyrus Kee et al. Moreover, critically, the selective destruction of adult-born neurons that recently had been incorporated into the hippocampal network impaired spatial memory in the Morris water maze task when animals were tested seven days after training Arruda-Carvalho et al.
This latter result indicates that these newly-incorporated neurons were substantially mediating the new spatial memory; indeed, it has been suggested that adult-born neurons in HPC are employed specifically for new learning i. A similar principle is emerging in the OB, within which the selective ablation of newly-incorporated adult-born neurons following appetitive odor conditioning eliminated animals' memory for that odor Akers et al.
Interestingly, some of the signaling mechanisms most strongly associated with LTM formation also appear to be involved in the learning-dependent survival of adult-born neurons. Besides a basic activity-dependence arising from glutamate and GABA receptor activation Platel et al. For example, infusions of BDNF into the hippocampus, when delivered to adult rats over 2 weeks, increased the number of adult-born granule cells when compared against control animals infused with saline vehicle or bovine serum albumin Scharfman et al.
In heterozygous BDNF knockout mice, the number of surviving new neurons in the hippocampus did not change despite increased proliferation in the SGZ ; however, adult-born neurons continued to express markers of immature neurons as well as reduced dendritic growth, suggesting that reduced BDNF levels impaired their processes of maturation and differentiation. Other studies have emphasized a role for BDNF in the survival, rather than the proliferation or differentiation, of adult-born neurons e.
Odor learning in the OB offers rare opportunities to study the molecular and structural mechanisms of learning and memory in concert with well-controlled perceptual and behavioral tasks. During appetitive learning, OB circuitry integrates information about the statistical properties of the conditioned stimulus, perhaps also incorporating other features of the odor environment, and supports persistent representations of this learning.
Insofar as has been studied, the molecular and structural determinants of OB memory appear similar to those described for hippocampal fear conditioning and other memory systems. The particular value of OB-dependent behavioral learning paradigms is that they enable study of these molecular and structural mechanisms in the more complex milieu of cumulative, multi-trial, representational learning, in which the instantiation of LTM is delayed and conditional in nature, and based on information acquired over time. The representational aspect of OB learning further enables study of how learning alters the form, as well as the strength and persistence, of acquired memories.
Intrinsic memory mechanisms within the OB appear to share common pathways and adhere to similar pharmacologically-elaborated phases as have been elucidated in IA-based neural plasticity and memory studies. For example, PKA activity in the neonatal rat OB increases 10 min after one-trial olfactory appetitive conditioning, and blocking PKA activation in the OB with the competitive inhibitor Rp-cAMPS disrupted odor preference memory when tested 5 or 24 h, but not 3 h, after training.
Moreover, exogenous administration of the PKA activator Sp-cAMPs into the OB prior to odor exposure sufficed to induce intermediate 5 h and long-term 24 h odor preference memory. Odor-reward conditioning, but not odor or reward alone, also induced increased CREB phosphorylation in neonatal OB mitral cell nuclei 10 min after training, suggesting that pCREB-related plasticity in mitral cells may be important for the formation of odor LTM McLean et al.
To the extent that a substantially common set of essential molecular mechanisms is employed, the important distinctions between one-trial learning and appetitive statistical learning become within which neurons, under what conditions, and to what extent these mechanisms are invoked. Most studies of olfactory learning and memory that measure the form of the odor memory typically via generalization gradients have been performed in adult animals and at STM timescales.
There is little research to date on the molecular mechanisms underlying bulbar STM, though there is a substantial literature on the effects of neuromodulators, hormones Dillon et al. Noradrenergic effects within OB, in particular, have been studied in both nonassociative and associative olfactory representational learning studies reviewed in Linster et al.
In neonatal rats, as noted in section 2. There is no evidence, however, that bulbar NE can serve as an unconditioned stimulus for adult odor learning, and even in neonates this property may be epiphenomenal. If NE serves to gate activity-dependent plasticity in OB circuits, then known properties of neonatal physiology ensure that in neonates this learning will always be strong, always depend on odor-induced activation of OB circuits, and always be appetitive neonates respond appetitively and can be positively conditioned to even normally-aversive unconditioned stimuli such as electric shocks; Sullivan, Consequently, simply gating circuit plasticity in the OB could be expected to directly generate a positive association in neonates.
In any event, analogous pairings of odor presentation with bulbar NE infusions in adult mice demonstrate that NE facilitates habituation to presented odors, but does not innately generate odor preferences as it does in neonatal animals Shea et al. Of course, other classical neuromodulators, notably acetylcholine acting at muscarinic receptors within OB, also exert effects within OB circuitry on odor learning and STM maintenance Devore and Linster, ; Devore et al.
While it has been much less thoroughly studied in the olfactory system, BDNF transcription is activated in OB and piriform cortex after odor conditioning Jones et al. Both mutants habituate normally to odors but exhibit greatly reduced spontaneous discrimination in the cross-habituation task Bath et al. The clearest effects of BDNF on the OB, however, are structural in nature, substantially affecting dendritic arborization and adult neurogenesis. Long-term potentiation has been clearly if sparsely observed in the early olfactory system, notably within piriform cortex and its ascending synapses into OB.
NMDA receptor-dependent LTP has been demonstrated at afferent and associative fiber synapses within piriform cortical slices, and coactivation of the two can facilitate a form of associative LTP if local inhibition is suppressed Kanter and Haberly, , Piriform pyramidal neuron feedback projections onto OB granule cells also exhibit spike timing-dependent LTP Gao and Strowbridge, , which may be a particularly powerful computational element given the importance of dynamical, timing-dependent interactions within OB circuitry.
This rich and structured plasticity requires further experimental and theoretical development, but exemplifies the capacities of the olfactory system as a model for understanding complex memory systems. Spine densities in OB and piriform cortex are affected by odor learning and by learning-associated trophic factors, notably BDNF. In combination with the integration of adult-born neurons into the OB network below , it is clear that the regulation of dendritic connectivity among OB neurons is a significant determinant of OB functional plasticity, and that BDNF is a crucial regulator of the underlying mechanisms.
Adult neurogenesis in the OB has been studied extensively with regard to its effects on, and mediation of, odor learning. The differentiation of adult-born neurons within OB and its relevance for olfactory perception and odor learning have been extensively studied and reviewed elsewhere Lazarini and Lledo, ; Lepousez et al.
Of particular interest for present purposes, though, is the regulation of these neuronal differentiation processes by signaling molecules and other established mediators of olfactory learning, as well as timing and task dependencies that may suggest points of particular mechanistic importance. The incorporation of new neurons is most widely associated with olfactory LTM; as described above, the selective ablation of newly differentiated OB neurons specifically disrupted a long-term odor memory Akers et al.
However, there also are indications that adult-born neurons may participate in STM processes. Infusions of the antimitotic drug AraC into the lateral ventricle of rats abolished the arrival of new neurons into the OB, while largely sparing hippocampal neurogenesis, and impaired short-term nonassociative memory for odors learned thereafter Breton-Provencher et al.
Specifically, the absence of new neurons in OB did not affect memory for a habituated odor after 30 min, but , , and min odor memories were disrupted compared with control animals. In contrast, AraC treatment did not affect h or 7-day preference memory for an odorant paired with reward over 4 days. It remains unclear whether this difference depends more on the multi-day spacing of the trials or on the associative nature of the task. Interestingly, it has been proposed that nonassociative and associative odor learning preferentially activate neurons of different ages within OB Belnoue et al.
This result is consistent with the results described above, in that the OBs of AraC-infused mice in that study were devoid of neurons younger than 3—4 weeks, as required for nonassociative odor learning, but possessed a full complement of neurons in the 5—9 week age range, as were most heavily utilized in the rewarded task.
These results still beg the question, of course, of what factors in these different training paradigms underlie the selective recruitment of different cohorts of new neurons. These results illustrate another advantage of the olfactory system for studies of complex and naturalistic learning, in which task parameters may determine the differential utilization of OB and non-OB; Luu et al.
Neuronal proliferation was not affected by these mutations, suggesting that the effects of BDNF primarily relate to survival and differentiation. The powerful effects of this neurotrophin on olfactory learning and neuronal differentiation, and its association with established learning-associated molecular cascades, render it a strong candidate for study in order to elucidate the complex relationships underlying these representational, statistical learning processes in naturalistic contexts.
Understanding the neurophysiological basis of natural learning and memory is one of the great challenges of neuroscience. Much of what is known about the cellular mechanisms underlying learning derives from one-trial learning paradigms of inhibitory avoidance fear conditioning , though research in other plastic neural systems has indicated that they share many, though not all, of the same underlying molecular and structural mechanisms of plasticity.
One-trial odor learning studies, which induce plasticity in olfactory bulb, suggest that these cortical circuits also rely on these common mechanisms for plasticity—although bulbar memory also depends on adult neurogenesis, a structural mechanism which it shares only with the hippocampus. Most natural learning, however, is less categorical than these one-trial paradigms, requiring multiple encounters in order to elucidate relevant stimuli and learn appropriate associations. Appetitive learning in adults, for example, tends to be gradual, conditional, and statistical in nature.
This raises new mechanistic questions: how does learning accumulate over multiple trials? How are the relevant features of the sensory scene identified, selected, and represented? How does learning change the form, or quality, of a sensory representation in response to accumulating information? Developing the olfactory system as a neurophysiological learning and memory model enables engagement with these rich questions.
Michelle T. Tong and Thomas A. Cleland conceived of and wrote the paper, and designed the figures. Shane T. Peace designed and performed the research featured in Figure 4. Tong designed and performed the research featured in Figure 5. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Abraham, N. Similar odor discrimination behavior in head-restrained and freely moving mice.
Long term functional plasticity of sensory inputs mediated by olfactory learning. Akers, K. Ablation of adult-generated olfactory bulb neurons produces retrograde impairment in an associative odor memory task. Alonso, M. Activation of adult-born neurons facilitates learning and memory.
BDNF—triggered events in the rat hippocampus are required for both short- and long-term memory formation. Hippocampus 12, — Olfactory discrimination learning increases the survival of adult-born neurons in the olfactory bulb. Anderson, M. Associative learning increases adult neurogenesis during a critical period.
Arruda-Carvalho, M. Posttraining ablation of adult-generated neurons degrades previously acquired memories. Barnes, D. Olfactory perceptual stability and discrimination. Bath, K.
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Variant brain-derived neurotrophic factor Val66Met alters adult olfactory bulb neurogenesis and spontaneous olfactory discrimination. Bekinschtein, P. Persistence of long-term memory storage requires a late protein synthesis- and BDNF-dependent phase in the hippocampus. Neuron 53, — BDNF is essential to promote persistence of long-term memory storage. Belnoue, L. A critical time window for the recruitment of bulbar newborn neurons by olfactory discrimination learning.
Benraiss, A. Adenoviral brain—derived neurotrophic factor induces both neostriatal and olfactory neuronal recruitment from endogenous progenitor cells in the adult forebrain. Pubmed Abstract Pubmed Full Text.
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