Presynaptic stochasticity improves energy efficiency and helps alleviate the stability-plasticity dilemma.
Ontology highlight
ABSTRACT:
SUBMITTER: Schug S
PROVIDER: S-EPMC8716105 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:In natural environments with many options of uncertain value, one faces a difficult tradeoff between exploiting familiar, valuable options or searching for better alternatives. Reinforcement learning models of this exploration/exploitation dilemma typically modulate the rate of exploratory choices or preferentially sample uncertain options. The extent to which such models capture human behavior remains unclear, in part because they do not consider the constraints on remembering what is learned. Using reinforcement-based timing as a motivating example, we show that selectively maintaining high-value actions compresses the amount of information to be tracked in learning, as quantified by Shannon's entropy. In turn, the information content of the value representation controls the balance between exploration (high entropy) and exploitation (low entropy). Selectively maintaining preferred action values while allowing others to decay renders the choices increasingly exploitative across learning episodes. To adjudicate among alternative maintenance and sampling strategies, we developed a new reinforcement learning model, StrategiC ExPloration/ExPloitation of Temporal Instrumental Contingencies (SCEPTIC). In computational studies, a resource-rational selective maintenance approach was as successful as more resource-intensive strategies. Furthermore, human behavior was consistent with selective maintenance; information compression was most pronounced in subjects with superior performance and non-verbal intelligence, and in learnable vs. unlearnable contingencies. Cognitively demanding uncertainty-directed exploration recovered a more accurate representation in simulations with no foraging advantage and was strongly unsupported in our human study.
| S-EPMC6328060 | biostudies-literature
Project description:We provide a novel computational framework on how biological and artificial agents can learn to flexibly couple and decouple neural task modules for cognitive processing. In this way, they can address the stability-plasticity dilemma. For this purpose, we combine two prominent computational neuroscience principles, namely Binding by Synchrony and Reinforcement Learning. The model learns to synchronize task-relevant modules, while also learning to desynchronize currently task-irrelevant modules. As a result, old (but currently task-irrelevant) information is protected from overwriting (stability) while new information can be learned quickly in currently task-relevant modules (plasticity). We combine learning to synchronize with task modules that learn via one of several classical learning algorithms (Rescorla-Wagner, backpropagation, Boltzmann machines). The resulting combined model is tested on a reversal learning paradigm where it must learn to switch between three different task rules. We demonstrate that our combined model has significant computational advantages over the original network without synchrony, in terms of both stability and plasticity. Importantly, the resulting models' processing dynamics are also consistent with empirical data and provide empirically testable hypotheses for future MEG/EEG studies.
| S-EPMC6716678 | biostudies-literature
Project description:It is often assumed that in public goods games, contributors are either strong or weak players and each individual has an equal probability of exhibiting cooperation. It is difficult to explain why the public good is produced by strong individuals in some cooperation systems, and by weak individuals in others. Viewing the asymmetric volunteer's dilemma game as an evolutionary game, we find that whether the strong or the weak players produce the public good depends on the initial condition (i.e., phenotype or initial strategy of individuals). These different evolutionarily stable strategies (ESS) associated with different initial conditions, can be interpreted as the production modes of public goods of different cooperation systems. A further analysis revealed that the strong player adopts a pure strategy but mixed strategies for the weak players to produce the public good, and that the probability of volunteering by weak players decreases with increasing group size or decreasing cost-benefit ratio. Our model shows that the defection probability of a "strong" player is greater than the "weak" players in the model of Diekmann (1993). This contradicts Selten's (1980) model that public goods can only be produced by a strong player, is not an evolutionarily stable strategy, and will therefore disappear over evolutionary time. Our public good model with ESS has thus extended previous interpretations that the public good can only be produced by strong players in an asymmetric game.
| S-EPMC4128801 | biostudies-literature
Project description:When making decisions, should one exploit known good options or explore potentially better alternatives? Exploration of spatially unstructured options depends on the neocortex, striatum, and amygdala. In natural environments, however, better options often cluster together, forming structured value distributions. The hippocampus binds reward information into allocentric cognitive maps to support navigation and foraging in such spaces. Here we report that human posterior hippocampus (PH) invigorates exploration while anterior hippocampus (AH) supports the transition to exploitation on a reinforcement learning task with a spatially structured reward function. These dynamics depend on differential reinforcement representations in the PH and AH. Whereas local reward prediction error signals are early and phasic in the PH tail, global value maximum signals are delayed and sustained in the AH body. AH compresses reinforcement information across episodes, updating the location and prominence of the value maximum and displaying goal cell-like ramping activity when navigating toward it.
| S-EPMC7589536 | biostudies-literature
Project description:An electrophysiology-based forward genetic screen has identified two genes, pickpocket11 (ppk11) and pickpocket16 (ppk16), as being necessary for the homeostatic modulation of presynaptic neurotransmitter release at the Drosophila neuromuscular junction (NMJ). Pickpocket genes encode Degenerin/Epithelial Sodium channel subunits (DEG/ENaC). We demonstrate that ppk11 and ppk16 are necessary in presynaptic motoneurons for both the acute induction and long-term maintenance of synaptic homeostasis. We show that ppk11 and ppk16 are cotranscribed as a single mRNA that is upregulated during homeostatic plasticity. Acute pharmacological inhibition of a PPK11- and PPK16-containing channel abolishes the expression of short- and long-term homeostatic plasticity without altering baseline presynaptic neurotransmitter release, indicating remarkable specificity for homeostatic plasticity rather than NMJ development. Finally, presynaptic calcium imaging experiments support a model in which a PPK11- and PPK16-containing DEG/ENaC channel modulates presynaptic membrane voltage and, thereby, controls calcium channel activity to homeostatically regulate neurotransmitter release.
| S-EPMC3784986 | biostudies-literature
Project description:Presynaptic homeostatic plasticity (PHP) stabilizes synaptic transmission by counteracting impaired neurotransmitter receptor function through neurotransmitter release potentiation. PHP is thought to be triggered by impaired receptor function and to involve a stereotypic signaling pathway. However, here we demonstrate that different receptor perturbations that similarly reduce synaptic transmission result in different responses at the Drosophila neuromuscular junction. While receptor inhibition by the glutamate receptor (GluR) antagonist γ-D-glutamylglycine (γDGG) is not compensated by PHP, the GluR inhibitors Philanthotoxin-433 (PhTx) and Gyki-53655 (Gyki) induce compensatory PHP. Intriguingly, PHP triggered by PhTx and Gyki involve separable signaling pathways, including inhibition of distinct GluR subtypes, differential modulation of the active-zone scaffold Bruchpilot, and short-term plasticity. Moreover, while PHP upon Gyki treatment does not require genes promoting PhTx-induced PHP, it involves presynaptic protein kinase D. Thus, synapses not only respond differentially to similar activity impairments, but achieve homeostatic compensation via distinct mechanisms, highlighting the diversity of homeostatic signaling.
| S-EPMC8692748 | biostudies-literature
Project description:A key unresolved question in cognitive science is whether the brain uses asynchronous or synchronous patterns of information transmission. Using an auditory learning task combined with electrophysiological recordings, we reveal for the first time that cognitive plasticity during learning transforms an asynchronous into a synchronous transmission pattern to achieve rapid, error-free performance. We also present a new model showing how the brain may resolve its information processing and transmission dilemma.
| S-EPMC3790200 | biostudies-literature
Project description:BackgroundIntermittent severe energy restriction is popular for weight management. To investigate whether intermittent moderate energy restriction may improve this approach by enhancing weight loss efficiency, we conducted a study in mice, where energy intake can be controlled.MethodsMale C57/Bl6 mice that had been rendered obese by an ad libitum diet high in fat and sugar for 22 weeks were then fed one of two energy-restricted normal chow diets for a 12-week weight loss phase. The continuous diet (CD) provided 82% of the energy intake of age-matched ad libitum chow-fed controls. The intermittent diet (ID) provided cycles of 82% of control intake for 5-6 consecutive days, and ad libitum intake for 1-3 days. Weight loss efficiency during this phase was calculated as (total weight change) ÷ [(total energy intake of mice on CD or ID)-(total average energy intake of controls)]. Subsets of mice then underwent a 3-week weight regain phase involving ad libitum re-feeding.ResultsMice on the ID showed transient hyperphagia relative to controls during each 1-3-day ad libitum feeding period, and overall ate significantly more than CD mice (91.1±1.0 versus 82.2±0.5% of control intake respectively, n = 10, P<0.05). There were no significant differences between CD and ID groups at the end of the weight loss or weight regain phases with respect to body weight, fat mass, circulating glucose or insulin concentrations, or the insulin resistance index. Weight loss efficiency was significantly greater with ID than with CD (0.042±0.007 versus 0.018±0.001 g/kJ, n = 10, P<0.01). Mice on the CD exhibited significantly greater hypothalamic mRNA expression of proopiomelanocortin (POMC) relative to ID and control mice, with no differences in neuropeptide Y or agouti-related peptide mRNA expression between energy-restricted groups.ConclusionIntermittent moderate energy restriction may offer an advantage over continuous moderate energy restriction, because it induces significantly greater weight loss relative to energy deficit in mice.
| S-EPMC4718562 | biostudies-literature
Project description:Background/objectivesThe MATADOR (Minimising Adaptive Thermogenesis And Deactivating Obesity Rebound) study examined whether intermittent energy restriction (ER) improved weight loss efficiency compared with continuous ER and, if so, whether intermittent ER attenuated compensatory responses associated with ER.Subjects/methodsFifty-one men with obesity were randomised to 16 weeks of either: (1) continuous (CON), or (2) intermittent (INT) ER completed as 8 × 2-week blocks of ER alternating with 7 × 2-week blocks of energy balance (30 weeks total). Forty-seven participants completed a 4-week baseline phase and commenced the intervention (CON: N=23, 39.4±6.8 years, 111.1±9.1?kg, 34.3±3.0?kg?m-2; INT: N=24, 39.8±9.5 years, 110.2±13.8?kg, 34.1±4.0?kg?m-2). During ER, energy intake was equivalent to 67% of weight maintenance requirements in both groups. Body weight, fat mass (FM), fat-free mass (FFM) and resting energy expenditure (REE) were measured throughout the study.ResultsFor the N=19 CON and N=17 INT who completed the intervention per protocol, weight loss was greater for INT (14.1±5.6 vs 9.1±2.9?kg; P<0.001). INT had greater FM loss (12.3±4.8 vs 8.0±4.2?kg; P<0.01), but FFM loss was similar (INT: 1.8±1.6 vs CON: 1.2±2.5?kg; P=0.4). Mean weight change during the 7 × 2-week INT energy balance blocks was minimal (0.0±0.3?kg). While reduction in absolute REE did not differ between groups (INT: -502±481 vs CON: -624±557?kJ?d-1; P=0.5), after adjusting for changes in body composition, it was significantly lower in INT (INT: -360±502 vs CON: -749±498?kJ?d-1; P<0.05).ConclusionsGreater weight and fat loss was achieved with intermittent ER. Interrupting ER with energy balance 'rest periods' may reduce compensatory metabolic responses and, in turn, improve weight loss efficiency.
| S-EPMC5803575 | biostudies-literature
Project description:Presynaptic homeostatic plasticity (PHP) compensates for impaired postsynaptic neurotransmitter receptor function through a rapid, persistent adjustment of neurotransmitter release, an effect that can exceed 200%. An unexplained property of PHP is the preservation of short-term plasticity (STP), thereby stabilizing activity-dependent synaptic information transfer. We demonstrate that the dramatic potentiation of presynaptic release during PHP is achieved while simultaneously maintaining a constant ratio of primed to super-primed synaptic vesicles, thereby preserving STP. Mechanistically, genetic, biochemical and electrophysiological evidence argue that a constant ratio of primed to super-primed synaptic vesicles is achieved by the concerted action of three proteins: Unc18, Syntaxin1A and RIM. Our data support a model based on the regulated availability of Unc18 at the presynaptic active zone, a process that is restrained by Syntaxin1A and facilitated by RIM. As such, regulated vesicle priming/super-priming enables PHP to stabilize both synaptic gain and the activity-dependent transfer of information at a synapse.
| S-EPMC6250423 | biostudies-literature