scholarly journals A DROSOPHILA CIRCUIT FOR HABITUATION OVERRIDE

2021 ◽  
Author(s):  
Swati Trisal ◽  
Marcia Maria Aranha ◽  
Ankita Chodankar ◽  
K Vijayraghavan ◽  
Mani Ramaswami
Keyword(s):  
Tyrosine Hydroxylase ◽  
Sensory Neuron ◽  
Sensory Neurons ◽  
Transmitter Release ◽  
Dopaminergic Neurons ◽  
Proboscis Extension Reflex ◽  
Trigger Activity ◽  
Proboscis Extension ◽  
Inhibitory Plasticity ◽  
Familiar Stimuli

Habituated animals retain a latent capacity for robust engagement with familiar stimuli. In most instances, the ability to override habituation is best explained by postulating: (a) that habituation arises from the potentiation of inhibitory inputs onto stimulus-encoding assemblies; and (b) fast habituation override occurs through disinhibition. Previous work has shown that inhibitory plasticity contributes to specific forms of olfactory and gustatory habituation in Drosophila. Here we analyze how exposure to a novel stimulus causes override of gustatory (proboscis-extension reflex or ″PER″) habituation. While brief sucrose contact with tarsal hairs causes naīve Drosophila to extend their proboscis, persistent tarsal exposure to sucrose reduces PER to subsequent sucrose stimuli. We show that in so habituated animals, either brief exposure of the proboscis to yeast or direct thermogenetic activation of sensory neurons restores the PER response to tarsal sucrose stimulation. Similar override of PER habituation can also be induced by brief thermogenetic activation of a population of TH (Tyrosine-Hydroxylase) positive neurons, a subset of which send projections to the SEZ. Significantly, sensory-neuron induced habituation override requires transmitter release from these TH-positive cells. Treatments that cause override specifically influence the habituated state, with no effect on the naīve sucrose response across a range of concentrations. Taken together, these and other findings are consistent with a model in which novel taste stimuli trigger activity in dopaminergic neurons which, directly or indirectly, inhibit GABAergic cells that drive PER habituation. The implications of these findings for general mechanisms of attentional and sensory override of habituation are discussed.

Simulation of synaptic depression, posttetanic potentiation, and presynaptic facilitation of synaptic potentials from sensory neurons mediating gill-withdrawal reflex in Aplysia

1985 ◽  
Vol 53 (3) ◽  
pp. 652-669 ◽  
Author(s):  
K. J. Gingrich ◽  
J. H. Byrne
Keyword(s):  
Action Potential ◽  
Sensory Neuron ◽  
Sensory Neurons ◽  
Transmitter Release ◽  
Neurotransmitter Release ◽  
Synaptic Depression ◽  
Posttetanic Potentiation ◽  
Withdrawal Reflex ◽  
Classic Conditioning ◽  
Presynaptic Facilitation

The defensive gill-withdrawal reflex in Aplysia has proven to be an attractive system for analyzing the neural mechanisms underlying simple forms of learning such as habituation, sensitization, and classic conditioning. Previous studies have shown that habituation is associated with synaptic depression and sensitization with presynaptic facilitation of transmitter release from sensory neurons mediating the reflex. The synaptic depression, in turn, is associated with a decrease in Ca2+ currents in the sensory neurons, whereas presynaptic facilitation with increased Ca2+ currents produced indirectly by a decrease in a novel serotonergic sensitive K+ current. The present work represents an initial quantitative examination of the extent to which these mechanisms account for each of these types of synaptic plasticity. To address these issues a lumped parameter mathematical model of the sensory neuron release process was constructed. Major components of this model include Ca2+-channel inactivation, Ca2+-mediated neurotransmitter release and mobilization, and readily releasable and upstream feeding pools of neurotransmitter. In the model, release of neurotransmitter has a linear function of Ca2+ concentration and is not affected directly by residual Ca2+. The model not only simulates the data of synaptic depression and recovery from depression, but also qualitatively predicts other features of neurotransmitter release that it was not designed to fit. These include features of synaptic depression with high and low levels of transmitter release, posttetanic potentiation, a steep relationship between action potential duration and transmitter release, enhanced release produced by broadening the sensory neuron action potential (presynaptic facilitation), and dramatic synaptic depression with two closely spaced tetraethylammonium (TEA) spikes. The model cannot account fully for synaptic depression with empirically observed somatic Ca2+-current kinetics. Rather a large component of synaptic depression is due to reduction to the pools of releasable neurotransmitter (depletion). In the model when spike durations are greater than 15-20 ms, spike broadening produces little facilitation. However, when spike durations are more physiological, spike broadening leads to enhanced transmitter release.

scholarly journals Temporal coherency of mechanical stimuli modulates tactile form perception

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Masashi Nakatani ◽  
Yasuaki Kobayashi ◽  
Kota Ohno ◽  
Masaaki Uesaka ◽  
Sayako Mogami ◽  
...  
Keyword(s):  
Sensory Neuron ◽  
Sensory Neurons ◽  
Contact Surface ◽  
Relative Magnitude ◽  
Form Perception ◽  
Tangential Displacement ◽  
Surface Geometry ◽  
Tactile Stimuli ◽  
Surface Patterns ◽  
Temporal Coherency

AbstractThe human hand can detect both form and texture information of a contact surface. The detection of skin displacement (sustained stimulus) and changes in skin displacement (transient stimulus) are thought to be mediated in different tactile channels; however, tactile form perception may use both types of information. Here, we studied whether both the temporal frequency and the temporal coherency information of tactile stimuli encoded in sensory neurons could be used to recognize the form of contact surfaces. We used the fishbone tactile illusion (FTI), a known tactile phenomenon, as a probe for tactile form perception in humans. This illusion typically occurs with a surface geometry that has a smooth bar and coarse textures in its adjacent areas. When stroking the central bar back and forth with a fingertip, a human observer perceives a hollow surface geometry even though the bar is physically flat. We used a passive high-density pin matrix to extract only the vertical information of the contact surface, suppressing tangential displacement from surface rubbing. Participants in the psychological experiment reported indented surface geometry by tracing over the FTI textures with pin matrices of the different spatial densities (1.0 and 2.0 mm pin intervals). Human participants reported that the relative magnitude of perceived surface indentation steeply decreased when pins in the adjacent areas vibrated in synchrony. To address possible mechanisms for tactile form perception in the FTI, we developed a computational model of sensory neurons to estimate temporal patterns of action potentials from tactile receptive fields. Our computational data suggest that (1) the temporal asynchrony of sensory neuron responses is correlated with the relative magnitude of perceived surface indentation and (2) the spatiotemporal change of displacements in tactile stimuli are correlated with the asynchrony of simulated sensory neuron responses for the fishbone surface patterns. Based on these results, we propose that both the frequency and the asynchrony of temporal activity in sensory neurons could produce tactile form perception.

Triggering the proboscis extension reflex (PER) in Rhodnius prolixus

2021 ◽  
pp. 104249
Author(s):  
Raquel A. Ferreira ◽  
Marcelo G. Lorenzo ◽  
Claudio R. Lazzari
Keyword(s):  
Rhodnius Prolixus ◽  
Proboscis Extension Reflex ◽  
Proboscis Extension

scholarly journals The role of intra-articular neuronal CCR2 receptors in knee joint pain associated with experimental osteoarthritis in mice

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Shingo Ishihara ◽  
Alia M. Obeidat ◽  
David L. Wokosin ◽  
Dongjun Ren ◽  
Richard J. Miller ◽  
...  
Keyword(s):  
Knee Joint ◽  
Sensory Neuron ◽  
Sensory Neurons ◽  
Direct Stimulation ◽  
Sensory Afferents ◽  
Neuronal Marker ◽  
The Right ◽  
Experimental Osteoarthritis ◽  
In Vivo Calcium Imaging

Abstract Background C–C chemokine receptor 2 (CCR2) signaling plays a key role in pain associated with experimental murine osteoarthritis (OA) after destabilization of the medial meniscus (DMM). Here, we aimed to assess if CCR2 expressed by intra-articular sensory neurons contributes to knee hyperalgesia in the early stages of the model. Methods DMM surgery was performed in the right knee of 10-week-old male wild-type (WT), Ccr2 null, or Ccr2RFP C57BL/6 mice. Knee hyperalgesia was measured using a Pressure Application Measurement device. CCR2 receptor antagonist (CCR2RA) was injected systemically (i.p.) or intra-articularly (i.a.) at different times after DMM to test its ability to reverse knee hyperalgesia. In vivo Ca2+ imaging of the dorsal root ganglion (DRG) was performed to assess sensory neuron responses to CCL2 injected into the knee joint cavity. CCL2 protein in the knee was measured by ELISA. Ccr2RFP mice and immunohistochemical staining for the pan-neuronal marker, protein gene product 9.5 (PGP9.5), or the sensory neuron marker, calcitonin gene-related peptide (CGRP), were used to visualize the location of CCR2 on intra-articular afferents. Results WT, but not Ccr2 null, mice displayed knee hyperalgesia 2–16 weeks after DMM. CCR2RA administered i.p. alleviated established hyperalgesia in WT mice 4 and 8 weeks after surgery. Intra-articular injection of CCL2 excited sensory neurons in the L4-DRG, as determined by in vivo calcium imaging; responses to CCL2 increased in mice 20 weeks after DMM. CCL2, but not vehicle, injected i.a. rapidly caused transient knee hyperalgesia in naïve WT, but not Ccr2 null, mice. Intra-articular CCR2RA injection also alleviated established hyperalgesia in WT mice 4 and 7 weeks after surgery. CCL2 protein was elevated in the knees of both WT and Ccr2 null mice 4 weeks after surgery. Co-expression of CCR2 and PGP9.5 as well as CCR2 and CGRP was observed in the lateral synovium of naïve mice; co-expression was also observed in the medial compartment of knees 8 weeks after DMM. Conclusions The findings suggest that CCL2-CCR2 signaling locally in the joint contributes to knee hyperalgesia in experimental OA, and it is in part mediated through direct stimulation of CCR2 expressed by intra-articular sensory afferents.

scholarly journals Olfactory Learning in the Stingless Bee Melipona eburnea Friese (Apidae: Meliponini)

Insects ◽  
2019 ◽  
Vol 10 (11) ◽  
pp. 412 ◽  
Author(s):  
Marisol Amaya-Márquez ◽  
Sergio Tusso ◽  
Juan Hernández ◽  
Juan Darío Jiménez ◽  
Harrington Wells ◽  
...  
Keyword(s):  
Unconditioned Stimulus ◽  
Stingless Bees ◽  
Olfactory Learning ◽  
Learning Performance ◽  
Taste Receptors ◽  
Proboscis Extension Reflex ◽  
Adaptive Traits ◽  
Proboscis Extension ◽  
Cognition And Learning ◽  
Plant Pollinator

Olfactory learning and floral scents are co-adaptive traits in the plant–pollinator relationship. However, how scent relates to cognition and learning in the diverse group of Neotropical stingless bees is largely unknown. Here we evaluated the ability of Melipona eburnea to be conditioned to scent using the proboscis extension reflex (PER) protocol. Stingless bees did not show PER while harnessed but were able to be PER conditioned to scent when free-to-move in a mini-cage (fmPER). We evaluated the effect of: 1) unconditioned stimulus (US) reward, and 2) previous scent–reward associations on olfactory learning performance. When using unscented-US, PER-responses were low on day 1, but using scented-US reward the olfactory PER-response increased on day 1. On day 2 PER performance greatly increased in bees that previously had experienced the same odor and reward combination, while bees that experienced a different odor on day 2 showed poor olfactory learning. Bees showed higher olfactory PER conditioning to guava than to mango odor. The effect of the unconditioned stimulus reward was not a significant factor in the model on day 2. This indicates that olfactory learning performance can increase via either taste receptors or accumulated experience with the same odor. Our results have application in agriculture and pollination ecology.

scholarly journals Spatial odor discrimination in hawkmoth, Manduca sexta (L.)

2020 ◽  
Author(s):  
P. Kalyanasundaram ◽  
M. A. Willis
Keyword(s):  
Spatial Distribution ◽  
Manduca Sexta ◽  
Flight Control ◽  
Spatial Information ◽  
Egg Laying ◽  
Proboscis Extension Reflex ◽  
Flying Insects ◽  
Odor Learning ◽  
Odor Plumes ◽  
Proboscis Extension

AbstractFlying insects track turbulent odor plumes to find mates, food and egg-laying sites. To maintain contact with the plume, insects are thought to adapt their flight control according to the distribution of odor in the plume using the timing of odor onsets and intervals between odor encounters. Although timing cues are important, few studies have addressed whether insects are capable of deriving spatial information about odor distribution from bilateral comparisons between their antennae in flight. The proboscis extension reflex (PER) associative learning protocol, originally developed to study odor learning in honeybees, was modified to show hawkmoths, Manduca sexta, can discriminate between odor stimuli arriving on either antenna. We show moths discriminated the odor arrival side with an accuracy of >70%. The information about spatial distribution of odor stimuli is thus available to moths searching for odor sources, opening the possibility that they use both spatial and temporal odor information.

Mutant PINK1 upregulates tyrosine hydroxylase and dopamine levels, leading to vulnerability of dopaminergic neurons

2014 ◽  
Vol 68 ◽  
pp. 220-233 ◽  
Author(s):  
Zhi Dong Zhou ◽  
Fathima Shaffra Refai ◽  
Shao Ping Xie ◽  
Shin Hui Ng ◽  
Christine Hui Shan Chan ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Dopaminergic Neurons

Molecular Biology of Vertebrate Olfactory Receptors and Circuits

2021 ◽  
Author(s):  
Richard P. Tucker ◽  
Qizhi Gong
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Olfactory Bulb ◽  
Gene Family ◽  
Sensory Neuron ◽  
Sensory Neurons ◽  
Odorant Receptor ◽  
Vomeronasal Organ ◽  
Odorant Receptors ◽  
The Central Nervous System

Animals use their olfactory system for the procurement of food, the detection of danger, and the identification of potential mates. In vertebrates, the olfactory sensory neuron has a single apical dendrite that is exposed to the environment and a single basal axon that projects to the central nervous system (i.e., the olfactory bulb). The first odorant receptors to be discovered belong to an enormous gene family encoding G protein-coupled seven transmembrane domain proteins. Odorant binding to these classical odorant receptors initiates a GTP-dependent signaling cascade that uses cAMP as a second messenger. Subsequently, additional types of odorant receptors using different signaling pathways have been identified. While most olfactory sensory neurons are found in the olfactory sensory neuroepithelium, others are found in specialized olfactory subsystems. In rodents, the vomeronasal organ contains neurons that recognize pheromones, the septal organ recognizes odorant and mechanical stimuli, and the neurons of the Grüneberg ganglion are sensitive to cool temperatures and certain volatile alarm signals. Within the olfactory sensory neuroepithelium, each sensory neuron expresses a single odorant receptor gene out of the large gene family; the axons of sensory neurons expressing the same odorant receptor typically converge onto a pair of glomeruli at the periphery of the olfactory bulb. This results in the transformation of olfactory information into a spatially organized odortopic map in the olfactory bulb. The axons originating from the vomeronasal organ project to the accessory olfactory bulb, whereas the axons from neurons in the Grüneberg ganglion project to 10 specific glomeruli found in the caudal part of the olfactory bulb. Within a glomerulus, the axons originating from olfactory sensory neurons synapse on the dendrites of olfactory bulb neurons, including mitral and tufted cells. Mitral cells and tufted cells in turn project directly to higher brain centers (e.g., the piriform cortex and olfactory tubercle). The integration of olfactory information in the olfactory cortices and elsewhere in the central nervous system informs and directs animal behavior.

Sensitization of the gill and siphon withdrawal reflex of Aplysia: multiple sites of change in the neuronal network

1993 ◽  
Vol 70 (3) ◽  
pp. 1210-1220 ◽  
Author(s):  
L. E. Trudeau ◽  
V. F. Castellucci
Keyword(s):  
Sensory Neuron ◽  
Sensory Neurons ◽  
Motor Neurons ◽  
Neuronal Network ◽  
Feedback Inhibition ◽  
Excitatory Input ◽  
Major Mechanism ◽  
Withdrawal Reflex ◽  
The Difference ◽  
Central Synapses

1. Recent studies have emphasized the major contribution of interneuronal transmission to the mediation and learning-associated modulation of the gill and siphon withdrawal (GSW) reflex of Aplysia. We wish to provide more direct support for the hypothesis that inhibitory junctions are crucial sites of plasticity. 2. In parallel experiments we investigated modulation at five major sites of synaptic transmission in the GSW network: 1) from sensory neurons to motor neurons, 2) from sensory neurons to excitatory interneurons (INTs+) 3) from INTs+ to motor neurons (MNs), 4) from inhibitory interneurons (INTs-) to INTs+, and 5) from INTs+ to INTs-. 3. While recording simultaneously from a single sensory neuron of the LE cluster, an INT+, and a MN, we found that both LE-MN and LE-INTs+ synapses were facilitated by the activation of modulator neurons by stimulation of the left pleuroabdominal connective (185 and 93%, respectively) as well as by serotonin (5-HT) (191 and 84%). Junctions of the second type were therefore less facilitated. The difference in the magnitude of facilitation at these two sites is an indication of a branch-specific, differential efficacy in the modulation of different central synapses made by a single neuron. 4. Although INT(+)-MN junctions have the capacity to display marked posttetanic potentiation, they are not significantly potentiated after connective stimulation. Sensitization of the GSW reflex is therefore not necessarily accompanied by a modification of transmission at these synapses. 5. Inhibitory transmission to INTs+ is significantly reduced by connective stimulation (36%) and by 5-HT (71%). This supports the hypothesis that a reduction of feedback inhibition into INTs+ is a major mechanism of reflex sensitization and may account for the increased evoked firing of INTs+ that is observed after connective stimulation. 6. The excitatory input to INTs- is selectively decreased by 5-HT (50%) and by the molluscan neuropeptide small cardioactive peptide B (38%). This latter effect, which could produce disinhibition of INTs+, may explain the previous observation that this peptide is able to potentiate the evoked input to MNs of the reflex at a concentration (1 microM) that fails to modify monosynaptic sensory-motor transmission. 7. These results indicate that transmission through a small neuronal network that mediates a withdrawal reflex in Aplysia may be modulated at multiple sites and by different mechanisms. These mechanisms include: 1) branch-specific facilitation of sensory neuron outputs and 2) inhibition of INT(-)-INT+ inhibitory postsynaptic potentials by endogenous modulatory neurons and by 5-HT.(ABSTRACT TRUNCATED AT 400 WORDS)

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