g , γ dynamic drive, γ static drive, α motor neuron drive) within

g., γ dynamic drive, γ static drive, α motor neuron drive) within a forward model of the system can inferences be made to interpret the state of the system from ambiguous afferent

signals. There have been many studies that have investigated whether forward models can be found within the sensorimotor system. However, conclusive evidence for a forward model in the sensorimotor find more system has been very difficult to produce. This is because the output of the forward model, a prediction of a future event, is not a measurable output but, instead, used to guide the control of the motor system (Mehta and Schaal, 2002). Several studies supporting the use of forward models in the sensorimotor system have used different techniques, for example sinusoidal tracking with induced delays (Miall et al., 1993) or virtual pole balancing with feedback blanking (Mehta and Schaal, 2002). In one study the existence of a forward Cell Cycle inhibitor model was probed by asking subjects to report the final hand position at the end of reaching movements that had been physically perturbed without visual feedback (Wolpert et al., 1995). The systematic errors and the

variability in the errors in the estimated positions were indicative of a forward model similar to the Kalman filter. Using saccades during reaching movements to probe the underlying predicted hand position, several studies have provided evidence that estimates of body state use both sensory unless feedback and a model of the world (Ariff et al., 2002 and Nanayakkara and Shadmehr, 2003). They asked subjects to visually track the position of their

hand during full-limb reaching movements. They found that saccades tended to move to a position 196 ms in advance of the position of the hand (Ariff et al., 2002). By disturbing the arm position with unexpected perturbations, they demonstrated that saccades were initially suppressed (100 ms following the disturbance), then following a recalculation of predicted position, the eyes moved to a predicted position (150 ms in advance, suggesting access to efferent copy information). In contrast when the perturbation also changed the external dynamics (i.e., adding a resistive or assistive field), this recalculation was incorrect, and subjects were unable to accurately predict future hand position. This work suggests that the prediction of future hand position was updated using both the sensory feedback of the perturbation and a model of the environment. When the model of the environment was incorrect, the system was unable to accurately predict hand position. On the other hand, when the altered environment could be learned, the saccade accurately shifted to the actual hand position, demonstrating that the model of the environment could be adaptively reconfigured (Nanayakkara and Shadmehr, 2003). Prediction can also be used for perception.

In essence, the precise positioning of motor columels ensures tha

In essence, the precise positioning of motor columels ensures that specific motor pools are strategically placed to receive input from functionally relevant classes of proprioceptive sensory axons. What then explains the higher-order register that exists between dorso-ventral columelar selleck position in the spinal cord and proximodistal joint and muscle position in the limb? Such matching could be a reflection of developmental strategies used to assemble sensory-motor reflex arcs. In this view, inductive signals arrayed along the proximodistal axis of the limb might act on the peripheral endings of proprioceptive sensory axons to impose neuronal

subtype identities that assign their later termination zone along the dorsoventral axis of the spinal cord. Studies of chick sensory-motor circuits have provided some support for this view, in the sense that they show that limb-derived signals are able to direct central patterns

of sensory-motor connectivity (Wenner and Frank, 1995). More generally, the emerging appreciation of Romanes’s classical findings may warrant a re-evaluation of the strategies and mechanisms used to convert neuronal identity into selective connectivity. A Sperry-like view of connectivity holds that neuronal identity can be translated directly into the selectivity of expression of neuronal surface labels and argues that these labels are the primary cues recognized by incoming axons. Current thinking on the molecular underpinnings of selective synaptic connectivity is dominated by this view, despite the still scant evidence for the workings of such synaptic recognition cues. Bortezomib Viewed with seventy year hindsight (Figure 4), Romanes’s studies of neuronal order in the spinal cord serve as a timely reminder that neuronal subtype identity is as clearly reflected in the stereotypic positioning of neuronal cell bodies

as in the diversity of surface labels. Indeed, there is emerging evidence that neuronal location is a determinant of connectivity patterns, Bumetanide beyond the immediate confines of the monosynaptic sensory-motor reflex system. Recent studies of interneuron organization in the spinal cord indicate that the local inhibitory circuits that are charged with patterning the output of flexor and extensor motor neuron subtypes actually settle in different coordinate locations in the spinal cord and that such positional distinctions have consequences for patterned sensory input (Tripodi et al., 2011). In addition, the dorsoventral and mediolateral termination positions of sensory axons in the ventral nerve cord of Drosophila are established by target-independent positioning cues that, conceptually, resemble the strategy that appears to operate in mammalian spinal cord ( Zlatic et al., 2009). Finally, neuromuscular connectivity patterns in the vertebrate limb are established by mesenchymal signals that coordinate motor axonal trajectory and muscle cleavage patterns, rather than through motor recognition of target muscle ( Lewis et al.

, 2003 and Nässel and Elekes, 1992) To identify the specific TH-

, 2003 and Nässel and Elekes, 1992). To identify the specific TH-Gal4 neurons that trigger proboscis extension, we employed a genetic mosaic analysis to restrict dTRPA1 expression to small subsets of TH-Gal4 neurons ( Gordon and Scott, 2009). Briefly, the repressor Gal80 flanked by FRT recombination sites was expressed ubiquitously to inhibit Gal4-dependent expression. Induction of Flp recombinase under the control of a heat-shock promoter led to the stochastic excision of Gal80 and the expression of UAS-dTRPA1 in different TH-Gal4 subpopulations ( Gordon and Scott, 2009). The inclusion of UAS-mCD8-GFP allowed for visualization of cells expressing dTRPA1. Mosaic animals were tested for

proboscis extension to heat and classified as extenders and nonextenders. The neurons labeled in Selleckchem Bosutinib the brains and thoracic ganglia of extenders and nonextenders were Verteporfin compared to test whether specific TH-Gal4 neurons were associated with the extension phenotype. Eleven different cell populations were frequently labeled by this method ( Figure 4). Most cell

populations showed a similar frequency distribution in both behavioral categories; however, one cell was present in 93% of extenders (51/55) and rarely present in nonextenders (1%; 1/99). In addition, three extenders showed Gal4 expression in just two cells in the entire nervous system; each contained the cell found in 93% of extenders and a second cell that was different in each fly. These results argue that a single TH-Gal4 cell is sufficient to drive proboscis extension. Other cells

may modestly influence proboscis extension but would not be uncovered by mosaic analyses. Instead, the mosaic analysis is biased toward identifying single neurons sufficient to activate proboscis extension. The TH-Gal4 neuron that generates extension shows broad arborizations in the ventral anterior SOG, the primary taste relay ( Figure 5 and Figure S2). This brain region receives gustatory axons from the proboscis, mouthparts, legs, and motor neuron dendrites that drive proboscis extension ( Figure S2). Previous studies characterizing the anatomy of TH-Gal4 neurons have classified this neuron as a ventral unpaired medial neuron based on cell-body position ( Nässel and Elekes, 1992). We name this Liothyronine Sodium neuron TH-VUM. As expected, TH-VUM expresses tyrosine hydroxylase by immunohistochemistry ( Figure 5C), demonstrating that it is indeed a dopaminergic neuron. To determine whether processes are dendrites or axons, a marker for presynaptic terminals, Synaptobrevin-GFP (Syn-GFP) ( Estes et al., 2000), was expressed in single-cell TH-Gal4 clones. Syn-GFP labeled all arbors of TH-VUM, suggesting that the neuron releases transmitter throughout the SOG ( Figure 5D). Based on its localization in the primary taste region and its extensive arborizations, the TH-VUM neuron is well situated to modulate taste behaviors.

Interestingly, animals that had been conditioned and returned to

Interestingly, animals that had been conditioned and returned to their normal rearing environment for 7–9 hr had thresholds at higher spatial frequencies (13.1 ± 1.14 cycles cm-1) than nonconditioned controls (10.3 ± 0.8 cycles cm-1, p < 0.05, Figures 6E and 6F). To determine if

the enhanced BDNF signaling resulting from visual conditioning played a role in this change, we injected K252a twice into the tectal ventricle at 3.5 and 4.5 hr after conditioning, corresponding to the period when we found facilitation of synaptic plasticity. Animals were then tested at 7–9 hr after conditioning. TrkB inhibition (n = 16), but not control vehicle injection (n = 12), prevented the improvement in spatial sensitivity produced by conditioning (K252a: 9.2 ± AZD2281 datasheet 1.0 cycles cm-1; vehicle: 9.8 ± 1.11 cycles Z-VAD-FMK solubility dmso cm-1) (Figure 6F). The fact that only about half the tadpoles responded to three or more of the counterphasing gratings most likely

reflects independent modulation of the behavioral output rather than low-order visual system differences between animals as the fall-off of visually evoked responses measured electrophysiologically in tectal neurons correlated well with spatial frequency in nearly all animals tested (Figure 5). Thus, the data show that the observed increase in tectal cell sensitivity to finer gratings can affect the visually-evoked behavior of the awake unrestrained animal in a BDNF-dependent manner. However, for the reasons mentioned above, this behavioral assay provides an estimate of the visual sensitivity of the animals rather than a measurement of absolute acuity. To confirm that the observed change in swimming acceleration in response to visual stimuli involved retinotectal transmission, we thermally lesioned the optic tract just anterior Bay 11-7085 to the optic

tectum using the two-photon microscope with the infrared laser set at high intensity (∼200 mW on the stage at 810 nm) (Figure S5). At 5 hr after lesioning, we performed the behavioral test. Although animals that had undergone optic tract lesions still exhibited normal startle responses to full-screen ON stimuli, their response to counterphasing gratings was dramatically impaired. This finding is in agreement with previous studies attributing the visual acuity of behavioral responses to sensory processing in the optic tectum (Yolen and Hodos, 1976). Taken together, our data demonstrate that BDNF signaling induced by visual conditioning is able to facilitate bidirectional retinotectal synaptic plasticity, resulting in a behaviorally significant improvement in the response thresholds of tectal neurons to visual stimuli. We previously reported that a repeating visual stimulus was able to upregulate plasticity-related gene transcription in the Xenopus optic tectum ( Schwartz et al., 2009).

e , which room the animal is in) (Kjelstrup et al , 2008) Accord

e., which room the animal is in) (Kjelstrup et al., 2008). Accordingly, the mPFC, whose inputs arise mostly from ventral and intermediate hippocampus, exhibits no evidence of place cell-like responses but does discriminate between rooms (Hyman et al., learn more 2012; Jung et al., 1998; Poucet, 1997). Recent evidence has established that the firing of hippocampal

place cells is modulated by environmental stimuli (Leutgeb et al., 2005). Given its strong connectivity with limbic structures, ventral hippocampus may encode nonspatial contextual signals for such things as odors, bodily states, and emotions (Pennartz et al., 2011). Hence, as has been previously suggested, the hippocampal input is a plausible source of spatial and emotional context (Jung et al., 1998; Pennartz et al., 2011). The other possible role for hippocampal MDV3100 concentration input to mPFC is to support rapid learning. Wise and Murray (2000) have provided evidence that arbitrary visual-motor mappings formed within premotor cortex initially depend on rapid associative mechanisms within the hippocampus but, through consolidation, become hippocampally independent. A similar principle may apply to the mPFC. To wit, the rapid formation and consolidation of associations between contexts, events, and responses

within mPFC may depend on hippocampus, whereas long-term storage may be mediated mostly by mPFC. The aforementioned evidence for coordinated memory replay in mPFC and hippocampus during consolidation

supports this claim. The role of communication between hippocampus and mPFC has been studied via functional disconnection, in which the mPFC is inactivated in one hemisphere and the hippocampus is inactivated in the other. Because the connections between hippocampus and mPFC are unilateral, the animal is left with one intact hippocampus and one intact mPFC but no pathway between them (Floresco et al., 1997). This technique Ketanserin has been used to demonstrate that mPFC-hippocampal communication is necessary for short-term memory in paradigms including the water maze (Wang and Cai, 2008), the T maze (Wang and Cai, 2006), spatial win-shift on the radial arm maze (Floresco et al., 1997; Goto and Grace, 2008), and the Hebb-Williams maze, a spatial maze requiring a specific set of turns to reach reward (Churchwell et al., 2010). In fact, the effects of mPFC-hippocampal disconnection are nearly the same as those seen after bilateral mPFC inactivation, supporting the claim that mPFC is dependent upon the hippocampal-mPFC pathway either for context or for rapid learning. As further evidence for a functional interaction between mPFC and hippocampus, electrophysiological rhythms in these two structures are coupled, particularly in the theta range. Roughly half of mPFC cells exhibit phase locking to hippocampal theta while rats engage in spatial tasks (Hyman et al., 2005; Siapas et al., 2005).

We propose that a rhythmic molecular clock in the DN1s of per01;

We propose that a rhythmic molecular clock in the DN1s of per01; DN1 > per larvae drives rhythmic signals from DN1s that regulate LNv neuronal activity. Because DN1s seem to be most active at dusk, this would allow LNvs to promote light avoidance at dawn even in the absence of their own functional clock. This result directly

parallels observations from adult flies, in which restoring per to only non-LNv clock neurons in per01 mutant flies restored the morning peak of locomotor activity ( Stoleru et al., 2004). Conversely, we propose that larvae lacking per expression in DN1s (per01; Pdf > per; Figure 4B) remain rhythmic because high CLK/CYC activity in per01 DN1s ( Figure 3C) renders them excitable and able to release their essential signal, while the functional LNv SCH727965 clock controls the timing of behavior. This contrasts with DN1 ablation, which prevents rhythms ( Figure 4A). Therefore, the DN1 signal is both necessary (ablated DN1s; Figure 4A) and sufficient (per+ DN1s with per mutant LNvs; Figure 4B) for light avoidance rhythms. If CLK/CYC activity regulates DN1 excitability (Figure 3), low CLK/CYC activity should block release of the essential DN1 signal and be phenotypically similar to ablating DN1s. To test this,

we assayed the effect of stopping the DN1 molecular clock with low CLK/CYC activity on light avoidance rhythms at 150 lux (Figure 4C). We found that DN1 > ClkDN larvae lost light avoidance rhythms, with larvae constitutively sensitive to light at both 150 lux and 50 lux, similar to DN1 ablation. It should be noted that the experiments in Galunisertib clinical trial Figures 4B and 4C are complementary rather than identical because expression of ClkDN or cycDN in a single neuronal group blocks the clock in those cells but leaves the other clock neurons wild-type, whereas restoration of per Carnitine dehydrogenase to a single neuronal group leaves the rest of the larva in a mutant

per01 state. Overall, our LD and DD data suggest that the DN1 molecular clock regulates DN1 neuronal activity, with DN1s least active when CLK/CYC activity is lowest at dawn. Next, we sought to directly test when DN1s normally signal by using a transgene that expresses the heat-activated cation channel, TrpA1 (Hamada et al., 2008). Because TrpA1 is activated at temperatures >25°C, it can be used to transiently activate neurons in which it is expressed (Pulver et al., 2009). We used TrpA1 to transiently stimulate DN1s at CT12 and CT24 and measure the effect on light avoidance (Figure 4D). At 20°C, DN1 > TrpA1 larvae displayed normal light avoidance rhythms. However, activating DN1s via TrpA1 at 26°C blocked the rhythm, with levels of light avoidance constitutively low at both CT12 and CT24. No reduction in light avoidance at CT24 was observed between 20°C and 26°C for either UAS-TrpA1 / + or DN1 / + control larvae ( Figure S3).

, 2009) Similarly in this study in cattle, it is plausible that

, 2009). Similarly in this study in cattle, it is plausible that the QuilA in the vaccine may provoke an adequate immune response to viral and bacterial infection despite concurrent infection with F. hepatica. It is also noteworthy that the immunoregulatory effects described by Flynn et al. (2007) relates to the suppressive effect of F. hepatica on the type IV delayed hypersensitivity (antibody independent) reaction, as modelled on the intradermal skin test. The vaccine used in this trial has a combination of bacterial and viral antigens, which is likely to induce a different immune response to that caused by Mycobacterium bovis

and therefore may relate to the difference between immune mechanisms involved in an antibody independent Inhibitor Library clinical trial hypersensitivity reaction and an antibody dependent immune response to vaccination.

Relative to other comparable studies (Waldvogel Selleckchem Olaparib et al., 2004) where a higher dose of F. hepatica metacercariae was used, the low dose used in this study could have resulted in a parasite burden too low to have a demonstrable effect on vaccine responsiveness. However, all animals in the experimental group were infected, and did mount an immunological response to liver fluke infection as indicated by seroconversion and increased liver enzymes. Low number of calves with a positive faecal egg count reflects the fact that the analysis was conducted early in the patent Mephenoxalone period. Also, detection of F. hepatica eggs in bovine faeces is a relatively insensitive diagnostic method ( Anderson et al., 1999). The increase in eosinophils as well as liver enzymes was significantly higher in the experimental group relative to the non-infected group, where no or little increase in these parameters was identified. In contrast, neutrophil numbers, which were elevated relative to the reference range at the start of the experiment, followed by a decline in both groups, were significantly lower in the infected group relative to the non-infected group. This observation in the neutrophil count was in contrast to other studies (Egbu et al., 2013) where a

significant increase was identified. A reasonable explanation to account for this response is not forthcoming. Stress, as a cause of the initial elevated numbers, is an unlikely explanation, given the animals were on the farm for 2 months prior to the commencement of the experiment. However, it is possible that an unknown sub-clinical infection may account for the unusual neutrophil profile, with the concurrent F. hepatica infection potentially hampering the neutrophil response in the infected group. The expected cytokine profile following liver fluke infection of elevated Th2 and inhibited Th1 profiles was not identified. In contrast to previous research, we found IL-4 concentrations produced by unstimulated and stimulated PBMC to be higher in the control group.

By deleting GluN2A or GluN2B during early postnatal development,

By deleting GluN2A or GluN2B during early postnatal development, a period of rapid synaptogenesis, we found that

both subunits negatively regulate synaptic AMPAR expression, but by distinct means. We show that, similar to GluN1 deletion (Adesnik et al., 2008), deletion of GluN2B increases the number of functional synapses, suggesting a basal role for GluN2B-containing NMDARs in Imatinib in vitro maintaining silent synapses in early development. Conversely, deletion of GluN2A increases synaptic strength without affecting the number of unitary connections. These results suggest that when significant bursts of activity drive the synaptic insertion of AMPARs and the recruitment of GluN2A-containing receptors, GluN2A functions to dampen further synapse potentiation. The hippocampal

CA3-to-CA1 synapse is a model excitatory synapse that has been used to delineate the mechanisms of synaptic plasticity. Using conditional KO alleles for GluN2A (Grin2afl/fl; see Figure S1A available online) and GluN2B (Grin2bfl/fl) ( Akashi et al., 2009), we eliminated the target gene in a small subset of hippocampal neurons by transcranial stereotactic injection of P0-P1 mice with a recombinant adeno-associated Dinaciclib concentration virus expressing a Cre-GFP fusion protein (rAAV1-Cre-GFP) ( Kaspar et al., 2002). Figure 1A shows a typical acute slice made from a P18 mouse after P0 injection demonstrating sparse infection of CA1 pyramidal neurons. It has long been suspected Ribonucleotide reductase from in situ hybridization, single-cell reverse-transcriptase polymerase chain reaction, and pharmacologic studies that hippocampal CA1 pyramidal neurons express primarily GluN2A and

GluN2B subunits (Garaschuk et al., 1996, Watanabe et al., 1992 and Zhong et al., 1995). By cross-breeding the Grin2afl/fl (ΔGluN2A) and Grin2bfl/fl (ΔGluN2B) mice, we generated Grin2afl/flGrin2bfl/fl (ΔGluN2AΔGluN2B) mice and simultaneous whole-cell recording from a Cre-expressing cell (green trace in inset), and a control cell in the presence of NBQX revealed a complete loss of NMDAR-EPSCs ( Figure 1B, inset). We followed the time course of subunit depletion by measuring the ratio of NMDAR-EPSCs from Cre-expressing cells to control cells after P0 injection, and demonstrated a gradual decrease in NMDAR-EPSCs and complete loss consistently by P15 ( Figure 1B), similar to the rate of loss of NMDAR-EPSCs in Grin1fl/fl mice (ΔGluN1). These data indicate that, in addition to obligatory GluN1 subunits, synaptic NMDA receptors in CA1 pyramidal neurons contain only GluN2A and GluN2B. Since the NMDA-EPSCs were entirely gone by P15 in the double conditional KO mice, we performed all subsequent analyses of ΔGluN2A and ΔGluN2B mice after P17 unless indicated.

, 2007 and Volgraf et al , 2006), this class of ion channel has b

, 2007 and Volgraf et al., 2006), this class of ion channel has been surprisingly underexploited as a tool to couple recognition of different types this website of chemicals with cellular physiological responses. The existence of many hundreds of divergent IRs of presumed distinct specificity reveals a natural exploitation of this ligand-gated ion channel for chemical sensing (Croset et al., 2010 and Liu et al., 2010). The molecular properties of IRs uncovered here provide a basis for their rational modification to generate custom-designed chemoreceptors of

desired specificity. Such sensors could offer invaluable tools as genetically encoded neuronal activators or inhibitors as well as have broad practical applications, for click here example, in environmental pollutant detection or clinical diagnosis. Standard methods were used for Drosophila genetics, as described together with a

list of strains used, in the Supplemental Experimental Procedures. Standard methods were used in construction of all plasmids; details are provided in the Supplemental Experimental Procedures. Standard methods were employed for immunofluorescence as described, together with all antibodies used, in the Supplemental Experimental Procedures. Extracellular recordings in single sensilla of 2- to 14-day-old flies were performed and quantified essentially as described (Benton et al., 2007 and Benton et al., 2009); details are provided, together with odor sources, in the Supplemental Experimental Procedures. Oocyte preparation and injection was carried out essentially as described (Vukicevic et al., 2006); details are provided in the Supplemental Experimental Procedures. Solutions containing agonists were applied once every minute for 10 s; between applications, the recording chamber was perfused with standard bath solution (110 mM NaCl, 2 mM BaCl2, 10 mM HEPES-NaOH, pH adjusted to 7.4 with NaOH) without agonist.

For current/voltage (IV) curves in the presence of different ions, NaCl was replaced 17-DMAG (Alvespimycin) HCl by 110 mM KCl or 40 mM CaCl2 and the osmolarity was adjusted with sucrose. The Na+ and K+ solutions contained 2 mM Ba2+ as divalent cation. Kaleidagraph (Synergy Software) was used to fit the inhibition curves to the Hill equation: I = I0/[1+([inh]/IC50)nH], where I0 is the current in the absence of inhibitor (inh), IC50 is the inhibitor concentration that induces 50% inhibition, and nH is the Hill coefficient. For IV curve measurements in high extracellular Ca2+, we injected 50 nl of 40 mM BAPTA 1-2 hr prior to the electrophysiological measurements to test the contribution of the Ca2+ currents by endogenous Ca2+-dependent chloride currents. Phenylacetaldehyde and propionic acid were prepared as 1 M stock solutions in DMSO and diluted in bath solution to the desired final concentration. Philanthotoxin 433 tris(trifluoroacetate) (Sigma) was diluted to 1 mM in standard bath solution containing 0.

The Weibull model provided the best description of survival kinet

The Weibull model provided the best description of survival kinetics for Salmonella survival in low-moisture foods. Secondary models were developed which predicted the time required for first decimal reduction (δ) and shape factor values (β) as influenced by

temperature and aw. These models were useful in predicting the survival of Salmonella in several tested low-moisture foods providing acceptable prediction performances. The models were more accurate in predicting the survival of Salmonella in non-fat food systems as compared to foods containing low-fat levels. These models provide baseline information to be used for research on risk mitigation strategies for low-moisture foods. In future research, the models developed will be expanded to include fat content and other food components that may affect Salmonella survival. Available literature data on Salmonella survival studies in low-moisture BMS-354825 price foods will be incorporated into future validation studies. Future research will also include survival studies using different initial inoculum levels, different inoculation preparation methods and experiments to determine the effects of salt and sugar on survival kinetics.

This project was supported by the International Life Sciences Institute, North America and by State and Hatch funds allocated to the Georgia Agricultural Experiment Station. Authors gratefully acknowledge Maria Sohail for the cocoa powder survival data and the assistance of John Glushka and William Kerr with NMR analyses. “
“Today, food chains are becoming more complicated in the handling, processing, and transportation Torin 1 ic50 about of food;

hence obtaining safe food is becoming more difficult day by day. Most of the antimicrobial substances and sanitizers used in the food industry for preservation and sanitation are dangerous for human health and harmful to the environment. In recent years, there has been an increasing demand for safe antimicrobial substances and sanitizers for the food industry (Lopez-Gomez et al., 2009). Similar trends are also valid for fresh fruits, vegetables, and organic foods. Thus, novel and complementary food preservation technologies are continuously being investigated. Among the alternative food preservation technologies, particular attention has been paid to the physical methods and biopreservation to extend the shelf-life and inhibit undesirable microorganisms, minimizing the impact on the nutritional and organoleptic properties of food products. No method of treatment or sanitation that is currently used in the food industry has been proven capable of inactivating microorganisms attached to fruit or vegetable tissues. Therefore, this review will summarize the basic knowledge and current applications of ultrasound technology as an alternative washing method for avoiding attachment of microorganisms to fruit and vegetable tissues.