*3.2.4 Sour taste*

Acidic pH and organic acids such as acetic acid evokes sour taste in the tongue. A subset of taste receptor cells in the tongue and palate epithelium that respond to acidic pH and weak organic acids with electrical activity detects the sour taste [78, 79]. PKD2L1-expressing cells respond are required for sensory response to acids [72, 78, 80] which is mediated by an unusual proton-selective ion channel [80]. Proton selectivity allows the cells to respond to acids without interference from Na<sup>+</sup> , which may vary independently in concentration. The taste of carbonation (CO2) is also detected by PKD2L1-expressing cells. This response is

dependent on a membrane anchored carbonic anhydrase isoform 4, Car4 [81], which interconverts CO2 + H2O to H<sup>+</sup> + HCO3 <sup>−</sup>. How Car4 contributes to the activation of sour cells is still not known.

Fruit flies reject foods that are too acidic and prefer the ones which are slightly acidic, such as carbonated water. Carbonated water triggers Ca2+ influx in the region of the SEZ innervated by taste peg GRNs, suggesting these neurons are involved in CO2 detection [82]. Fruit flies avoid many carboxylic acids with a low pH. Behavioral and physiological analysis reveals that the avoidance to carboxylic acid is mainly mediated by a subset of bitter GRNs [83]. The ionotropic receptor Ir7a has been shown for rejecting foods laced with high levels of acetic acid suggesting flies discriminate foods on the basis of acid composition rather than just pH [84].

#### *3.2.5 Amino acid receptors*

Umami (amino acid taste) is the sensation elicited by glutamate. In humans, umami is only elicited by glutamate, while mice are sensitive to a wider range of L-amino acids [1]. Addition of the nucleotides IMP or GMP potentiates the umami response, distinguishing it from a more general sensing of glutamate [85]. T1R1/ T1R3 is widely recognized as the umami receptor [1].

Fruit flies can taste amino acids too, although their preference is enhanced when raised on a food source devoid of amino acids [86]. Female fruit flies show greatest preference for cysteine, phenylalanine, threonine and tyrosine, while males prefer leucine and histidine. None of the 18 standard amino acids tested stimulates action potentials in GRNs in sugar responsive sensilla [8] raising the possibility of taste pegs in sensing amino acids. Another amino acid, L-canavanine is toxic and elicits an avoidance response in flies [87] and is sensed by GRNs in a subset of S-type sensilla [88]. Gr8a and Gr66a are both required for L-canavanine avoidance [88]. An ionotropic receptor Ir76b has been shown recently for amino acid taste in flies [89].

Activation of fly GRNs by sweet substances, bitter compounds and the amino acid, L-canavanine occur through direct activation of ion channels and G-protein signaling pathways. G proteins subunits Gγ, Goα, Gsα and Gqα are implicated in sugar signaling [90–93]. PLCβ is an effector for Gqα. Knockdown in sugar-responsive GRNs of *plc*β*21c* or any of the genes encoding TRPC channels (TRP, TRPL and TRPγ) alters the behavioral response to trehalose [92]. Role of G-protein coupled signaling pathways in sensation of bitter tastants has also been suggested for example AC78C is required for the response to caffeine [94], and the PLCβ encoded by *norpA* is required in *trpA1*-expressing GRNs for the behavioral and electrophysiological responses to the bitter compound, aristolochic acid [64] suggesting a role of Gq/PLC/TRPA1 pathway functions in the detection of aristolochic acid. Goα47A is needed for detection of L-canavanine [95]. The predicted role of G-protein coupled signaling pathways in insect taste is to enhance the responses to low concentrations of ligands, as seen for photo transduction cascade in amplifying the response to a photon of light.

#### **3.3 Taste coding**

Taste in flies and mammals use labeled line model of coding (in which each cell represents a distinct taste quality and communicates essentially without interruption to the central nervous system). Single taste neurons in flies can detect multiple taste qualities having the same valence (behavioral output) supported by the results that some GRNs are activated by sugars, and low levels of fatty acids,

**137**

be determined.

*Understanding Taste Using* Drosophila melanogaster *DOI: http://dx.doi.org/10.5772/intechopen.89643*

behaviors [77].

to behavior, as is the case in flies.

**3.4 Taste modulation in** *Drosophila*

both of which promote feeding [96] while other GRNs are activated by bitter compounds and high concentrations of salt and suppress feeding [20]. In addition, a subset of bitter GRNs is also activated by low pH carboxylic acids, which are feeding deterrents [83]. A complex model for salt coding in flies that combinatorially integrates inputs from across cell types to afford robust and flexible salt

The taste system of mice also uses a variant of the labeled line model. In mice, taste receptors are segregated into distinct populations such that bitter, sweet, sour and low concentrations of salt are detected by non-overlapping sets of cells [1, 58]. Whether this principle applies to sweet and umami is presently unclear. Recent evidence suggest that aversive high concentrations of salt are not detected by a separate subset of cells, but are instead detected by the populations of cells that detect bitter and sour [72] suggesting that the mammalian taste system is relatively hard-wired

Modulation of taste neuron activity prior to the first relay has been suggested. Presence of multiple molecular and cellular mechanisms by which tastant information is integrated in primary taste neurons has been proposed [97]. Various studies suggest that aversive tastants such as bitter compounds and acids, can inhibit the activity of appetitive taste circuits in adult flies and larvae [83, 98, 99]. The reduction of the firing rate of sweet neurons in mixtures of sucrose and the aversive tastants is independent of the activity of the deterrent neuron [83, 98, 99]. Bitter compounds suppress feeding by activating bitter—GRNs and by inhibiting sugar sensitive GRNs [11]. The suppression of sugar GRNs depends on a odorant binding proteins" (OBP), OBP49a, which is expressed in gustatory organs or indirectly via GABAergic interneurons that connect bitter taste neuron activity to that of sweet taste neurons [100, 101]. Accessory cells synthesized OBP49a and release it into endolymph fluid bathing the GRNs, which then acts non-cell autonomously on sugar activated GRNs. OBP49a binds directly to bitter compounds, and later interacts with the sugar receptor, Gr64a, on the cell surface of the GRNs to suppress its activity [101]. Such non-cell autonomous modulation of the sugar response ensures that bitter compounds in sugar-laden foods are not consumed. Low concentrations of acid tastants have also been observed to modulate detection of bitter compounds in the context of both sweet and deterrent neurons, suppressing their inhibitory effect in the former and their excitatory effect in the latter [102]. Although the mechanisms by which carboxylic acids or low pH inhibit taste neurons remains to

Internal state can change the gustatory sensitivity as well: starvation potentiates the responses of sweet GRN and suppresses bitter GRN responses; mating increases taste peg GRN sensitivity to polyamines and behavioral responses to low salt in females; and protein deprivation sensitizes taste peg GRNs to yeast and increases behavioral sensitivity to amino acids [86, 103–108]. Taste neuron sensitivity is also modulated by prior dietary experience. Response to camphor (non-toxic bitter compound) decrease after exposing flies to camphor for long [66]. An E3 ubiquitin ligase-regulated decline in the levels of Trpl caused the change in sensitivity. No calories diet also cause increase activity in the *Gr5a*+ sweet taste circuit [104, 109] and reduce sensitivity in the bitter taste circuit [105]. In the former case, dopamine signaling acting on the both primary and secondary neurons in the sweet circuit caused the change in sensitivity [104, 109]. The latter is dependent on sNPF acting via GABAergic interneurons [105]. A significant modulation of fly salt taste behav-

ior by salt deprivation has been shown recently [77].

*Understanding Taste Using* Drosophila melanogaster *DOI: http://dx.doi.org/10.5772/intechopen.89643*

*Animal Models in Medicine and Biology*

which interconverts CO2 + H2O to H<sup>+</sup>

just pH [84].

*3.2.5 Amino acid receptors*

activation of sour cells is still not known.

T1R3 is widely recognized as the umami receptor [1].

recently for amino acid taste in flies [89].

dependent on a membrane anchored carbonic anhydrase isoform 4, Car4 [81],

+ HCO3

Umami (amino acid taste) is the sensation elicited by glutamate. In humans, umami is only elicited by glutamate, while mice are sensitive to a wider range of L-amino acids [1]. Addition of the nucleotides IMP or GMP potentiates the umami response, distinguishing it from a more general sensing of glutamate [85]. T1R1/

Fruit flies can taste amino acids too, although their preference is enhanced when raised on a food source devoid of amino acids [86]. Female fruit flies show greatest preference for cysteine, phenylalanine, threonine and tyrosine, while males prefer leucine and histidine. None of the 18 standard amino acids tested stimulates action potentials in GRNs in sugar responsive sensilla [8] raising the possibility of taste pegs in sensing amino acids. Another amino acid, L-canavanine is toxic and elicits an avoidance response in flies [87] and is sensed by GRNs in a subset of S-type sensilla [88]. Gr8a and Gr66a are both required for L-canavanine avoidance [88]. An ionotropic receptor Ir76b has been shown

Activation of fly GRNs by sweet substances, bitter compounds and the amino acid, L-canavanine occur through direct activation of ion channels and G-protein signaling pathways. G proteins subunits Gγ, Goα, Gsα and Gqα are implicated in sugar signaling [90–93]. PLCβ is an effector for Gqα. Knockdown in sugar-responsive GRNs of *plc*β*21c* or any of the genes encoding TRPC channels (TRP, TRPL and TRPγ) alters the behavioral response to trehalose [92]. Role of G-protein coupled signaling pathways in sensation of bitter tastants has also been suggested for example AC78C is required for the response to caffeine [94], and the PLCβ encoded by *norpA* is required in *trpA1*-expressing GRNs for the behavioral and electrophysiological responses to the bitter compound, aristolochic acid [64] suggesting a role of Gq/PLC/TRPA1 pathway functions in the detection of aristolochic acid. Goα47A is needed for detection of L-canavanine [95]. The predicted role of G-protein coupled signaling pathways in insect taste is to enhance the responses to low concentrations of ligands, as seen for photo transduction cascade in amplifying the response to a

Taste in flies and mammals use labeled line model of coding (in which each cell represents a distinct taste quality and communicates essentially without interruption to the central nervous system). Single taste neurons in flies can detect multiple taste qualities having the same valence (behavioral output) supported by the results that some GRNs are activated by sugars, and low levels of fatty acids,

Fruit flies reject foods that are too acidic and prefer the ones which are slightly acidic, such as carbonated water. Carbonated water triggers Ca2+ influx in the region of the SEZ innervated by taste peg GRNs, suggesting these neurons are involved in CO2 detection [82]. Fruit flies avoid many carboxylic acids with a low pH. Behavioral and physiological analysis reveals that the avoidance to carboxylic acid is mainly mediated by a subset of bitter GRNs [83]. The ionotropic receptor Ir7a has been shown for rejecting foods laced with high levels of acetic acid suggesting flies discriminate foods on the basis of acid composition rather than

<sup>−</sup>. How Car4 contributes to the

**136**

photon of light.

**3.3 Taste coding**

both of which promote feeding [96] while other GRNs are activated by bitter compounds and high concentrations of salt and suppress feeding [20]. In addition, a subset of bitter GRNs is also activated by low pH carboxylic acids, which are feeding deterrents [83]. A complex model for salt coding in flies that combinatorially integrates inputs from across cell types to afford robust and flexible salt behaviors [77].

The taste system of mice also uses a variant of the labeled line model. In mice, taste receptors are segregated into distinct populations such that bitter, sweet, sour and low concentrations of salt are detected by non-overlapping sets of cells [1, 58]. Whether this principle applies to sweet and umami is presently unclear. Recent evidence suggest that aversive high concentrations of salt are not detected by a separate subset of cells, but are instead detected by the populations of cells that detect bitter and sour [72] suggesting that the mammalian taste system is relatively hard-wired to behavior, as is the case in flies.

## **3.4 Taste modulation in** *Drosophila*

Modulation of taste neuron activity prior to the first relay has been suggested. Presence of multiple molecular and cellular mechanisms by which tastant information is integrated in primary taste neurons has been proposed [97]. Various studies suggest that aversive tastants such as bitter compounds and acids, can inhibit the activity of appetitive taste circuits in adult flies and larvae [83, 98, 99]. The reduction of the firing rate of sweet neurons in mixtures of sucrose and the aversive tastants is independent of the activity of the deterrent neuron [83, 98, 99]. Bitter compounds suppress feeding by activating bitter—GRNs and by inhibiting sugar sensitive GRNs [11]. The suppression of sugar GRNs depends on a odorant binding proteins" (OBP), OBP49a, which is expressed in gustatory organs or indirectly via GABAergic interneurons that connect bitter taste neuron activity to that of sweet taste neurons [100, 101]. Accessory cells synthesized OBP49a and release it into endolymph fluid bathing the GRNs, which then acts non-cell autonomously on sugar activated GRNs. OBP49a binds directly to bitter compounds, and later interacts with the sugar receptor, Gr64a, on the cell surface of the GRNs to suppress its activity [101]. Such non-cell autonomous modulation of the sugar response ensures that bitter compounds in sugar-laden foods are not consumed. Low concentrations of acid tastants have also been observed to modulate detection of bitter compounds in the context of both sweet and deterrent neurons, suppressing their inhibitory effect in the former and their excitatory effect in the latter [102]. Although the mechanisms by which carboxylic acids or low pH inhibit taste neurons remains to be determined.

Internal state can change the gustatory sensitivity as well: starvation potentiates the responses of sweet GRN and suppresses bitter GRN responses; mating increases taste peg GRN sensitivity to polyamines and behavioral responses to low salt in females; and protein deprivation sensitizes taste peg GRNs to yeast and increases behavioral sensitivity to amino acids [86, 103–108]. Taste neuron sensitivity is also modulated by prior dietary experience. Response to camphor (non-toxic bitter compound) decrease after exposing flies to camphor for long [66]. An E3 ubiquitin ligase-regulated decline in the levels of Trpl caused the change in sensitivity. No calories diet also cause increase activity in the *Gr5a*+ sweet taste circuit [104, 109] and reduce sensitivity in the bitter taste circuit [105]. In the former case, dopamine signaling acting on the both primary and secondary neurons in the sweet circuit caused the change in sensitivity [104, 109]. The latter is dependent on sNPF acting via GABAergic interneurons [105]. A significant modulation of fly salt taste behavior by salt deprivation has been shown recently [77].

#### **3.5 Non-canonical taste qualities**

#### *3.5.1 Fats*

Vertebrates can sense a variety of other important taste qualities such as wetness and fattiness. Olfaction and somatosensation helps in the detection of fats, and they elicit post-ingestive effects that promote consumption. It has been shown that mice prefer water spiked with free fatty acids supports a role for the taste system in detecting this rich source of calories [110]. A fatty acid transporter (CD36) and two fat-sensitive GPCRs—GPR40 and GPR120 are putative receptors for fat taste including K+ channels that are sensitive to polyunsaturated fatty acids [111]. GPR120 is required for preference to fatty acids in mice [112] and is expressed in human TRCs as well [113].

In flies, sweet GRN activation requires the function of the three *Ionotropic receptor* genes *Ir25a*, *Ir76b* and *Ir56d*. *Ir25a and Ir76b* are expressed in several neurons per sensillum, while *IR56d* expression is restricted to sweet GRNs. *Ir25a* and *Ir76b* mutant flies loose appetitive behavioral responses to fatty acids. The phenotype can be rescued by expression of respective transgenes in sweet GRNs [114].

#### *3.5.2 Calcium taste*

Ca2+, an ion is required for a vast array of cellular functions. Ca2+-deprived animals show attraction and Ca2+-sated animals show rejection. The aversive response to Ca2+requires a functioning T1R3 receptor, a subunit of the umami and sweet receptor [115]. In human subjects an attenuation of the taste of Ca2+ by the T1R3 blocker lactisole has been shown [116].

Fruit flies avoids toxic levels of calcium. This repulsion is mediated by two mechanisms—activation of a specific class of GRNs that suppresses feeding, and inhibition of sugar-activated GRNs, which normally stimulates feeding. The distaste for Ca2+, and electrophysiological responses to Ca2+ require three members of the variant ionotropic receptor family Ir25a, Ir62a and Ir76b. The high concentrations of Ca2+ show decrease survival in flies [117].

#### *3.5.3 Water*

No water receptor has been identified in vertebrate so far. The somatosensory system of animals can detect wetness across their body and also contribute to the sensing of aqueous solutions in the oral cavity. Various tastes have been ascribed to distilled water, from bitter to salty and sweet. Notably, application of water after exposure to some artificial sweeteners, such as saccharin, elicits a sweet taste [118].

A member of the Degenerin/Epithelial Sodium Channel family, ppk28 (an osmosensitive ion channel) mediates the cellular and behavioral response to water in flies. *ppk28* is expressed in water-sensing neurons and loss of *ppk28* abolishes water sensitivity [119].

#### **3.6 Taste signal processing and taste sensory maps in the** *Drosophila* **brain**

In flies, after evaluation of taste input, the information translates into an appropriate behavioral response such as feeding, cessation of feeding, search for alternative food source, courtship, or egg-laying. Detection of sweet compounds by labellum GRs induces a sucking response and sugar detection by the tarsi induces extension of proboscis. It is a requirement to understand the flow of information

**139**

learning [97].

**4. Conclusions**

*Understanding Taste Using* Drosophila melanogaster *DOI: http://dx.doi.org/10.5772/intechopen.89643*

from peripheral activation of GRNs to behavioral output to gain insight into the

Unlike mammalian taste cells, fly GRNs from labellum and pharynx send projections of axons directly to the SEZ area of the brain. GRNs in the ovipositor, wings, and some leg sensilla send projections to the thoracic ganglia [24, 25]. Taste neurons send their axons to loosely defined, widely circumscribed zones in the SEZ or thoracic ganglia [32]. Labial palp *Gr5a* positive GRNs project to large areas in the lateral and anterior region of the SEZ, whereas the *Gr66a*-expressing GRNs project to the medial part of the SEZ [6, 7]. Information from GRNs of the legs activates non-overlapping areas of the SEZ than GRNs of the labial palps, suggesting different behavioral outputs of neurons responding to the same ligand but located in different taste tissues. Functional domains of taste have been mapped in the brain using live flies expressing the calcium-sensitive indicator G-CaMP [120] (G-CaMP protein is a fusion of the calmodulin-binding domain from the myosin chain kinase (M13 peptide), permutated EGFP and the calmodulin) in response to sugars and bitter compounds suggesting different taste compounds activate distinct neural ensembles in the SEZ. In terms of their taste quality, organ location, and in some cases sensillar type, at least 10 categories of patterns have been defined in the SEZ and nine in the thoracic abdominal ganglia. Each category is a unique combination

The SEZ is a primary gustatory center, the higher brain centers where taste information is conveyed from the SEZ are unknown. Recently, sweet second order projection neurons that relay sweet taste information from the SEZ to the antennal and mechanosensory motor center (AMMC) in the deutocerebrum were described [109]. The results support the role of AMMC (generally receives input from mechanosensory and olfactory neurons) in processing multisensory information. Various other studies have identified interneurons that impinge on taste circuits and feeding behavior routines, including a feeding promoting command neuron, feeding promoting dopaminergic neurons, bitter sensitive projection interneurons, feeding restrain GABAergic neurons and neurons in the ventral nerve cord that

The taste representations in the mushroom bodies (MB) (sites for associative learning) examined recently and found that input to the main calyx continues to be segregated according to taste modality and the location that taste information originates from. The bitter and sweet stimuli activate distinct areas, and stimuli from different taste organs activate partially overlapping but distinct patterns [127]. The information about water and sweet qualities, as well as nutritive and non-nutritive sugars is also separated in MB [128, 129]. Unraveling taste circuits, therefore, will be important not only for understanding how sensory input is translated to behavioral output, but also how taste associations are formed in reward and aversive

*Drosophila* Grs, IRs, Trp, and ppk receptors underlie detection of various categories of tastants but a lot remains undetermined about the composition and response properties of taste receptors. How combinations of GRs and IRs belonging to different receptor families (e.g. Gr and IR), coordinate within the neurons that house them is a subject of investigation. Feeding behavior is root cause of metabolic disorders. A better understanding of the biology of metabolic disorders in association with GRs, IRs, Trp, and ppk receptors is a need of the hour because of the burden of metabolic disorders, high incidences of cardiovascular diseases, faster

neuronal wiring of the taste at each level of information processing.

of discrete patterns elements that define taste neurons [97].

balance feeding and locomotion [121–126].

#### *Understanding Taste Using* Drosophila melanogaster *DOI: http://dx.doi.org/10.5772/intechopen.89643*

*Animal Models in Medicine and Biology*

**3.5 Non-canonical taste qualities**

Vertebrates can sense a variety of other important taste qualities such as wetness

channels that are sensitive to polyunsaturated fatty acids [111].

and fattiness. Olfaction and somatosensation helps in the detection of fats, and they elicit post-ingestive effects that promote consumption. It has been shown that mice prefer water spiked with free fatty acids supports a role for the taste system in detecting this rich source of calories [110]. A fatty acid transporter (CD36) and two fat-sensitive GPCRs—GPR40 and GPR120 are putative receptors for fat

GPR120 is required for preference to fatty acids in mice [112] and is expressed in

be rescued by expression of respective transgenes in sweet GRNs [114].

In flies, sweet GRN activation requires the function of the three *Ionotropic receptor* genes *Ir25a*, *Ir76b* and *Ir56d*. *Ir25a and Ir76b* are expressed in several neurons per sensillum, while *IR56d* expression is restricted to sweet GRNs. *Ir25a* and *Ir76b* mutant flies loose appetitive behavioral responses to fatty acids. The phenotype can

Ca2+, an ion is required for a vast array of cellular functions. Ca2+-deprived animals show attraction and Ca2+-sated animals show rejection. The aversive response to Ca2+requires a functioning T1R3 receptor, a subunit of the umami and sweet receptor [115]. In human subjects an attenuation of the taste of Ca2+ by the T1R3

Fruit flies avoids toxic levels of calcium. This repulsion is mediated by two mechanisms—activation of a specific class of GRNs that suppresses feeding, and inhibition of sugar-activated GRNs, which normally stimulates feeding. The distaste for Ca2+, and electrophysiological responses to Ca2+ require three members of the variant ionotropic receptor family Ir25a, Ir62a and Ir76b. The high concentra-

No water receptor has been identified in vertebrate so far. The somatosensory system of animals can detect wetness across their body and also contribute to the sensing of aqueous solutions in the oral cavity. Various tastes have been ascribed to distilled water, from bitter to salty and sweet. Notably, application of water after exposure to some artificial sweeteners, such as saccharin, elicits a sweet

A member of the Degenerin/Epithelial Sodium Channel family, ppk28 (an osmosensitive ion channel) mediates the cellular and behavioral response to water in flies. *ppk28* is expressed in water-sensing neurons and loss of *ppk28* abolishes

**3.6 Taste signal processing and taste sensory maps in the** *Drosophila* **brain**

In flies, after evaluation of taste input, the information translates into an appropriate behavioral response such as feeding, cessation of feeding, search for alternative food source, courtship, or egg-laying. Detection of sweet compounds by labellum GRs induces a sucking response and sugar detection by the tarsi induces extension of proboscis. It is a requirement to understand the flow of information

*3.5.1 Fats*

taste including K+

*3.5.2 Calcium taste*

*3.5.3 Water*

taste [118].

water sensitivity [119].

human TRCs as well [113].

blocker lactisole has been shown [116].

tions of Ca2+ show decrease survival in flies [117].

**138**

from peripheral activation of GRNs to behavioral output to gain insight into the neuronal wiring of the taste at each level of information processing.

Unlike mammalian taste cells, fly GRNs from labellum and pharynx send projections of axons directly to the SEZ area of the brain. GRNs in the ovipositor, wings, and some leg sensilla send projections to the thoracic ganglia [24, 25]. Taste neurons send their axons to loosely defined, widely circumscribed zones in the SEZ or thoracic ganglia [32]. Labial palp *Gr5a* positive GRNs project to large areas in the lateral and anterior region of the SEZ, whereas the *Gr66a*-expressing GRNs project to the medial part of the SEZ [6, 7]. Information from GRNs of the legs activates non-overlapping areas of the SEZ than GRNs of the labial palps, suggesting different behavioral outputs of neurons responding to the same ligand but located in different taste tissues. Functional domains of taste have been mapped in the brain using live flies expressing the calcium-sensitive indicator G-CaMP [120] (G-CaMP protein is a fusion of the calmodulin-binding domain from the myosin chain kinase (M13 peptide), permutated EGFP and the calmodulin) in response to sugars and bitter compounds suggesting different taste compounds activate distinct neural ensembles in the SEZ. In terms of their taste quality, organ location, and in some cases sensillar type, at least 10 categories of patterns have been defined in the SEZ and nine in the thoracic abdominal ganglia. Each category is a unique combination of discrete patterns elements that define taste neurons [97].

The SEZ is a primary gustatory center, the higher brain centers where taste information is conveyed from the SEZ are unknown. Recently, sweet second order projection neurons that relay sweet taste information from the SEZ to the antennal and mechanosensory motor center (AMMC) in the deutocerebrum were described [109]. The results support the role of AMMC (generally receives input from mechanosensory and olfactory neurons) in processing multisensory information. Various other studies have identified interneurons that impinge on taste circuits and feeding behavior routines, including a feeding promoting command neuron, feeding promoting dopaminergic neurons, bitter sensitive projection interneurons, feeding restrain GABAergic neurons and neurons in the ventral nerve cord that balance feeding and locomotion [121–126].

The taste representations in the mushroom bodies (MB) (sites for associative learning) examined recently and found that input to the main calyx continues to be segregated according to taste modality and the location that taste information originates from. The bitter and sweet stimuli activate distinct areas, and stimuli from different taste organs activate partially overlapping but distinct patterns [127]. The information about water and sweet qualities, as well as nutritive and non-nutritive sugars is also separated in MB [128, 129]. Unraveling taste circuits, therefore, will be important not only for understanding how sensory input is translated to behavioral output, but also how taste associations are formed in reward and aversive learning [97].
