A matter of taste And Brain
How are taste signals (which provide one of the most significant rewards for eating) processed through different stages in our brains, to produce (among other effects) activation of the lateral hypothalamic neurons described above .
Some of the brain connections and pathways in the macaque monkey. The monkey is used to illustrate these pathways because neuronal activity in non-human primates is considered to be especially relevant to understanding brain function and its disorders in humans. During the first few stages of taste processing (from the rostral part [rostral towards the head or front end of an animal, as opposed to caudal (towards the tail)] of the nucleus of the solitary tract, through the thalamus, to the primary taste cortex), representations of sweet, salty, sour, bitter and protein tastes are developed (protein represents a fifth taste, also referred to as ‘umami’). The reward value or pleasantness of taste is not involved in the processing of the signal as yet, because the primary responses of these neurons are not influenced by whether the monkey is hungry or satiated. The organization of these first few stages of processing therefore allows the primate to identify tastes independently of whether or not it is hungry. In contrast, in the secondary cortical taste area (the orbitofrontal cortex), [orbitofrontal cortex above the orbits of the eyes, part of the prefrontal cortex, which is the part of the frontal lobes in front of the motor cortex and the premotor cortex] the responses of taste neurons to a food with which the monkey is fed to satiety decrease to zero (Rolls et al., 1989, 1990). In other words, there is modulation or regulation of taste responses in this tasteprocessing region of the brain. This modulation is also sensoryspecific (see, for example, figure 5.6). So if the monkey had recently eaten a large number of bananas, then there would be a decreased response of neurons in this region of the orbitofrontal cortex to the taste of banana, but a lesser decrease in response to the taste of an orange or melon. This decreased responding in the orbitofrontal cortex neurons would be associated with a reduced likelihood for the monkey to eat any more bananas (and, to a lesser degree, any more orange or melon) until the satiety had reduced.
So as satiety develops, neuronal activity in the secondary taste cortex appears to make food less acceptable and less pleasant – the monkey stops wanting to eat bananas. In addition, electrical stimulation in this area produces reward, which also decreases in value as satiety increases (Mora et al., 1979). It is possible that outputs from the orbitofrontal cortex subsequently influence behaviour via the connections of this region to the hypothalamus, where it may activate the feeding-related neurons described earlier.
How are taste signals (which provide one of the most significant rewards for eating) processed through different stages in our brains, to produce (among other effects) activation of the lateral hypothalamic neurons described above .
Some of the brain connections and pathways in the macaque monkey. The monkey is used to illustrate these pathways because neuronal activity in non-human primates is considered to be especially relevant to understanding brain function and its disorders in humans. During the first few stages of taste processing (from the rostral part [rostral towards the head or front end of an animal, as opposed to caudal (towards the tail)] of the nucleus of the solitary tract, through the thalamus, to the primary taste cortex), representations of sweet, salty, sour, bitter and protein tastes are developed (protein represents a fifth taste, also referred to as ‘umami’). The reward value or pleasantness of taste is not involved in the processing of the signal as yet, because the primary responses of these neurons are not influenced by whether the monkey is hungry or satiated. The organization of these first few stages of processing therefore allows the primate to identify tastes independently of whether or not it is hungry. In contrast, in the secondary cortical taste area (the orbitofrontal cortex), [orbitofrontal cortex above the orbits of the eyes, part of the prefrontal cortex, which is the part of the frontal lobes in front of the motor cortex and the premotor cortex] the responses of taste neurons to a food with which the monkey is fed to satiety decrease to zero (Rolls et al., 1989, 1990). In other words, there is modulation or regulation of taste responses in this tasteprocessing region of the brain. This modulation is also sensoryspecific (see, for example, figure 5.6). So if the monkey had recently eaten a large number of bananas, then there would be a decreased response of neurons in this region of the orbitofrontal cortex to the taste of banana, but a lesser decrease in response to the taste of an orange or melon. This decreased responding in the orbitofrontal cortex neurons would be associated with a reduced likelihood for the monkey to eat any more bananas (and, to a lesser degree, any more orange or melon) until the satiety had reduced.
So as satiety develops, neuronal activity in the secondary taste cortex appears to make food less acceptable and less pleasant – the monkey stops wanting to eat bananas. In addition, electrical stimulation in this area produces reward, which also decreases in value as satiety increases (Mora et al., 1979). It is possible that outputs from the orbitofrontal cortex subsequently influence behaviour via the connections of this region to the hypothalamus, where it may activate the feeding-related neurons described earlier.
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