Bio 337 Neurbio of taste and feeding

The classic tastes

Sweet, salty, bitter, sour, umami

What do taste buds contain

Taste receptor cells which express specific taste receptor.

What type of channels mediate Salty and Sour

Specific ion channels

Amiloride sensitive NA+ channel and a cation channel. (PKD and TRP Family)

What type of channels mediate sweet and umami

Hetero-dimers formed by T1R3 and another subunit.

For sweet its T1R3/T1R2
For Umami is T1R3/T1R1

G PROTEIN COUPLED!!!!

What type of channels mediate bitter

Receptors are T2R (multiple subtypes) that are G Coupled proteins

Pathway for mouth to brain

1. Taste receptor Cells

2. Cranial Nerve ganglia

3. Brainstem NST

4. Thalamus VPMpc

5. Insular Cortex (gustatory cortex)

Chorda tympani branch of facial

ANT tongue and palate

Lingual Branch of Glossopharyngeal

Post tongue and palate

Laryngeal branch of vargus

Larynx

Two theories of gustatory system coding

Labeled line

1. There are specific sweet neurons that get activated and transfer the signal to other sweet neurons in the CNS.

Pattern Code

1. Nonspecific neurons send signals to other neurons in a specific pattern to code sweet versus other flavors.

Beyond the classic 5 tastes

Carbonation, Texture, Astringency, Cold (menthol), Temperature, and Spiciness (hot)

How is palatability encoded in the brain

The amygdala processes information from a stimulus and sends the signal about the reward value, expectation, motivated behaviors and learning.

Amygdala communicates with the gustatory cortex to mediate palatability.

What does the hypothalamus do for taste/feeding?

It sends signals to the Gustatory Cortex to regulate feeding behaviors (hunger/satiety)

How does the setpoint in control of feeding get set? How is it altered?

Many factors from genetic, behavioral, and environmental. If the hypothalamus is lesioned it will alter the setpoint.

What does lesions of the ventromedial hypothalamus produce?

Hyperphagia and obesity

What does lesions of the lateral hypothalamus produce?

Aphagia and weight lost

Short term control satiety signals

PYY: High lvl (after meal) promotes satiety

CCK: High lvl (after meal) promotes satiety

Gastric distention promotes satiety

Glucose

Ghrelin: High lvls (before meal) promote hunger

Adiposity signals (Longer term control of satiety)

Leptin: High levels promote satiety. Low lvls=hunger

Insulin: Levels promote satiety. Low lvls=hunger

What do satiety signals act on and where do adiposity signals act on?

Satiety signals act on the Gustatory cortex while Adiposity signals act on the hypothalamus.

How does the Lateral Hypothalamus promote food intake

Through orexin A and melanin concentrating hormone (MCH)

How does the Paraventricular nucleus decrease food intake and increase food expenditure

Through oxytocin and CRH

What does NPY/AgRP do

Inhibit the PVN and excite the Lateral hypothalamus

What does alpha-MSH/CART do?

Excite the PVN and inhibit LHA

Besides endocrine/hormonal signals, how else is food intake and hunger/satiety regulated? How?

Through cognitive and sensory signals

Reward and taste related areas receive inputs from the hypothalamus to control reward behavior. (acts on VTA and Insular cortex)

What kind of alterations do obese people show?

Both metabolic and gustatory/reward systems.

EX:
Lower sensitivity to Leptin/inability to produce leptin/alteraion of orexin

Anorexia

Alterations to AgRP and BDNF genes (hunger genes)

Alterations to serotoninergic system and dopaminergic in limbic areas.

What is associated with Bulimia

Decreased release of CCK, Increased release of ghrelin and alterations of several other hormones.