Taste & the Gustatory System June 16, 2011. Brainstorming Why is taste important? Why did we develop a sense of taste? What do you think is the neurological.

Taste & the Gustatory System

June 16, 2011

Brainstorming

• Why is taste important? Why did we develop a sense of taste?

• What do you think is the neurological basis of taste?

Mmm, Mmm Good.

• Chemicals in your food act on taste cells located in the taste buds of your tongue and mouth.

• 5 Basic Tastes– Bitter– Sweet– Sour– Salty– Umami

Chandrashekar, J., M. A. Hoon, et al. (2006). "The receptors and cells for mammalian taste." Nature 444(7117): 288-294.

First Tastes

• Information processing begins in the taste cells.– Receptors are

located on microvilli of the taste cells.

• Different tastes are represented by different receptor types.

http://faculty.washington.edu/chudler/taste.html

Tasting Ions: Salty & Sour

• Sour– H+ in acids (like acetic acid in vinegar)

• Salty– Na+ from NaCl

• Entry of H+ or Na+ through the respective receptors opens ion channels and directly generatesan electrical signal.

Sweet, Bitter, and Umami

• Involve G-Protein Coupled Receptors (GPCRs)– When a chemical binds

to these receptors, they activate a G-protein, which causes a downstream chemical cascade.

– A series of chemical events occurs that ultimately results in the opening or closing of ion channels.

Sheridan, C. (2004). "A taste of the future." Nat Biotech 22(10): 1203-1205.

• Sweet:– T1R2 and T1R3 receptors– Activates Ca2+ channels

• Umami:– T1R1 and T1R3 receptors– Activates Ca2+ channels

• Bitter:– T2R receptors interacting with gustducin

Sweet, Bitter, and Umami

Taste Cell Summary

• Ion Channels– Sour: H+– Salty: Na+

• GPCRs– Sweet:

T1R2 + T1R3– Umami:

T1R1 + T1R3– Bitter:

T2R

Eisenstein, M. (2010). "Taste: More than meets the mouth." Nature 468(7327): S18-S19.

Buds to Brains

• Taste cells form synapses with axons from the facial, glossopharyngeal, and vagus cranial nerves.– Taste cells from each of the 3

regions of taste buds connects with a different nerve.

• Nucleus of the Solitary Tract in the medulla (NST)– Once again, topographical

organization is at work—each of the 3 cranial nerves goes to a different portion of the NST.

http://universe-review.ca/I10-85-taste.jpg

Neural Taste Processing

• NST projects to Ventral Posterior Medial Nucleus of the thalamus and continues to the cortices, amygdala, and hypothalamus

http://faculty.washington.edu/chudler/taste.html

Tasty Visions Experiment

Class Discussion

• What Influences Taste?• Sound Medicine: Neurobiology of

Taste

Neurobiology of Eating

• What brain region controls eating?

• 1940, Hetherington & Ranson – Lesions of the

ventromedial hypothalamus cause obesity & excess food intake in rats

– Lesions of the lateral hypothalamus caused decreased eating & starvation

https://wiki.brown.edu/confluence/display/BN0193S04/Historical+Background

What Does This Mean?

• Could the lateral hypothalamus be the brain’s control center for hunger, while the ventromedial hypothalamus is the center for satiety (feeling full)

• Oversimplified…there’s more to this story than that!– The brain & body have a host of

chemicals to help induce hunger and satiety.

Gastrointestinal Peptides

• Ghrelin– Stimulates food intake & pre-meal hunger– Excess levels cause increased food intake &

weight gain.

• Peptide YY– Inhibits food intake after meals

• Glucagon-like-peptide-1– Inhibits food intake in response to

nutrients in the gut

• Cholecystokinin (CCK)– Reduces food intake

Peripheral Hormones

• Leptin & Insulin– Both hormones reduce food intake.

• Both circulate in the body in response to fat content and enter the central nervous system in proportionate levels.– Receptors expressed in brain areas

important for energy

• Leptin is a protein encoded for by the ob gene.

Leptin, Body Fat, & Food

• Douglas Coleman discovered in the 1960s that the ob genes indicates to the brain that fat reserves are at a normal level.

• So what would we expect from mice lacking the ob gene?

• In the 1990s, Jeffrey Friedman began studying leptin.– What happens if we give an ob/ob mouse

leptin?– Reverses the obesity until normal levels of

adipose tissue are reached.

Ob/Ob Mice

http://en.wikipedia.org/wiki/Ob/ob_mouse

Energy homeostasis

Schwartz et al Nature 2000 404:661

Central Food Signals

• Stimulate Food Intake (Orexigenic)– Neuropeptide Y

(NPY)– Agouti-related

protein (AgRP)

• Decrease Food Intake (Anorexigenic)– Melanocortins – Cocaine-&

amphetamine-regulated transcript (CART)

Barsh, G. S. and M. W. Schwartz (2002). "Genetic approaches to studying energy balance: perception and integration." Nat Rev Genet 3(8): 589-600.

Signaling Food Intake & Satiety

• To Stimulate Eating:– NPY is released from the

Paraventricular nucleus, lateral hypothalamic, and prefornical areas.

– Orexins and MCH from the prefornical areas and lateral hypothalamlus also play a role.

• To Reduce Eating: -MSH is derived from POMC in

the paraventricular nucleus to stop eating.

– Oxytocin, corticotrophin-releasing hormone, and thyrotrophin-releasing hormone may play roles as well.

Schwartz, M. W., S. C. Woods, et al. (2000). "Central nervous system control of food intake." Nature 404(6778): 661-671.

Other Factors

• Brain Stem• Reward Pathways

– Dopamine– Serotonin– Endocannabinoids– Opioids– Cholinergic systems

Anorectic Peptides (Inhibit Feeding Behavior) Orexigenic Peptides (Stimulate Feeding BehaviorAbbreviation Full Name Location Abbreviation Full Name Location-MSH Alpha-melanocyte-

stimulatinghormone

Arcuatenucleus

NPY Neuropeptide Y Arcuatenucleus

CART Cocaine- andamphetamine-regulated transcript

Arcuatenucleus

AgRP Agouti-relatedpeptide

Arcuatenucleus

OT Oxytocin PVN MCH Melanin-concentratinghormone

Lateralhypothalamicarea

TRH Thyrotropin-releasing hormone

PVN Orexin Lateralhypothalamicarea

Summary

Who Knew Eating Was So Complicated?!?

Schwartz, M. W., S. C. Woods, et al. (2000). "Central nervous system control of food intake." Nature 404(6778): 661-671.

Hypothalamus

Eating Disorder Treatment Plans

http://fitnesslines.com/health-tips/what-is-an-eating-disordercausessymptoms-and-treatment-for-eating-disorders-in-children/

Smell Discrimination Experiment

What is Smell?

• Chemical molecules enter the nasal passage and are mixed with mucus in the olfactory epithelium.

• Olfactory hair cells respond to these chemicals and relay an electrical message to the brain.

http://www.gunthersclass.com/lecture10p.html

Olfactory Receptors

• Another example of GPCRs– Allow Ca2+ & Na+ in, depolarizing the

cell

Firestein, 2001

Only expressed in select regions of the nasal cavity. A given receptor only maps to certain regions of the nasal passage.

Where Are Sensory Neurons?

From Lecture by Kerry Ressler, Emory University , 2006

From Lecture by Kerry Ressler, Emory University , 2006

Olfactory Bulb

• Olfactory information is processed in the olfactory bulb.– Consists of glomeruli:

round regions without cell bodies that receive input from olfactory nerves.

– Each neuron sends only 1 axon to 1 glomerulus in the olfactory bulb.

Firestein 2001

Does This Organization Seem Familiar?

From Lecture by Kerry Ressler, Emory University , 2006

Patterning Creates Scents

• The patterns of glomeruli that are stimulated is important for determining the odor sensed.

From Lecture by Kerry Ressler, Emory University , 2006

Imaging techniques in anesthetized rats allow visualization of odor-induced activation of specific glomeruli Belluscio & Katz, 2001

Special Scent Processing

• Further processing occurs in the olfactory cortex, hippocampus, amygdala, and hypothalamus

From Lecture by Kerry Ressler, Emory University , 2006

Changes in Smell

• NPR “Five Senses, Minus One: Living Without Smell”

• “The Dog Beneath the Skin”

Current Research in Taste and Smell