Chemoreceptors

Central chemoreceptors

Central chemoreception involves the detection of alterations in carbon dioxide (CO₂) and hydrogen ion (H⁺) levels within the brain, which subsequently influences respiratory rate and depth. The central chemoreceptors are primarily located on the ventral medulla and especially in the retrotrapezoid nucleus. They monitor the acidity (pH) of the cerebrospinal fluid, which is a good indicator of blood carbon dioxide levels. Although H⁺ can not cross the blood-brain barrier, CO₂ can easily diffuse across the barrier and enter the brain, where it reacts with water to form carbonic acid. This acid then breaks down into hydrogen ions (H⁺) and bicarbonate ions. The increase in H⁺ ions in the cerebrospinal fluid triggers the central chemoreceptors.

When CO₂ levels rise, the pH decreases, and the central chemoreceptors send signals to the respiratory centers to increase breathing rate and depth, expelling more carbon dioxide and restoring normal pH. They provide real-time feedback to the brainstem's respiratory control center. The elevated CO₂ levels, particularly in arterial blood and alveolar gas, stimulate these receptors and this stimulation, in turn, leads to increased alveolar ventilation. The hyperventilation helps to reduce CO₂ levels and restore balance. By continuously monitoring and adjusting ventilation, these chemoreceptors ensure adequate oxygenation and carbon dioxide elimination, maintaining a delicate equilibrium between metabolism and respiration.

On the contrary, when the level of CO₂ in the blood decreases, the amount of H⁺ ions in the CSF decreases, so the CSF becomes less acidic. The chemoreceptors are less stimulated and the brain sends fewer signals to the breathing muscles, which causes the rate and depth of breathing to slow down. In short, lower blood CO₂ levels lead to slower breathing and this helps maintain a balance in blood gasses, ensuring proper oxygen levels and CO₂ removal.

Central chemoreceptors also exert an indirect influence on cardiac function by modulating blood pressure. Elevated respiratory rates can result in a minor decrease in blood pressure due to reduced pulmonary blood volume. Conversely, in cases of severe respiratory compromise characterized by significantly elevated carbon dioxide levels, central chemoreceptors can initiate a reflexive increase in sympathetic nervous system activity, causing a subtle elevation in heart rate and myocardial contractility.

Peripheral chemoreceptors

Peripheral chemoreceptors are sensors located outside the CNS that act faster than the central chemoreceptors and help regulate blood osmolarity.

They are found in carotid bodies, bilaterally in the division of the common carotid arteries, and in the aortic bodies in the aortic arch. The carotid body (CB) is composed of clusters of type I cells, the primary chemoreceptors for oxygen and carbon dioxide, surrounded by supporting type II cells. Despite its small size, the CB has an exceptionally high blood flow, essential for its function as a chemoreceptor. This blood flow is regulated by both sympathetic and parasympathetic innervation. Information from the carotid and aortic bodies reaches the brain via the glossopharyngealand vagus nerves, respectively.

Peripheral chemoreceptors primarily detect changes in blood oxygen levels (O₂), which is the most powerful stimulus, with lesser sensitivity to changes in CO₂ and pH. A decrease in the partial pressure of oxygen (PO₂) in the arterial blood or, respectively, an increase in CO₂ levels triggers these peripheral chemoreceptors to transduce the signal. The electrical impulse is transmitted to the respiratory center in the brainstem and the breathing rate and depth are adjusted to restore blood osmolarity and pH in normal.
When PO₂ falls below a certain threshold, around 60 mmHg a condition called hypoxemia, the peripheral chemoreceptors increase their firing rate. This signal is transmitted to the respiratory control center in the brainstem, where the respiratory control center then increases the rate and depth of ventilation in an attempt to increase O₂ intake and eliminate CO₂.

Peripheral chemoreceptors are primarily sensitive to low oxygen levels. However, when oxygen levels become excessively high, a condition called hyperoxia, their activity diminishes, as they are not designed to regulate breathing in such conditions. In hypoxia, additionally, the peripheral chemoreceptors send signals to the cardiovascular control center, which increases heart rate and contractility to improve oxygen delivery to tissues. The chemoreceptors can also cause vasoconstriction in certain blood vessels, which helps to redirect blood flow to vital organs like the heart and brain.

Olfactory chemoreceptors

Olfactory sensory neurons are located in the upper region of each nasal cavity, within the olfactory epithelium. These primary neurons are bipolar, featuring an axon that projects to the olfactory bulb and a dendrite that extends to the olfactory epithelium. Each olfactory chemoreceptor is a type of metabotropic receptor and it is associated with a G-protein on the cytoplasmic side. Volatile odorant molecules diffuse within the mucus of the nasal cavity and bind to the olfactory receptors on the extracellular side of the cilia. This binding triggers the activation of a specific intracellular G-protein complex called Golf, to which the receptor attaches. This activation prompts eventually the opening of the gated sodium ion channels across the cilia membrane, resulting in an influx of sodium ions into the cell. Neurons transmit their signal to the olfactory cortex, where the brain interprets the collective information to generate the perception of the various odors a human can smell.

Each olfactory neuron has a specific type of receptors that bind to a particular range of odorants. For an odorant to be detectable, it must be partially water-soluble to reach the cilia in the mucus and partially lipid-soluble to pass through the cilium membrane. The olfactory pathway is the only sensory pathway in the cerebral cortex where the signals bypass the thalamus and directly reach the cortex.

The olfactory nerve is only one of the 12 cranial nerves. Learn about all 12 of them with our time-saving cranial nerves quizzes and labeling exercises. 

Gustatory chemoreceptors

Gustatory information is detected by specialized chemoreceptors located in taste buds situated on the lingual papillae, on the dorsum of the tongue, as well as in the epithelium of various areas such as the tonsillar pillars, the palate and the lining parts of the larynx, the pharynx and the epiglottis. Each taste bud consists of approximately 100 taste receptor cells, supported by sustentacular cells and regenerative basal cells, organized around a central taste pore. Taste receptor cells activate a complex terminal network of taste nerve fibers that surround them with some fibers penetrating folds in the taste cell membranes. Beneath the cell membrane, numerous vesicles store a neurotransmitter substance. Upon taste stimulation, these vesicles release the neurotransmitter through the cell membrane, stimulating the nerve fiber endings. These receptors identify different chemical compounds dissolved in saliva and transmit signals to the gustatory cortex, where they are interpreted as distinct tastes, including sweet, salty, sour, bitter, and umami.

During mastication, chemicals in food dissolve in saliva and interact with taste receptors in the mouth, each sensitive to one of five tastes. Low concentrations activate specific receptors, while high concentrations may activate multiple.

• Sour: Hydrogen ions (H⁺) enter type III cells, increasing calcium and releasing serotonin, which excites neurons.
• Salty: Sodium ions enter type I cells, leading to neuron activation.
• Sweet: Type II cells detect sweet by binding organic compounds to G-protein receptors, raising calcium and releasing ATP to excite neurons.
• Bitter: Type II cells also detect bitter compounds via G-proteins, releasing ATP and exciting neurons, often as a defense against harmful substances.
• Umami: Type II cells detect umami, triggered by L-glutamate, stimulating ATP release and promoting protein-rich food intake.

When a taste substance interacts with taste hairs, it creates a receptor potential that activates sensory neurons. These neurons send signals via cranial nerves VII, IX, and X to the pons and the medulla, then to the thalamus, and finally to the insular gustatory cortex for interpretation. Saliva clears the taste chemical, ending the sensation. Different tastes need varying concentrations to be sensed. For example, sour requires 0.0009 M HCl, salty and sweet about 0.01 M, and bitter (from quinine) only 0.000008 M, making it highly sensitive as a defense against toxins.