Gustation: Taste Buds, Receptors & Labeled Lines | MCAT

GPCRs possess a characteristic seven-transmembrane domain structure spanning the cell membrane seven times. This architecture includes an extracellular N-terminal region, seven hydrophobic transmembrane helices, and an intracellular C-terminal tail. The receptor binds to G proteins located on the cytoplasmic side of the membrane. Upon ligand binding, the receptor undergoes conformational changes that activate the associated G protein, initiating downstream signaling cascades.

G-protein coupled receptors (GPCRs) span the cell membrane with seven transmembrane domains. The extracellular portion binds ligands, while the intracellular portion interacts with G-proteins. When activated, G-proteins exchange GDP for GTP, becoming active. GPCRs have slower response but longer duration compared to direct ligand-gated channels. Examples include adrenergic and muscarinic receptors.

G protein-coupled receptors (GPCRs) are the largest class of cell membrane receptors found only in eukaryotic organisms, with over 1,000 types in humans. They are characterized by their distinctive 7-transmembrane alpha-helix structure. GPCRs regulate diverse physiological processes including immune function, growth, sensory perception, and neurotransmitter systems. G proteins, which interact with GPCRs, are specialized proteins that bind GTP or GDP. Those associated with GPCRs are heterotrimeric, consisting of alpha, beta, and gamma subunits. The alpha and gamma subunits span the cell membrane through lipid anchor domains. In the inactive state, G proteins bind GDP to their alpha subunit.

Cell surface receptors are primary drug targets located on the plasma membrane. Ion channel receptors (ligand-gated) function by opening channels upon drug binding, allowing ion flow that changes membrane potential. Examples include nicotine and muscarinic receptors (increasing sodium influx) and GABA receptors (increasing chloride influx). G-protein coupled receptors (GPCRs) are seven-transmembrane proteins that activate G-protein complexes (alpha, beta, gamma subunits). These activate second messenger systems: Gs increases cAMP via adenylyl cyclase, Gi decreases cAMP, and Gq activates phospholipase C producing IP3/DAG. These pathways regulate cellular functions including gene expression, metabolism, and cell growth.

There are three major types of cell surface receptors: G-protein coupled receptors (GPCRs), receptor tyrosine kinases (RTKs), and ligand-gated ion channels. GPCRs activate G-proteins that initiate intracellular signaling cascades. RTKs are dimeric receptors that phosphorylate each other upon ligand binding, activating multiple downstream pathways. Ligand-gated ion channels form pores in the cell membrane that open or close in response to ligand binding, controlling ion flow across the membrane.

Synaptic transmission involves action potentials arriving at presynaptic terminals, calcium influx triggering vesicle fusion and neurotransmitter release, neurotransmitters binding to postsynaptic receptors, and postsynaptic membrane potential changes. Synaptic vesicles contain neurotransmitters and are stored in the presynaptic terminal. When calcium enters, vesicles move to the membrane and fuse, releasing contents into the synaptic cleft. Acetylcholine is an excitatory neurotransmitter that binds to postsynaptic receptors and opens sodium channels, depolarizing the postsynaptic cell. Acetylcholine receptors are ligand-gated ion channels composed of five subunits with a binding site and pore.

Synaptic transmission is the process by which action potentials travel from one neuron to another at specialized junctions called synapses. This process involves several key components: mitochondria provide energy for the complex transmission process, synaptic vesicles store neurotransmitters, and the synaptic cleft is the gap where communication occurs. When an action potential arrives at the presynaptic terminal, it triggers voltage-gated calcium channels to open, allowing calcium ions to flow into the terminal. This calcium influx causes synaptic vesicles to dock and prime at the presynaptic membrane. SNARE proteins on both membranes facilitate vesicle fusion, leading to the release of neurotransmitters into the synaptic cleft through exocytosis. Different types of neurotransmitters such as glutamate, glycine, and GABA are released depending on the specific synaptic connection.

Synaptic transmission involves: (1) Impulse conduction to presynaptic terminal, (2) Neurotransmitter release via calcium-triggered exocytosis, (3) Neurotransmitter binding to postsynaptic receptors, (4) Generation of postsynaptic potentials, (5) Termination through metabolism, reuptake, or diffusion. Excitatory neurotransmitters increase sodium permeability, causing depolarization and generating Excitatory Postsynaptic Potentials (EPSP). Inhibitory neurotransmitters increase chloride permeability, causing hyperpolarization and generating Inhibitory Postsynaptic Potentials (IPSP). The resting membrane potential is approximately -70 mV, with sodium higher outside and potassium higher inside. Action potentials propagate by depolarizing adjacent membrane regions. When reaching the presynaptic terminal, calcium influx triggers synaptic vesicle fusion and neurotransmitter release. Neurotransmitter action is terminated through: (1) Local degradation by enzymes (acetylcholine by acetylcholinesterase), (2) Reuptake into presynaptic neuron (norepinephrine by norepinephrine transporter), (3) Diffusion away from synaptic cleft. Cotransmission involves release of multiple neurotransmitters from the same neuron, with cotransmitters modulating primary neurotransmitter effects and acting on presynaptic autoreceptors for feedback regulation.

Action potentials are electrical signals generated when a neuron is stimulated. The resting membrane potential is approximately -70 mV, maintained by selective permeability to potassium and chloride ions, and the sodium-potassium pump. When a stimulus reaches threshold, sodium channels open, allowing sodium ions to enter and depolarize the membrane. The action potential propagates along the axon, with the membrane potential changing from negative to positive and back to negative. In myelinated axons, action potentials jump between nodes of Ranvier (saltatory conduction), significantly increasing transmission speed. Synaptic transmission is the process by which neurons communicate with each other. Chemical synapses are the most common type and involve the release of neurotransmitters from the presynaptic neuron to the postsynaptic neuron. Synapses consist of the presynaptic membrane, postsynaptic membrane, and synaptic cleft. Synaptic vesicles store neurotransmitters, which are released when calcium ions enter the presynaptic terminal. Neurotransmitters bind to specific receptors on the postsynaptic membrane, causing depolarization or hyperpolarization. Excitatory synapses (using glutamate) depolarize the postsynaptic membrane, while inhibitory synapses (using GABA) hyperpolarize it.

Synaptic transmission converts electrical signals (action potentials) into chemical signals (neurotransmitter release) at synapses. Synaptic vesicles contain neurotransmitters released when calcium ions enter the presynaptic terminal. Neurotransmitters bind to receptors on the postsynaptic membrane, causing ion channels to open. In excitatory synapses, neurotransmitters like acetylcholine allow sodium ions to enter, depolarizing the membrane and bringing it closer to threshold. In inhibitory synapses, neurotransmitters like GABA allow chloride ions to enter, hyperpolarizing the membrane and moving it further from threshold. The resulting postsynaptic potentials can summate temporally or spatially to determine whether an action potential will be generated in the postsynaptic neuron.

The Peripheral Nervous System (PNS) consists of nerves extending from the Central Nervous System (CNS) - brain and spinal cord - to different body parts. The PNS is classified into spinal nerves (emerging from the spinal cord) and cranial nerves (emerging from the brainstem). Humans have 12 pairs of cranial nerves, numbered using Roman numerals (I through XII). These nerves are classified into three functional types: sensory nerves (carry sensory information to the brain), motor nerves (carry motor commands from the brain to effectors), and mixed nerves (carry both sensory and motor information). The sensory cranial nerves include Olfactory (I), Optic (II), and Vestibulocochlear (VIII). The motor cranial nerves include Oculomotor (III), Trochlear (IV), and Abducens (VI). The mixed cranial nerves include Trigeminal (V), Facial (VII), Glossopharyngeal (IX), Vagus (X), Accessory (XI), and Hypoglossal (XII). Each nerve has specific functions related to sensory perception, motor control, or both, enabling the body to respond appropriately to environmental stimuli.

The peripheral nervous system consists of nerves and ganglia connecting the central nervous system to body tissues. Nerves are bundles of axons that transmit information bidirectionally: sensory nerves carry impulses to the CNS, while motor nerves carry responses from the CNS to effectors. Mixed nerves contain both sensory and motor neurons. The system is classified into cranial nerves (12 pairs connecting directly to the brain) and spinal nerves (communicating with the spinal cord). Cranial nerves include olfactory (smell), optic (vision), oculomotor (eye movement), trochlear (eye movement), trigeminal (face sensation and jaw movement), abducens (eye movement), facial (facial expression and taste), vestibulocochlear (hearing and balance), glossopharyngeal (swallowing and taste), vagus (visceral regulation), accessory (head and neck muscles), and hypoglossal (tongue movement).

The peripheral nervous system consists of cranial nerves (12 pairs) and spinal nerves (31 pairs). Cranial nerves originate from the brainstem (10 pairs) and other brain regions (2 pairs). They are classified as sensory, motor, or mixed. Purely sensory: CN I (olfactory) and CN II (optic). Purely motor: CN III, IV, VI (eye muscles). Mixed: CN V (trigeminal), VII (facial), VIII (vestibulocochlear), IX (glossopharyngeal), X (vagus), XI (accessory), XII (hypoglossal). Each nerve has specific functions related to sensory perception, motor control, or both.

The peripheral nervous system includes 12 pairs of cranial nerves. Sensory nerves include olfactory (I), optic (II), and vestibulocochlear (VIII). Motor nerves include oculomotor (III), trochlear (IV), abducens (VI), accessory (XI), and hypoglossal (XII). Mixed nerves include trigeminal (V), facial (VII), glossopharyngeal (IX), and vagus (X). The vagus nerve is particularly important for innervating thoracic and abdominal viscera.

The peripheral nervous system consists of sensory nerves (afferent) and motor nerves (efferent). Sensory nerves carry signals from receptors to the CNS, while motor nerves carry signals from the CNS to effectors. There are 12 pairs of cranial nerves, with four being particularly important: Oculomotor nerve (III) controls eye movements, Facial nerve (VII) controls facial muscles, Glossopharyngeal nerve (IX) controls the tongue and pharynx, and Vagus nerve (X) is called the 'master nerve' because it controls many important body functions.