Cell Communication Processes in Biology PDF

Communication Between Cells cell signals and signaling cascades responses to external signals modes of cell signaling the chemical synapse: -signaling at the synapse -excitatory and inhibitory signals -the neuromuscular junction neurotransmitters and their modulation R...

Communication Between Cells cell signals and signaling cascades responses to external signals modes of cell signaling the chemical synapse: -signaling at the synapse -excitatory and inhibitory signals -the neuromuscular junction neurotransmitters and their modulation References: p. 554-560, 434-438, 574-575  Cell communication between yeast mating types “Shmoo” The fusion of haploid yeast cells of opposite mating types (a and a) results in a diploid cell (a/a). The cells synthesize and secrete mating factors to communicate with each other and initiate fusion. The initial response to receiving the signal from the other cell is a change in cell shape (B).  Effects of external signals on cells in animals Cells need signals for survival and function. cells need signals to survive (A, B, and C) external signals (D & E) can induce a cell to divide (to enter the cell division cycle) cells also require signals (F & G) to differentiate (to become specialized during development if a cell receives no signals: death by apoptosis  Effects of external signals on cells in animals  A signal molecule can induce different responses in different target cells Acetylcholine (Ach): the neurotransmitter is released by parasympathetic neurons of the autonomous nervous system, causing a reduced frequency of cardiac muscle contraction and an increase in salivary secretions it is also the neurotransmitter released by motor neurons in neuromuscular junctions, causing skeletal muscle contraction  Effect of acetylcholine in parasympathetic regulation Decreased Food heart rate digestion Lower AP frequency Effect of acetylcholine on skeletal muscle cells Note: while the receptor for acetylcholine from parasympathetic neurons is a G protein-coupled receptor, the receptor for acetylcholine from motor neurons is an acetylcholine-gated ion channel. Force generation  Requirements for cell-to-cell communication 1. A signal (and the means to deliver it). 2. A receptor in the responsive cell. 3. Intracellular signaling proteins. 4. The modification of target proteins. Result: a response. Signaling cascades Responses  Responses to external signals Fast: the intracellular cascade depends on already present enzymes and target proteins, and does not require gene expression (takes < one second to a few minutes). No gene expression is induced. Fast responses are short-lived. Slow: the signal results in gene expression, and the response to the signal depends on the gene products (this slows down the process: it takes minutes to hours). Slow responses are longer lasting. Responses to external signals  Modes of cell signaling communication junctions Communication junctions: gap junctions plasmodesmata Gap junctions occur in animals the cytoplasms of adjacent cells are connected through connexons: hollow transmembrane complexes of connexin proteins  Modes of cell signaling communication junctions Gap junctions p. 701  Modes of cell signaling communication junctions Plasmodesmata occur in plants no transmembrane protein systems plasma membranes of adjacent cells are fused through holes in the cell walls  Modes of cell signaling: juxtacrine Juxtacrine signaling direct cell-to-cell contact the signal and the receptor are both cell surface molecules Modes of cell signaling: signaling through secreted molecules Endocrine signaling: hormones the secreted signals enter the circulatory system the signals are stable and can reach distant target cells  Modes of cell signaling: signaling through secreted molecules Autocrine signaling: the secreted signal can trigger responses in the same cell that secretes it. Paracrine signaling: the secreted signals can only reach neighboring cells the signals do not enter the circulatory system Modes of cell signaling: signaling through secreted molecules Synaptic signaling a special type of paracrine signaling: the target is a specific cell (the postsynaptic cell) in a permanent interaction the signals are neurotransmitters (stored in synaptic vesicles at the axon terminal of the neuron) that are released and reach the target cell (or cells) over a small space, or gap (the chemical synapse)  The neuron Electric signals travel along the axon to the nerve terminal. The propagation of electric signals is caused by ion currents through the axon membrane by the alternating opening, inactivation, and closing of voltage-gated ion channels.  Signaling to the post synaptic cell In the neuron (the presynaptic cell): the electrical signal (voltage changes due to Na+/K+ currents through voltage gated channels) reaches the axon terminal where it opens voltage-gated Ca2+ channels the inflow of Ca2+ causes the neurotransmitter-containing synaptic vesicles to fuse to the presynaptic membrane, and the neurotransmitters are released to the synapse => The signal is converted to a chemical signal. In the synapse and postsynaptic cell: the released signals reach receptors on the post-synaptic cell (typically, neurotransmitter-gated ion channels) ion channels in the post-synaptic membrane open ion currents occur, changing the voltage of the membrane => The signal is converted back to an electrical signal. Conversion of an electrical signal into a chemical signal AP Presynaptic membrane: in the axon terminal. Postsynaptic membrane: in the target cell. Conversion of an electrical signal into a chemical signal and then back to an electrical signal  Two types of neurotrasmitters The ions that flow through the postsynaptic membrane after a neurotransmitter opens ion channels may have an excitatory or inhibitory effect. 1. Excitatory neurotransmitters cause the depolarization of the post-synaptic membrane. they open Na+ channels on the postsynaptic membrane and cause an inflow of the ion, causing: membrane depolarization: an excitatory post-synaptic potential (EPSP) this can trigger action potentials  Two types of neurotrasmitters The ions that flow through the postsynaptic membrane after a neurotransmitter opens ion channels may have an excitatory or inhibitory effect. 2. Inhibitory neurotransmitters cause the hyperpolarization of the post-synaptic membrane. they open Cl- channels on the postsynaptic membrane and cause an inflow of the ion membrane hyperpolarization: inhibitory post-synaptic potential (IPSP) this blocks action potentials from happening  Two types of neurotrasmitters Why are neurotransmitters categorized as either excitatory or inhibitory? Excitatory neurotrasmitters bring the cell membrane closer to the threshold potential, increasing the probability of triggering action potentials. Inhibitory neurotrasmitters decrease the probability of triggering action potentials by hyperpolarizing the cell membrane.  Examples of neurotransmitters and their regulation Excitatory neurotransmitter in the neuromuscular junctions: Acetylcholine (ACh) is the neurotransmitter that crosses the synapse between a motor neuron and a skeletal muscle. opens ACh-gated Na+ channels its overall effect is the depolarization of the muscle cell membrane (EPSP) the depolarization of the membrane due to the Na+ current triggers action potentials and the contraction of the muscle cell (and force generation) The innervation of a muscle to form neuromuscular junctions (the synapses between motor neurons and muscle fibers): the axon terminal of a motor neuron branches to innervate multiple muscle fibers (muscle cells).  Examples of neurotransmitters and their regulation Na+ The acetylcholine receptor in the neuromuscular junction is an example of a ligand-gated ion channel: the ligand (Ach) opens Na+ channels for facilitated diffusion. Acetylcholinesterase is an enzyme that degrades ACh to terminate the signal and allow the muscle to relax.  Amino acid neurotransmitters Excitatory amino acid neurotransmitter in the CNS: Glutamate (glutamic acid) the glutamate receptors are gated Na+ and Ca2+ channels modulated by reuptake into the neuron also modulated by GABA excessive stimulation by glutamate results in neurodegeneration (Huntington’s disease)  Amino acid neurotransmitters Inhibitory amino acid neurotransmitter in the CNS: GABA (gamma-aminobutyric acid) GABA receptors are gated Cl- channels important for the neural control of body movements and other brain functions modulated by reuptake Valium and Xanax (sedative drugs) enhance the binding of GABA to its receptor  Amino acid-derived neurotransmitters (Biogenic amines) Excitatory biogenic amine in the CNS: Dopamine causes EPSP it is a controller of body movements and pleasure sensations if dopamine-releasing neurons degenerate: tremors occur (Parkinson’s disease)  The vertebrate limbic system The limbic system are functionally and anatomically interconnected structures that are located in the brain. Their main role is the control of functions necessary for self preservation and species preservation.  Modulation of dopamine activity in limbic system Dopamine is active in the pleasure pathways in the amygdalae (part of the limbic system of the brain). the activity of dopamine is controlled by reabsorption: neurotransmitter molecules are removed from the synapse by transporters The reabsorption of dopamine can be blocked by cocaine: cocaine resembles dopamine and binds to the transporters dopamine is not removed from the synapse and remains stimulating the limbic system pleasure sensations are heightened if too much dopamine is present in the synapses (and excessive stimulation persists): the down-regulation of the dopamine receptors in the post-synaptic cell begins Modulation of dopamine activity in limbic system  Modulation of dopamine activity in limbic system (dopamine) (cocaine) Normal stimulation of Excessive stimulation due to the post-synaptic cell. the presence of the analog.  Modulation of dopamine activity in limbic system The post-synaptic cell responds by decreasing the number of surface dopamine receptors (down-regulation). The cell balances the signal received by controlling the activity of the receptor Drug dependence: insufficient neurotransmitter stimulation if no drug is present (fewer receptor means more neurotransmitter is needed for normal stimulation) withdrawal symptoms occur if the drug is removed  Modulation of dopamine activity in limbic system The number of dopamine The synapse is less sensitive receptors in the postsynaptic when the drug is removed membrane decreases. (drug addiction).  Amino acid-derived neurotransmitters (Biogenic amines) Biogenic amine in the CNS: Serotonin effect: EPSP/IPSP, depending on the receptor a regulator of sleep and emotional states its activity is controlled by reabsorption insufficient serotonin activity in the synapses may result in clinical depression Serotonin and depression Prozac ® is a selective serotonin reuptake inhibitor (SSRI).  Peptide neurotransmitters (neuropeptides) Neuropeptides are short chains of amino acids. Substance P released at the synapses in the CNS by sensory neurons activated by painful stimuli (P: pain) excitatory (EPSP): results in pain sensations the intensity of the pain is modulated by the effect of endogenous opiates (enkephalins and endorphins, which are inhibitory neuropeptides)  Peptide neurotransmitters (neuropeptides) Endorphins and enkephalins are endogenous opiates. They are produced by the brain to block the perception of pain. Endorphin Morphine and heroin are exogenous opioids. They have an analgesic (pain-reducing) effect because they can bind to enkephalin and endorphin receptors.  Gas signals Synthesis of Nitric oxide (NO) from the deamination of arginine NO synthase Gas signals such as NO are synthesized upon the stimulation of the secreting cell. They diffuse to the target cell rapidly but are very short-lived: 1/2 life of only a few seconds.  Effects of nitric oxide The synthesis of NO in endothelial cells is stimulated by acetylcholine, which activates NO synthase (NOS). the specific ACh-releasing neurons do not synapse with smooth muscle cells, but instead synapse with the endothelial cells inside blood vessel NO is synthesized and diffuses rapidly to the surrounding smooth muscle cells Results: the relaxation of the smooth muscles surrounding the blood vessels the dilatation of the blood vessels and increased blood flow not to be confused with laughing gas (nitrous oxide, N2O) Effects of nitric oxide