Neuron Function & Neurotransmission: Anatomy, Ion Gradients, Action Potentials, Synapses -, Study notes of Philosophy of psychiatry

Download Neuron Function & Neurotransmission: Anatomy, Ion Gradients, Action Potentials, Synapses - and more Study notes Philosophy of psychiatry in PDF only on Docsity! Notes are online at http://cogsci.ucsd.edu/~clovett/NeuroNotesCogs17.pdf The Neuron A. What is a neuron? 1. A neuron is a type of cell that receives and transmits information in the Central Nervous System (CNS – brain and spinal cord) and the Peripheral Nervous System (PNS – afferent & efferent nerves). 2. Parts of the neuron: cell body (soma), dendrites, axon, axon hillock, synaptic boutons . The Nerve Impulse A. The Resting Potential 1. When a neuron is at rest, the neuron maintains an electrical polarization (i.e., a negative electrical potential exists inside the neuron's membrane with respect to the outside). This difference in electrical potential or voltage is known as the resting potential. At rest, this potential is around -70mV. 8. After the action potential, the neuron has more Na+ and fewer K+ ions inside for a short period (this is soon adjusted by the sodium-potassium pumps to the neuron's original concentration gradient). 9. Local anesthetic drugs (e.g., Novocain, Xylocaine, etc.) hinder the occurrence of action potentials by blocking voltage-activated Na+ gates (preventing Na+ from entering a membrane). 10. General anesthetics (e.g., ether and chloroform) cause K+ gates to open wider, allowing K+ to flow outside of a neuron very quickly, thus preventing an action potential from occurring (no pain signal). 11. Action potentials only occur in axons as cell bodies and dendrites do not have voltage-dependent channels. 12. All-or-none law: The size, amplitude, and velocity of an action potential are independent of the intensity of the stimulus that initiated it. If threshold is met or exceeded an action potential of a specific magnitude will occur, if threshold is not met, an action potential will not occur. 13. Refractory period: A period of immediately after an action potential occurs when the neuron will resist the production of another action potential. a. Absolute refractory period: Na+ gates are incapable of opening; hence, an action potential cannot occur regardless of the amount of stimulation. b. Relative refractory period: Na+ gates are capable of opening, but K+ channels remain open; a stronger than normal stimulus (i.e., exceeding threshold) will initiate an action potential. C. Propagation (movement) of the Action Potential 1. The action potential begins at the axon hillock (a swelling located where an axon exits the cell body). 2. The action potential is regenerated due to Na+ ions moving down the axon, depolarizing adjacent areas of the membrane. 3. Propagation of the action potential: Transmission (movement) of an action potential down an axon. The action potential moves down the axon by regenerating itself at successive points on the axon. 4. The refractory periods prevent the action potentials from moving in the opposite direction (i.e., back toward the axon hillock). D. Myelin Sheath and Saltatory Conduction 1. Myelinated axons : Axons covered with a myelin sheath. The myelin sheath is found only in vertebrates and is composed mostly of fats. 2. Nodes of Ranvier: Short unmyelinated sections on a myelinated axon. 3. Saltatory conduction: The "jumping" of the action potential from node to node. 4. Multiple sclerosis: A disease characterized by the loss of myelin along axons; the loss of the myelin sheath prevents the propagation of action potentials down the axon. The Concept Of The Synapse A. Synapse: A gap between neurons where a specialized type of communication occurs. B. C. S. Sherrington deduced the properties of the synapse from his experiments on reflexes (an automatic response to stimuli). C. Sherrington discovered that: 1. Reflexes are slower than conduction along an axon; thus, there must be a delay at the synapse. 2. Synapses are capable of summating stimuli. 3. Excitation of one synapse leads to a decreased excitation or inhibition of others. D. Temporal summation: Repeated stimulation of one presynaptic neuron (the neuron that delivers the synaptic potential) occurring within a brief period of time having a cumulative effect on the postsynaptic neuron (the neuron that receives the message). E. Graded potentials: Either depolarization (excitatory) or hyperpolarization (inhibitory) of the postsynaptic neuron. A graded depolarization is known as an excitatory postsynaptic potential (EPSP) and occurs when Na+ ions enter the postsynaptic neuron. EPSP'S are not action potentials: The EPSP's magnitude decreases as it moves along the membrane. F. Spatial summation: Several synaptic inputs originating from separate locations exerting a cumulative effect on a postsynaptic neuron. G. Inhibitory postsynaptic potential (IPSP): A temporary hyperpolarization of a postsynaptic cell (this occurs when K+ leaves the cell or Cl- enters the cell after it is stimulated). H. Spontaneous firing rate : The ability to produce action potentials without synaptic input (EPSP's and IPSP's increase or decrease the likelihood of firing action potentials). Chemical Events At The Synapse A. In most cases, synaptic transmission depends on chemical rather than electrical stimulation. This was demonstrated by Otto Loewi's experiments where fluid from a stimulated frog heart was transferred to another heart. The fluid caused the new heart to react as if stimulated. B. The major events at a synapse are: 1. Neurons synthesize chemicals called neurotransmitters. 2. Neurons transport these chemicals to the axon terminal. 3. Action potentials travel down the axon. 4. At the axon or presynaptic terminal, the action potentials open voltage-gated calcium channels to open, allowing calcium to enter the cell. This leads to the release of the neurotransmitters from the terminal into the synaptic cleft (space between the presynaptic and postsynaptic neuron). 5. Neurotransmitters, once released into the synaptic cleft, attach to receptors and alter activity of the postsynaptic neuron. 6. The neurotransmitters will separate from their receptors and (in some cases) are converted into inactive chemicals. 7. In some cells much of the released neurotransmitters are taken back into the presynaptic neuron for recycling. This is called reuptake. 2. Acetylcholinesterase (AchE): Found in acetylcholine (Ach) synapses; AchE quickly breaks down Ach after it releases from the postsynaptic receptor. 3. Myasthenia gravis: Motor disorder caused by a deficit of acetylcholine transmission. This disease is treated with drugs which block AchE activity (thus allowing more Ach to stay in the synapse). 4. Serotonin and the catecholamines are taken up by the presynaptic neuron which released them after they separated from postsynaptic receptors. This process is called reuptake; it occurs through specialized proteins called transporters . 5. Some serotonin and catecholamine molecules are converted into inactive chemicals by enzymes such as COMT (converts catecholamines) and MAO (converts both catecholamines and serotonin). Synapses, Abused Drugs, and Behavior A. Drugs can affect synapses by either blocking the effects (an antagonist) or increasing the effects (an agonist) of a neurotransmitter. B. Drugs can influence synaptic activity in many ways including altering synthesis of the neurotransmitter, disrupting the vesicles, increasing release, decreasing reuptake, blocking its breakdown into inactive chemical, or directly simulating or blocking postsynaptic receptors. C. Affinity: How strongly the drug attaches to the receptor. D. Efficacy: The tendency of the drug to activate a receptor. E. Olds and Milner (1954) conducted the first brain reinforcement experiments by implanting electrodes in the brains of rats and allowing them to press a lever to produce self-stimulation of the brain. 1. Later experiments showed that the brain stimulation is reinforcing almost exclusively in tracts of axons that release dopamine, especially in an area called the nucleus accumbens . Cells located in the nucleus accumbens are inhibited by increased DA activity (most abused drugs, as well as ordinary pleasures, lead to increased DA activity); some hypothesize this phenomenon occurs with drug addiction. 2. Because of their roles in reinforcement the nucleus accumbens is regarded by many as the pleasure area and dopamine as the pleasure chemical. However, several lines of evidence conflict with this interpretation and more recent studies suggest dopamine and the nucleus accumbens play an important role in attention-getting. F. Stimulant drugs (e.g., amphetamines, cocaine, etc.) produce excitement, alertness, elevated mood, decreased fatigue, and sometimes motor activity. Each of these drugs increases activity at dopamine receptors. Stimulant drugs are often highly addictive. 1. Amphetamine increases dopamine release from presynaptic terminals by reversing the flow of the dopamine transporter. 2. Cocaine blocks the reuptake of catecholamines and serotonin at synapses. The behavioral effects of cocaine are believed to be mediated primarily by dopamine and secondarily on serotonin. 3. The effects of amphetamine and cocaine are both short lived because of depletion of dopamine stores and tolerance. 4. Methylphenidate (Ritalin): Stimulant currently prescribed for Attention Deficit Disorder (ADD); works like cocaine by blocking reuptake of dopamine at presynaptic terminals. The effects of methylphenidate are much longer lasting and less intense as compared to cocaine. G. Nicotine : Compound found in tobacco. Stimulates the nicotinic receptor (a type of acetylcholine receptor) both in the central nervous system and neuromuscular junction of skeletal muscles; can also increase dopamine release by attaching to receptors that release dopamine in the nucleus accumbens. H. Opiate Drugs : Derived from (or similar to those derived from) the opium poppy. Common opiates include morphine, heroin, and methadone. Opiates have a net effect of increasing the release of dopamine by stimulating endorphin synapses. I. Marijuana : Contains the chemical D9-tetrahydrocannabionol (D9-THC) and other cannabinoids (chemicals related to D9-THC); D9-THC works by attaching to cannabinoid receptors. Anandamide is a brain chemical that binds to cannabinoid receptors. J. Hallucinogenic drugs : Drugs that distort perception. Many hallucinogenic drugs resemble serotonin and bind to serotonin type 2 (5-HT2) receptors, although their exact mechanism of action remains unclear (some ligands that bind to 5-HT2 receptors have no psychoactive effects at all).