Psyc 6 Week 2
Popular in Introduction to Neuroscience
Popular in Psychology (PSYC)
This 5 page Class Notes was uploaded by Sabrina Straus on Friday September 23, 2016. The Class Notes belongs to PSYC 6 at Dartmouth College taught by Catherine Cramer in Fall 2016. Since its upload, it has received 5 views. For similar materials see Introduction to Neuroscience in Psychology (PSYC) at Dartmouth College.
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Date Created: 09/23/16
6. 092316 Intro to Neuro Class Notes PSYCHOPHARMACOLOGY I. Exogenous substances that affect endogenous processes Agonistsstimulate a naturally occurring process by mimicking a neurotransmitter Ex: LSD is agonist for serotonin Antagonists (competitive and noncompetitive)oppose Ex: curare to nicotinic receptor > can’t move muscles Competitive and noncompetitive II. A dozen ways to mess with your neurons 1. Affect synthesis of NT Ex: deactivates enzyme in synthesis 2. Block conduction of AP via channel block Ex: tetrodotoxin by messing with voltagegated channels 3. Block axonal transport of NT Ex: colchicine used to treat gout 4. Modulate release of NT [e.g., black widow spider venom] Ex: block calcium channels or snares> less release of neurotransmitters 5. Modulate storage of NT [e.g., reserpine] 6. Modulate presynaptic receptors Ex: block autoreceptors negative feedback > caffeine is a stimulator 7. Modulate reuptake Ex: Prozac~ specific for serotonin 8. Modulate breakdown of NT in cleft Ex: reduce amt. Of neurotransmitter to be recycled by blocking enzymes} cholinesterase inhibitors Postsynaptic membrane 9. Modulate # of postsynaptic receptors Ex: more > more effective [e.g., alcohol upregulation of Gaba receptor (more inhibitory postsynaptic potentials] 10. Block receptors [e.g., curare] 11. Activate receptors [e.g., nicotineagonists] 12. Modulate second messengers [e.g., lithiumbipolar disorder by blocking it] III. Effects of some psychoactive drugs A. Stimulants (e.g., amphetamine (agonistic dopamine), cocaine+Ritalin (blocks reuptake of dopamine)) B. Opiates (stimulates endorphin) (e.g., heroin, morphine)} relaxation C. Cannabinoids (marijuanaretrograde) D. Hallucinogens (e.g., LSDstimulates serotonin) E. Sedatives (e.g., barbituates, alcohol) IV. Some consequences of repeated exposure to psychoactive drugs 1. Tolerance and withdrawal to opiates> change dosage 2. Up and downregulation of receptors Chapter Notes Chapter 6:Neurotransmitter Systems 3 major neurotransmitters: amino acids, amines, and peptides Studying neurotransmitter systems >Neurotransmitter: 1. The molecule must be synthesized and stored in the presynaptic neuron. 2. The molecule must be released by the presynaptic axon terminal upon stimulation. 3. The molecule, when experimentally applied, must produce a response in the postsynaptic cell that mimics the response produced by the release of neurotransmitter from the presynaptic neuron. ● Localization of Transmitters and transmittersynthesizing enzymes: prove that located in and synthesized by neurons ○ Immunocytochemistry: anatomically localizes particular molecules to particular cells ■ Inject neurotransmitter in blood>antibodies form and bind to antigen (transmitter candidate)>color antibodies and stick in brain cells to distinguish dif. cells ○ In situ hybridization: useful for confirming that a cell synthesizes a particular protein or peptide ■ Create complementary strand of mRNA (probe~chemically labeled) > bonds (hybridization) > ● make them radioactive and stick on film} autoradiography ● Or use fluorescence ● Transmitter release ○ Brain slices in K+ and Ca2+ solution to stimulate depolarization ○ Hard to see if released from terminal ● Synaptic Mimicry: microiontophoresis ○ Apply drug by passing electrical current and stimulate axon> record Vm at neuron ● Receptors: no two neurotransmitters bind to the same receptor but one neurotransmitter can bind to many different receptors ○ Receptor subtype: Each of the different receptors a neurotransmitter binds to ○ Studies ■ Neuropharmacological analysis: different receptor subtypes can be distinguished with different drugs or selective antagonists *neurotransmitter > agonists > receptors ■ Ligandbinding methods: Any chemical compound that binds to a specific site on a receptor ● Ligand can be agonist, antagonist, or chemical neurotransmitter itself ■ Molecular analysis ● neurotransmitter receptor proteins ○ Transmittergated ion channels ○ Gprotein coupled receptors Neurotransmitter Chemistry >Dale’s principle: neuron has only one neurotransmitter} violated by cotransmitters ● Cholinergic neurons: synthesized by motor neurons > choline transporter allows ChAT to be made into ACh and transported in a vesicle } powered by Na+ and choline determines amt of ACh } rate limiting step ○ AChE degrades ACh into choline and acetic acid in the synaptic cleft ● Catecholaminergic neurons~involved in regulation of movement, mood, attention, and visceral function ○ Contain tyrosine hydroxylasecatalyzes synthesis } rate limiting ■ Controlled by endproduct inhibition ○ Transmitters ■ Dopamine ■ Norepinephrine ■ epinephrine/adrenaline ● Serotonergic neurons: regulate mood, emotional behavior, and sleep ○ Limited by availability of trptophan ○ Synthesis: ■ Tryptophan is converted first into an intermediary ■ 5HTP is then converted to 5HT ○ Then reuptake or degraded ● Amino acidergic neurons ○ Glu, Gly, and Gaba are neurotransmitters at CNS synapses ■ Gaba not used to construct proteins only transmitter/ major source of synaptic inhibition in the nervous system ● Can easily become inhibitory ● Other Neurotransmitter Candidates and Intercellular Messengers ○ ATP: released into the cleft by presynaptic spikes in a Ca 2 dependent manner ○ Endocannabinoids: small lipid molecules released from post and act on pre} retrograd signaling ■ Stimulated by elevated [Ca 2 ] ■ Qualities: 1. They are not packaged in vesicles like most other neurotransmitters; instead, they are manufactured rapidly and on demand. 2. They are small and membrane permeable; once synthesized, they can diffuse rapidly across the membrane of their cell of origin to contact neighboring cells. 3. They bind selectively to the CB1 type of cannabinoid receptor, which is mainly located on certain presynaptic terminals. ■ CB1: G protein/ reduce Ca2+ ○ Nitric Oxide: causes smooth muscle of blood vessels to relax TransmitterGated channels ● Structure: ACh: 5 subunits to create a pore ○ Stretches where the receptor has similar sequences of amino acids ○ In general most have: ■ 4 hydrophobic segments that span the membrane of the receptor in subunits ■ Exceptions: ATP and Glu ● Amino acidgated channels: mediate most of the fast synaptic transmission in the CNS ○ The pharmacology of their binding sites describes which transmitters affect them and how drugs interact with them. ○ The kinetics of the transmitter binding process and channel gating determine the duration of their effect. ○ The selectivity of the ion channels determines whether they produce excitation or inhibition and whether Ca 2 enters the cell in significant amounts. ○ The conductance of open channels helps determine the magnitude of their effects. 1. GlutamateGated channels a. AMPAgated (permeable to Na+ and K+) and NMDAgated channels (permeable to Ca2+ + inward ionic current is voltage dependent and at rest, pore is blocked by Mg2+) mediate the bulk of fast excitatory synaptic transmission in the brain by admitting an excess of Na+ 2. GABAgated and Glycinegated (chloride) channels a. Gaba: mediates synaptic inhibitions b. Glycine: mediates the rest c. Affected by drugs to enhance inhibition Gproteincoupled receptors and effectors ● Structure: ○ Single polypeptide: 7 membranespanning alpha helices ○ Two of the extracellular loops of the polypeptide form the transmitter binding sites ■ Structural variations in this region determine which neurotransmitters, agonists, and antagonists bins to the receptor ● Ubiquitous GProteins: links neurotransmitter and effector protein 1. Each Gprotein has three subunits> In the resting state, a guanosine diphosphate (GDP) molecule is bound to the G subunit, and the whole complex floats around on the inner surface of the membrane. 2. If this GDPbound Gprotein bumps into the proper type of receptor and if that receptor has a transmitter molecule bound to it, then the Gprotein releases its GDP and exchanges it for a GTP that it picks up from the cytosol. 3. The activated GTPbound Gprotein splits into two parts: the G subunit plus GTP and the G complex. Both can then move on to influence various effector proteins. 4. The G subunit is itself an enzyme that eventually breaks down GTP into GDP. Therefore, G eventually terminates its own activity by converting the bound GTP to GDP. 5. The G and G subunits come back together, allowing the cycle to begin again. >Gs: stimulatory >GI: inhibitory ● Gprotein coupled effector systems ○ Bind to Gprotein gated ion channels ○ Bind to Gprotein activated enzymes ○ Shortcut pathway: localized (action occurs within membrane) ○ Second messenger cascades: activating certain enzymes ■ Protein kinases esp important (ATP) ○ Phosphorylation and dephosphorylation ■ Protein phosphatase: act rapidly to remove phosphates ○ Signal cascades ■ Although it is slow signal amplification is one advantage ■ The use of small messengers that can diffuse quickly allows signaling at a distance, over a wide stretch of cell membrane ■ Provide many sites for further regulation ■ generate very longlasting chemical changes in cells divergence and convergence in neurotransmitter systems ● Divergence: ability of one transmitter to activate more than one subtype of receptor, and cause more than one type of postsynaptic response ● Convergence: Multiple transmitters, each activating their own receptor type, can converge to influence the same effector system
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