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Oct 2 Lec 4.docx

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Michael Inzlicht

Oct 2, Lec 4 Recap from last lec: • intracellular is negative bc of the proteins, and the proteins are too large to fit through the channels • resting membrane potential = potassium membrane = it’s called this bc some of the potassium channels are open so K+ can move freely and it’s balance by the llbm of the diffusion wanting it to leave and electrical forces wanting to pull it in. Sodium channels are primarily closed though. • Hyperpolarizing = making it more negative and thus even farther away from the threshold, so no action potential • Depolarizing = makes it more positive and only if we get it past threshold will we have an AP • AP’s travel down the axon. Myelinated is better because it’s quicker since you only have to jump from one node of renvier to the next • Voltage-gated sodium channel = the channel opens or closes depending on the voltage(must be threshold, generally) • One neuron communicates with another at the synapse 2 Type of Synapses (Specialized Junctions): • Human brain contains about 100 billion neurons with each neuron forming an avg of 1000 synapses • 1)Electrical: o fairly rare but widespread o narrow cleft (gap junction) = 2-4 nanometers o membranes have large channels o transmission along synapse resembles conduction along axon o nearly instantaneous o frequently found in neural circuits such as escape behv o cells directly stimulate each other by sending ions through across gaps through channels that actually touch o Excitatory signals ONLY o Requires large presynaptic neuron to influence a small postsynaptic • 2)Chemical: o exocytosis results in the release of neurotrans o wider synaptic gap = 20 nanometers o stimulate adjacent cells by sending chem messengers o can take up to several milliseconds o excitatory or inhibitory o neurotrans release, binds to postsynaptic receptor cite, termination of chem. signal, postsynaptic potential, and neural integration o small pre can influence large post Types of Receptors and Detection on the Postsynaptic Side: • 1) Ionotropic: o Neurotransmitters attach to the ~ receptor site: o Ions are released from pre an attach directly to an ion channel, causing it to open o Everything occurs at one particular point in one step. Receptor = ion channel o faster • 2) Metabotropic: o Neurotrans attaches to a G-protein receptor (G-proteins are active) and causes the G-protein to separate and attach to an ion channel o This causes the ion channel to open o 2-step process. Receptor is not the ion channel o Slower, often deals with modulation bc it has the time delay Methods to Deactivate Neurotransmitters in the synaptic cleft: • 1) Diffusion (neurotrans can be diffused away) • 2) Deactivation (broken down) • 3) Reuptake (reabsorbed) Neural Integration • Excitatory  membrane will be more positive, enough to hit threshold, thus AP fired • Inhibitory  membrane will be more negative, therefore, farther away from threshold, no AP • However since there are many synapses for a given neuron, it is the net effect that really matters. Ex. 1 excitatory and 1 inhibitory of equal strengths = no effect • 2 types of integration: o 1) Spatial Summation = inputs from all over cell converge at axon hillock and exert a cumulative effect on the neuron (AP only if threshold reached) o 2) Temporal Summation = excitation from one active synapse is sufficient to initiate AP , across time if there’s enough rapid firing to cause enough depolarization Postsynaptic Potential Summary • Action potential o 1 to 2 ms o Signalling within neuron o About 100 mV o All or none o Active o Voltage dependent Na and K • Excitatory (EPSPs)  slight depolarization, allows sodium in (ligand-gated) o Signalling between neurons o 5-10ms up to 100ms o Up to 20mV o Graded depolarization (not all or none = small changes that can sum together) o Small, local o Passive • Inhibitory (IPSPs)  slight hyperpolarization bc chloride in or potassium out (ligand- gated) o Signalling between neurons o Up to 15mV o 5 to 10 ms up to 100 ms o Graded hyperpolarization (not all or none = small changes that can sum together) o Passive o Small, local • * ligand-gated = opposite voltage-gated, dependent on neurotrans (= ligand) and how well it bound to ion channel. And presence or absence of ligand determines whether channel opens Neuromodulation: • Synapses between an axon terminal and another axon fiber • Axo-axonic synapses have modulating effect on release of neurotrans of target axon. Two types of this modulation: o 1) Presynaptic facilitation: makes it easier for axon to release neurotrans o 2) Presynaptic Inhibition: makes axon releasing neurotrans less likely • A 3 neuron apart from pre and post is the one that can modulate *Tetanus related to GABA = inhibitory CHAPTER 4 PSYCHOPHARMACOLOGY (lec content/slides only! No textbook readings needed.) Identifying Neurotrans: • Must be synthesized within neuron • In response to an AP, the substance is released in sufficient quantities to produce an effect on post cell • This effect should be possible to duplicate experimentally • There needs to be some mechanism to be able to stop the interaction between pre and post 3 Types of Neurotransmitters • 1) Small Molecule Transmitters: meets all or most of criteria, plays a vital role in neurotransmission. Ex. Ach • 2) Neuropeptides: at least 40. Act as neurotrans, neuromod, and neurohormones • 3) Gaseous Neurotrans: some gases transfer info from one cell to another o Most recently discovered form Characteristics of Specific Neurotrans: • Ach = Acetylcholine: o Found in neuromuscular junction, basal projections of hippocampus to amygdale o Involved with learning and memory, autonomic fxn, movement • Dopamine: o Basal ganglia and substantia nigra o Reinforcement, reward o Parkinsons’ • Norepinephrine: o Mood, arousal o Hypothalamus o Not really going to talk about this one • Serotonin: o Pons o Not gonna talk about this much o Sleep though, and appetite • Glutamate o Most widely distributed excitatory o Long-term memory • GABA o Most widely distributed inhibitory o Mood, seizure thresholds o Ex. Alcohol • Not gonna talk about ATP (energy molecule, pain modulation, CNS inhibition) • End
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