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Lecture 2

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PSYC 3030
Rob Foster

SYNPATIC STRUCTURE AND FUNCTION AXONAL TRANSPORT  Anterograde transport (communication from the cell body to the axon in a neuron) o Cytoskeletal and soluble proteins o Vesicles containing: proteins for growth o Mitochondria o Proteins/enzymes needed for neurotransmitter synthesis & secretion  Retrograde transport o Vesicle membrane material and excess or degenerated axon proteins o Nerve growth factor (NGF) – are neurotropic factors, they’re very specific SYNAPSE Three types of synaptic connections between neurons: a. Axodendritic – most common synapses in the brain b. Axosomatic – the target here is a cell body, and not a dendrite c. Axoaxonic – this is modulation, changing the pattern of activity of the other synapse. Activity at an axoaxonic synapse may cause presynaptic inhibition or presynaptic facilitation. NEUROTRANSMITTERS Criteria 1. The presynaptic terminal should contain a store of the suspected transmitter substance. 2. The effects of application of a suspected transmitter substance to a synapse should mimic the effects caused by stimulation of the presynaptic terminal at the synapse. 3. Application of an antagonist drug that blocks the receptors should inhibit both the action of the applied substance and the effect of stimulation the presynaptic neuron. 4. A mechanism must exist for the synthesis of the neurotransmitter. Therefore, the precursor and the appropriate enzymes should be present in the presynaptic terminal. 5. A mechanism must exist for inactivating the transmitter, such as catabolic enzyme to degrade the transmitter, or an active re-uptake system in the presynaptic terminal or in adjacent glial cells. Synthesis Chemical classes: I. Amino Acids – a few, play other metabolic roles besides their role as neurotransmitters. II. Monoamines – possesses a single amine group. III. Acetylcholine – typically they’re small and soluble, but are ionized at physiological pH, thus reducing their tendency to diffuse through the blood-brain barrier. Synthesized from dietary precursors, and transformed in active compounds by a series of biochemical reactions. IV. Neuropeptides – long or short chains (3-40) of amino acids derived from proteins precursors synthesized in the cell body. V. Lipids – e.g. cannabinoids VI. Gases – e.g. nitric oxide. Now we know that many neurons make and release two, three and occasionally even more, different transmitters. Except for the neuropeptides, transmitter are synthesized by enzymatic reactions that can occur anywhere in the cell. Typically, the enzymes are shipped out in large quantities to the axon terminals, so they’re an important site of transmitter synthesis. The protein precursor for neuropeptides must be made in the cell body, and the protein is packaged into large vesicles, along with enzymes that will break down the precursor and liberate the neuropeptide. Neuromodulator They are substances that don’t act exactly like typical neurotransmitters. It might alter the action of a standard neurotransmitter by enhancing, reducing or prolonging the transmitter’s effectiveness. Another common property is diffusion away from the site of release to influence cells more distant from the releasing cell. Neurotransmitter release – exocytosis 1. Neurotransmitter is synthesized and then stored in vesicles. 2. An action potential invades the presynaptic terminal 2+ 3. Depolarization of presynaptic terminal causes opening of voltage-gated Ca channels 4. Influx of calcium ions through channels  it is the direct trigger for neurotransmitter release. 5. Ca causes vesicles to fuse with presynaptic membrane (docking at the active zones) 6. Neurotransmitter is released into synaptic cleft via exocytosis. 7. Neurotransmitter binds to receptor molecules in postsynaptic membrane. 8. Opening or closing of postsynaptic channels. 9. Postsynaptic current causes excitatory or inhibitory postsynaptic potential that changes the excitability of the postsynaptic cell. 10. Retrieval of vesicular membrane from plasma membrane. Endocytosis Release and re-formation of vesicles is termed vesicle recycling. Release of neurotransmitters – rate-controlling factors Rate of cell firing The more action potentials, the higher rate of release. Transport of precursor amino acids If you can’t produce fast enough, you won’t be able do release. Synthesizing enzymes and precursor proteins Heteroreceptors They can control how much and how fast the neurotransmitter will be released: a. Facilitation: speeding up the machine of production b. Inhibition: changing the polarization The main difference between hetero and autoreceptors is the neurotransmitter, because in the heteroreceptor can be any neurotransmitter, and the autoreceptor will only bind with its own neurotransmitters. Autoreceptors It is on axon terminals or cell bodies and dendrites. It is a receptor for the same neurotransmitter released by that neuron. a. Terminal autoreceptors – located on axon terminals. When they are activated by the neurotransmitter, their main function is to inhibit further transmitter release. It’s a form of auto regulation. b. Somatodendritic autoreceptors - when they are activated, they slow the rate of cell firing. Inactivation 1. Enzymatic breakdown (Ach, neuropeptides, lipids and gases) 2. Reuptake (amino acids – glutamate and GABA, and dopamine) – this is an active process, you need specific proteins that use energy (transporters). Transporters fish the NT from the synaptic cleft and bring it back, where it can be broken down or repacked. 3. Glutamine is one of the kind that can be picked by glial cells. It is important that it is not broken down or repacked, so they’re transformed into an inert version and sent back to the axon where they can be released again. - Some drugs block NT transporters: cocaine blocks dopamine transporter, and then the neuron doesn’t shut down (neurotransmission enhanced). CRF (corticotropin-releasing factor) and ACTH (adrenocorticotropic hormone) The secretion of glucocorticoids regulates the CRF production by hypothalamus (negative feedback). Dexamethasone is a synthetic glucocorticoid that supresses hypothalamic release of CRF. However, in depressed individuals, there is a missing brick in the stress system, so it cannot be regulated properly by glucocorticoids, and the system doesn’t shut off. Schluger et al (2001) Methadone – opioid agonist (safe and effective treatment for opiate addiction). HPA – hypothalamic-pituitary-adrenal axis Metyrapone – inhibitor that block cortisol production in the adrenals, removing negative feedback normally exerted by endogenous glucocorticoids. Metyrapone administration thus produces an HPA axis response paralleling that which is normally precipitated by stressors. Hypothesis: alt
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