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| Frage | Antworten |
| Structure of the neuron | |
| Structure of the nervous system |
- Sympathetic/parasympathetic nerves have an opposite effect on the nervous system
- Sympathetic nerves: long ganglion connecte
Image:
Ns (binary/octet-stream)
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| Neurotransmitters | - Noradrenaline- primary transmitter at the sympathetic nerve terminals - Acetylcholine- Primary parasympathetic neurotransmitter at nerve terminals, ganglia and neuromuscular junctions - Dopamine and serotonin- part of the CNS |
| Anatomy of the sympathetic nervous system | - Most nerves of sympathetic NS emanate from thoracolumbar segments of the spinal cord - A few emenate from the ganglia |
| Anatomy of the parasympathetic nervous system | - Most emenate from the caraniosacral outflow, which is made up of cranial and sacral nerves - Others emenate from the ganglia, which are close to/inside the target tissue |
| Anatomy of the Sympathetic and parasympathetic nervous systems | |
| The neuroeffector junction: of the terminal region of the nerve | 1. Action potential reaches the nerve terminal, resulting in depolarisation 2. Depolarisation causes voltage gated calcium channels in the nerve terminal membrane to open 3. Calcium enters the nerve terminal through these channels, triggering a vesicle containing neurotransmitter to be released from the NT by exocytosis into the synapse 4. The neurotransmitter then interacts with postsynaptic receptors on the tissue, evoking a response (agonism). 5. Autoinhibition- stopping more neurotransmitter being released from the nerve terminal. |
| Synthesis and storage of neurotransmitter | Synthesis: 1. chemical precursor taken into the nerve terminal by active uptake process 2. Enzyme cascade: which changes the structure of the precursor into that of the neurotransmitter Storage: - Neurotransmitter taken up into vesicles for storage in the nerve terminals. * Drugs can affect this process by being inhibitory (AMPT, Hemicholinium) or stimulatory (L-DOPA- used in the treatment of parkinson's) |
| How drugs can interfere with the release of a neurotransmitter | - Guanethidine can inhibit terminal depolarisation and displace neurotransmitter in the nerve terminal. - Conotoxin can disrupt the uptake of calcium ions. - Botulinium can interfere with vesicle fusion - Amphetamine can cause neurotransmitter to be displaced in the nerve terminal. - Clonidine interferes with presynaptic receptors that control autoinhibition. |
| Termination of neurotransmission | - Local enzymes in the synapse convert neurotransmitters into inert metabolites - Neurotransmitters can also be reuptaken into terve terminal. Inhibition of this termination enhances transmission. Drugs that do this eg SSRIs- flouxotine inhibit breakdown and reuptake of serotonin, neostigmine inhibits degregation of Ach |
| Agonist action on receptors | - Agonist: a drug that activates receptors - Properties of agonists: Have affinity (bind to receptor) Have efficacy (activate the receptor) Have the ability to mimic transmitter |
| Antagonist action on receptors | - Antagonist: a drug that effects the activity of an agonist - Properties of antagonists: Have affinity (bind to receptors) Do NOT have efficacy (do not activate receptors) Block binding of the agonist to the receptor |
| Major therapeutic applications of agonists | - Salbutamol- used in asthma to activate B2 receptors - Diazepam activates A GABA receptors in order to relieve anxiety (however acts on a slightly different binding site so not strictly an agonist) |
| Major therapeutic applications of antagonists | - Propanolol blocks betanoradrenaline receptors to reduce blood pressure |
| Drugs affecting the neurotransmitter response | Drugs affecting neuroeffector response effect the neurotransmitter from nerve terminal to neuroeffector cell EG Benzodiazapeine tranquillizers- bind to GABA receptor/cl channel mcomplex to enhance channel opening and potentiate inhibitory effects of GABA Sidenafil- inhibits breakdown of secondary messenger GMP produced by nitric oxide in erectile tissue |
| Summary of neurotransmission | 1. Synthesis 2. Storage 3. Release 4. Activation of receptors 5. Cessation |
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