8917957
Description
Flashcards by Alex Aspel, updated more than 1 year ago
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Created by Alex Aspel
over 7 years ago
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| Question | Answer |
| Primary Neurotransmitters; 2 Types | Glutamate and GABA |
| Glutamate | Excitatory Transmitter INCREASES membrane potential of post-synaptic cell Amino Acid Activates NMDA and AMPA receptors |
| AMPA | AMPA Receptor controls Na+ gate -> EPSP |
| NMDA | NMDA Receptor controls Na+ and Ca2 gates Receptor blocked by Mg+ ion |
| Ca2 | Is involved in changes to AMPA receptors, producing Long Term Potential (LTP) |
| GABA | Inhibitory Transmitter DECREASES membrane potential of post-synaptic cells PREVENTS excessive excitation GABA A controls Cl- GABA B controls K+ channels |
| Neurotransmitter | Diffuses across the synaptic cleft to affect one post-synaptic neuron (or muscle cell) |
| Neuromodulator | Affects groups of neurons ( or effector cells) that have the appropriate receptors. May not be released at synaptic sites. Can produce long lasting effects. |
| Neurohormone | Released by neurons into the haemolymph, therefore may affect very distant targets. It may differ only in degree from a neuromodulator in the extent of it's action. |
| Receptor Types; 2 | Ionotropic Receptors and Metabotropic Receptors |
| Ionotropic Receptors | Directly control an ion channel Fast information transmission |
| Metabotropic Receptors | Indirectly control an ion channel Slower- long lasting modulatory effects. |
| Acetylcholine (Ach) | Cholinergic receptors located throughout brain, spinal cord and neurotransmitter junctions. Cell bodies located in limbic system. Ach released along axon and acts diffusively on receptor on the soma and dendrites. |
| Dopamine | Dopaminergic projections from SN, VTA. Modulate activity in limbic & cortical areas. SN modulates input areas of basal ganglia. Degeneration causes Parkinson's Disease. Effect can be inhibitory, excitatory or modulatory depending on receptor. |
| Norepinephrine (Noradrenaline) | LC sends Noradrinergic projections throughout brain. Involved in vigilance and alertness. Increased firing before & during focused attention. Arousal effect on rest of the brain. Noradrinergic systems reduce distraction. |
| Serotonin (H5T) | Inhibits transmission of pain signals from nociceptors. Modulates moto-neuron excitability. Involved in satiety. Involved in antidepressant Prozac. Lesions induce aggression & increased motor activity. |
| Prozac | Antidepressant. Serotonin re-uptake inhibitor. |
| Blood Brain Barrier | Aids the regulation of the brain's chemical environment. Molecules, such as drugs, must be transported across this barrier. |
| Therapeutic Window | The range of drug doses which can treat a disease effectively without toxic effects. |
| Drug Action | Drugs typically affect processes in the synapses. |
| Agonist | FACILITATE post-synaptic effects |
| Antagonist | INHIBIT post-synaptic effects |
| Cocaine | Ach AGONIST. Blocks re-uptake of dopamine and norepinephrine. |
| Benzodiazepines (e.g. Valium) | GABA AGONIST Binds to one site on the GABA receptor. Aids binding of GABA molecules -> Post-synaptic hyperpolarization and subsequent inhibitory effects. |
| Alcohol | GABA AGONIST NMDA ANTAGONIST Increases dopamine release (reward) Interferes with LTP (memory & cognition) |
| Positive Reinforcement | Appetitive stimulus (e.g. heroin rush) in association with a behaviour |
| Negative Reinforcement | Removal of an adversive stimulus (e.g. anxiety) in association with a behaviour. |
| Reinforcement | Linked to the release of dopamine in the NA. |
| Tolerance | Increased sensitivity to the drug, following chronic use. |
| Sensitivity | Increased drug effect following prolonged use. Long-time users show hypo-frontality. Damage to this area disrupts decision making. |
| Heroin | Stimulates opiate receptors and produces analgesia, sedation and reinforcement. |
| Heroin withdrawal | Blocking heroin in the LC leads to over activation of the serotonergic system which was repressed by the heroin. |
| Cocaine | Blocks re-uptake of dopamine |
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