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Details of the synapse cytoplasm

Synaptic vesicles
contain molecules of neurotransmitter. They attach to the presynaptic membrane and release neurotransmitter into the synaptic cleft

Synaptic cleft is the space between the pre- and postsynaptic membranes. It is filled with an extracellular fluid.

1

Postsynaptic Potentials (PSP)

Neurotransmitters attach to binding site. Cause opening ING of ion channel. Affects potential of OSM creating psp determined by ion receptor opened. Sodium, potassium, cl, and ca2+

When sodium channels are opened, the influx of Na+ causes a depolarisation -
Excitatory Postsynaptic Potential (EPSP)

Potassium is positively charged. It’s efflux causes a hyperpolarisation -
Inhibitory Postsynaptic Potential (IPSP)

PSP’s are influenced by other ions depending on the state of the membrane. E.g. if the membrane is resting, Cl ̄ will have no effect, but if the membrane has been depolarised, Cl ̄ channels will permit Cl ̄ to enter the cell thus neutralising the EPSP.

2

Neural Integration


The interaction of the excitatory and inhibitory synapses on a particular neuron is called neural integration.

Rate of firing controlled by rate of epsp and ipsp

3

Imp. Neural inhibition does not always produce behavioural inhibition. Likewise Neural excitation does not always produce behavioural excitation


For example, a group of neurons may prevent me from putting my hand in the fire. If, however, those neurons are inhibited (i.e. prevented from producing an IPSP), those neurons will NOT suppress my behaviour and I will put my hand in the fire.
Ø Inhibition of inhibitory neurons makes the behaviour more likely to occur

For example, when we are dreaming, a group of inhibitory neurons are activated to prevent us from acting out our dreams. If this activation fails to occur, people will act out their dreams.
Ø Excitation of neurons that inhibit a behaviour, suppresses that behaviour

4

Auto receptors

Do not effect membrane potential. Effect, tram otter synthesis. And are mostly inhibitory.
Imp. For transmission of info for reuptake,
Do not control ion channels. See text book section,

5

Axoaxonix, between two terminal buttons, 2.38

A third type of axon. Modulate neurotransmitter release between.

6

Physopharmacology.

Drugs and their effectiveness.

7

Psychopharmacology

is the study of the effects of drugs on the nervous system and behaviour.

Many definitions of a drug, perceived beneficial effects, recreational. PHARMACOLOGICAL: A chemical substance used for treatment OR
An exogenous chemical that significantly alters the function of certain cells when taken in relatively low doses.

Must be constructed to pass blood brain barrier if desired.
Have effect on our Behaviour.

8

Routes of Drug Administration

Drugs have to reach their site of action which is the point where drug molecules interact with molecules located on or in cells of the body.
1. Intravenous (i.v.) injection - into the vein
2. Intraperitoneal (i.p.) injection - into the abdominal wall (peritoneal cavity)
3. Intramuscular (i.m.) injection - into the muscle
4. Subcutaneous (s.c.) injection - into the space between the skin
5. Oral administration - by mouth
6. Sublingual administration - under the tongue
7. Intrarectal administration - as suppositories
8. Inhalation - by smoking
9. Topical administration - through the skin
10. Intracerebral administration - directly into the brain but not for humans. Only for animals. Exception is brain stimulation by neurologists for Parkinson's. Motor conditions helped.

9

Dose Response Curve

A dose response curve is the magnitude of an effect of a drug as a function of the amount that is administered. It is obtained by giving subjects various doses of drug (according to weight).

Free a point, drug has maximum effect.
Morphine though: is a depressant. Has two curves. Analgesic. Relatively low dose. High for depressive effect, dose must be within margin of safety.

10

Drug Efficacy

Drugs vary in effectiveness because:
§ They have different sites of action.
§ They have different affinities for the molecules to which they attach. The affinity of a drug is the readiness with which two molecules join together.
A drug with a high affinity will produce an effect at low doses whereas a drug with a low affinity may have to be administered at a high dose.
The same drug may have a high affinity at one site of action and a low affinity at a different site of action.

Aspirin vs morphine
Aspirin is peripheral, morphine is central effect, has better effect.

11

Effects of Repeated Administration

1. Tolerance is when the effect of drug diminishes because of repeated administration.
§ E. g. A regular heroin user must take larger and larger amounts for the drug to be effective. Having developed tolerance to heroin, the user will suffer withdrawal symptoms which are opposite effects of the drug (i.e. euphoria vs dysphoria).
§ Tolerance is the body’s attempt to compensate for the effects of the drug.
Hmm, what about health products.

2. Sensitization occurs when a drug becomes more and more effective through repeated use.
§ E. g. barbiturates have sedative and depressive effects. The
sedative effect shows tolerance but the depressive effect does not. Thus, if larger doses of barbiturates are taken to achieve a sedative effect, you run the risk of taking a dangerously high dose of the drug. Context also important, hold reinforcing properties
. Think pubs,

3. A placebo is an inert substance which has no physiological effect. It is given to subjects to control the effects of mere administration of the drug. § Is the observed behavioural effect a specific cause of the drug? Test effect of drug.

12

The Neurotransmitters

Amino Acids
Glutamate
Gamma-aminobutyric acid (GABA)
Glycine spinal chord, inhibitory.
Aspartate


Monoamines
-Catecholamines
Dopamine (DA) Norepinehprine (NE) Epinephrine
-Idolamines
Serotonin (5-HT) different by structure, tryptophan,

Cholinergic
Acetylcholine (ACh)


Neuropeptides
Endorphins: opium like analgesics
Other neuropeptides

Widespread effect on brain!

13

Mechanisms of Drug Action: Competitive Binding

Neurotransmitter release stimulates the postsynaptic receptor. Drugs can bind to these neurotransmitters. These drugs can be an:
§ An agonist, a drug that facilitates postsynaptic transmission
§ An antagonist, a drug that blocks or inhibits postsynaptic transmission

Competitive binding
§ An direct agonist will attach itself to the binding site where the neurotransmitter would normally bind.
§ The binding causes ion channels to open.
§ The ions pass through and causing a postsynaptic potential.
§ A direct antagonist (receptor blocker) can also occupy the binding site therefore preventing the opening of the ion channel.

Non-competitive binding
§ Some receptors have multiple binding sites.
§ The neurotransmitter binds with one site while the drug binds with another.
§ An indirect agonist binds with an alternative binding site and facilitates the opening of the ion channel.
§ An indirect antagonist binds with an alternative binding site and prevents the channel from opening.

Know about reuptake,
And degradation of vesicles.

14

Psychoactive Drugs

§ Cocaine
- A potent catecholamine agonist that is highly addictive
- Increases activity of DA and NE by blocking their reuptake from the synapse
- cause euphoria, insomina, loss of appetite, and addiction
§ Benzodiazepines (e.g. diazepam)
- Acts as a GABA agonist but do not mimick GABA's action.
- Reduce anxiety (anxiolytic), sleep inducing (sedative) and
anticonvulsant.
§ Botox (Botulinium toxin)
- A nicotinic antagonist which blocks ACh release.
- At minute doses it can reduce tremor and reduce wrinkles
§ Curare
- A cholinergic receptor blocker (works specifically on nicotonic
receptors)
- Blocks transmission at neuromuscular junctions causing paralysis