Download doc Behavioural_Neuroscience_Jan_16

Behavioural Neuroscience
4/19/2012 5:30:00 PM
How do neurons communicate with each other?
The Synapse:
 A synapse is a junction between the terminal button of the sending
neuron and a portion of the dendritic membrane of the receiving
neuron.
 Synaptic transmission is the transmission of messages from one
neuron to another through a synapse
Detail of the Synapse:
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Synaptic vesicles contain molecules of neurotransmitter
o 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.
Presynaptic membrane is the membrane of the terminal button (the
sending cell). This is where neurotransmitter is released
Postsynaptic membrane is the membrane of the receiving cell either
on the soma or the dendrite
Postsynaptic Potentials (PSP):
 Excitatory Postsynaptic Potential (EPSP): Sodium-potassium
channels keep Na+ outside the cell. When sodium channels are
opened, the influx of Na+ causes a depolarisation
 Inhibitory Postsynaptic Potential (IPSP): If potassium channels
open, K+ leave the cell. Potassium is positively charged. It’s efflux
causes a hyperpolarisation
 PSP’s are influenced by other ions depending on the state of the
membrane.
o 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.
Neural Integration Neural Integration:
 Neural Integration: The interaction of the excitatory and inhibitory
synapses on a particular neuron
o If several excitatory synapses are active at the same time,
the EPSP will travel toward the axon and the axon will fire
o If several inhibtitory synapses are active at the same time as
the EPSP, the IPSP will diminish the size of the EPSP and
prevent the axon from firing
Neural inhibition does not always produce behavioural inhibition:
 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.
o Inhibition of inhibitory neurons makes the behaviour more
likely to occur
Neural excitation does not always produce behavioural excitation:
 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.
o Excitation of neurons that inhibit a behaviour, suppresses that
behaviour
Psychopharmacology: Drugs and their Effectiveness
What is a Drug?:
 a) A chemical substance used in the treatment, cure, prevention or
diagnosis of disease or used to enhance physical or mental well
being.
 b) A chemical substance that has “perceived” beneficial effects on
perception, consciousness, personality and behaviour (e.g.
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narcotics, hallucinogens). Some drugs can cause addiction if abused
(e.g. cocaine, heroin)
c) An exogenous chemical that significantly alters the function of
certain cells when taken in relatively low doses.
Psychopharmacology is the study of the effects of drugs on the
nervous system and behaviour.
Routes of Drug Administration:
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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 (IV) injection - into the vein
2. Intraperitoneal (IP) injection - into the abdominal wall
(peritoneal cavity)
3. Intramuscular (IM) injection - into the muscle
4. Subcutaneous (SC) injection - into the space between the skin
5. Oral administration - by mouth
6. Sublingual administration - under the tongue
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7. Intrarectal administration - as suppositories
8. Inhalation - by smoking
9. Topical administration - through the skin
10. Intracerebral administration - directly into the brain
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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).
o Higher doses cause larger effects until the point of maximum
effect
o The difference between the two curves is the drugs margin of
safety
Drug Efficacy:
 Drugs vary in effectiveness because:
o They have different sites of action.
o They have different affinities for the molecules to which they
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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. o The same drug may have a high affinity at one site of action
and a low affinity at a different site of action.
Effects of Repeated Administration:
 1. Tolerance is when the effect of drug diminishes because of
repeated administration.
o 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).
o Tolerance is the body’s attempt to compensate for the effects
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of the drug.
2. Sensitization occurs when a drug becomes more and more
effective through repeated use.
o E. g. barbiturates have sedative and depressive effects. The
sedative effect shows tolerance but the depressive effect does
not.
o 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.
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.
o Is the observed behavioural effect a specific cause of the
drug?
How drugs influence synaptic transmission
The Neurotransmitters:
 Amino Acids
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o Glutamate
o Gamma-aminobutyric acid (GABA)
o Glycine Aspartate
Monoamines
o Catecholamines
 Dopamine (DA)
 Norepinehprine (NE)
 Epinephrine
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o Idolamines
 Serotonin (5-HT)
Cholinergic
o Acetylcholine (ACh)
Neuropeptides
o Endorphins
o Other neuropeptides
Distribution of Neurotransmitters in Rat Brain:
Mechanisms of Drug Action: Competitive Binding:
 Neurotransmitter release stimulates the postsynaptic receptor.
o Drugs can bind to these neurotransmitters.
o 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:
o A direct agonist will attach itself to the binding site where the
neurotransmitter would normally bind.
o The binding causes ion channels to open.
o The ions pass through and causing a postsynaptic potential.
o A direct antagonist (receptor blocker) can also occupy the
binding site therefore preventing the opening of the ion
channel.
Mechanisms of Drug Action: Noncompetitive Binding:
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Neurotransmitter release stimulates the postsynaptic receptor.
o Drugs can bind to these neurotransmitters.
o These drugs can be an:
 An agonist, a drug that facilitates postsynaptic
transmission
 An antagonist, a drug that blocks or inhibits
postsynaptic transmission
Noncompetitive binding:
o Some receptors have multiple binding sites.
o The neurotransmitter binds with one site while the drug binds
with another.
o An indirect agonist binds with an alternative binding site and
facilitates the opening of the ion channel.
o An indirect antagonist binds with an alternative binding site
and prevents the channel from opening.
The Basics of Neurotransmitter Action:
Psychoactive Drugs:
 Cocaine
o A potent catecholamine agonist that is highly addictive
o Increases activity of DA and NE by blocking their reuptake
from the synapse
o cause euphoria, insomina, loss of appetite, and addiction
 Benzodiazepines (e.g. diazepam)
o Acts as a GABA agonist but do not mimick GABA's action.
o Reduce anxiety (anxiolytic), sleep inducing (sedative) and
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anticonvulsant.
Botox (Botulinium toxin)
o A nicotinic antagonist which blocks ACh release.
o At minute doses it can reduce tremor and reduce wrinkles
Curare
o A cholinergic receptor blocker (works specifically on nicotonic
receptors)
o Blocks transmission at neuromuscular junctions causing
paralysis
4/19/2012 5:30:00 PM
4/19/2012 5:30:00 PM