Download E.4 Neurotransmitters and Synapses

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Artificial general intelligence wikipedia , lookup

History of neuroimaging wikipedia , lookup

Cognitive neuroscience wikipedia , lookup

Axon wikipedia , lookup

Environmental enrichment wikipedia , lookup

Neuropsychology wikipedia , lookup

Neuroplasticity wikipedia , lookup

Biological neuron model wikipedia , lookup

Brain wikipedia , lookup

Haemodynamic response wikipedia , lookup

Brain Rules wikipedia , lookup

Time perception wikipedia , lookup

Neuroeconomics wikipedia , lookup

Premovement neuronal activity wikipedia , lookup

Long-term depression wikipedia , lookup

Optogenetics wikipedia , lookup

Development of the nervous system wikipedia , lookup

Signal transduction wikipedia , lookup

Feature detection (nervous system) wikipedia , lookup

Nonsynaptic plasticity wikipedia , lookup

Single-unit recording wikipedia , lookup

Holonomic brain theory wikipedia , lookup

Circumventricular organs wikipedia , lookup

Aging brain wikipedia , lookup

Neuromuscular junction wikipedia , lookup

Spike-and-wave wikipedia , lookup

Activity-dependent plasticity wikipedia , lookup

Pre-Bötzinger complex wikipedia , lookup

End-plate potential wikipedia , lookup

Metastability in the brain wikipedia , lookup

Neuroanatomy wikipedia , lookup

Channelrhodopsin wikipedia , lookup

Synaptogenesis wikipedia , lookup

Nervous system network models wikipedia , lookup

Synaptic gating wikipedia , lookup

Stimulus (physiology) wikipedia , lookup

Neurotransmitter wikipedia , lookup

Chemical synapse wikipedia , lookup

Endocannabinoid system wikipedia , lookup

Molecular neuroscience wikipedia , lookup

Clinical neurochemistry wikipedia , lookup

Neuropsychopharmacology wikipedia , lookup

Transcript
E.4
Neurotransmitters
and Synapses
E.4.1. Some Pre-synaptic neurons excite
postsynaptic transmission and others inhibit
postsynaptic transmission
E.4.2. Explain how decision-making in the CNS can result
from the interaction between the activities of excitatory and
inhibitory presynaptic neurons at synapses.
• Nerve signals are processed and
integrated through the adding together of
small changes in membrane potential
caused by the binding of neurotransmitters
to the receptors.
Neurone
Post-Synaptic Potentials (PSPs) can be
Excitatory (EPSP)(+) or
Inhibitory (IPSP) (-)
+
-
Neurone
+
• The EPSP must build up in the
postsynaptic neuron to the threshold level
to allow the formation of an action
potential.
+
Neurone
+
For example this
Neuron needs a 2
more “+” than “-”
before it will fire.
+
• Neurons can integrate signals from other
neurons
1) through spatial summation (a number
synaptic inputs combine to cause a
depolarization event).
+
Neurone
+
+
2) through temporal summation where a number
of Excitory Post Synaptic Potentials occur quickly
without enough recovery time between the Excitory
Post Synaptic Potentials to cause a depolarization
event.
+
+ ++ +
+ Neurone
-
+
• Neurons can integrate both
excitatory and inhibitory signals
from other neurons.
• Thus the adding together of the
inputs from synapses leads to
whether or not an action potential
is formed in the postsynaptic
neuron.
E.4.3 Explain how psychoactive drugs affect the brain and
personality by either increasing or decreasing postsynaptic
transmission.
E.4.4 List three examples of excitatory and three
examples of inhibitory psychoactive drugs.
• Excitatory drugs:
• nicotine,
• cocaine
• amphetamines
• Inhibitory drugs:
• benzodiazepines,
• alcohol
• tetrahydrocannabinol (THC).
E.4.5 Explain the effects of THC and Cocaine in terms of
their action at synapses in the brain.
Marijuana is the buds and
leaves of the Cannabis sativa
plant. This plant contains more
than 400 chemicals, including
tetrahydrocannabinol (THC),
the plant's main psychoactive
chemical.
THC is known to affect our
brain’s short-term memory.
Additionally, marijuana affects
motor coordination, increases
your heart rate and raises
levels of anxiety. Studies also
show that marijuana contains
cancer-causing chemicals
typically associated with
cigarettes.
An intravenous dose of only 1 milligram can produce
serious mental and psychological effects. Once in
your bloodstream, THC typically reaches the brain
within seconds after it is inhaled.
A neurotransmitter such as Acetylcholine
is released from one neuron and binds to
receptors on adjacent neurons.
• Neurotransmitters fill the gap, or synapse,
between two neurons and bind to protein
receptors, which enable various functions and
allow the brain and body to be turned on and off.
• Some neurons have thousands of receptors that
are specific to particular neurotransmitters.
• Foreign chemicals, like THC, can mimic or block
actions of neurotransmitters and interfere with
normal functions.
In your brain, there are groups of
cannabinoid receptors concentrated
in several different places. These
cannabinoid receptors have an
effect on several mental and
physical activities, including:
• Short-term memory
• Coordination
• Learning
• Problem solving
Cannabinoid receptors are activated by a neurotransmitter
called anandamide. Anandamide belongs to a group of
chemicals called cannabinoids. THC is also a cannabinoid
chemical. THC mimics the actions of anandamide, meaning
that THC binds with cannabinoid receptors and activates
neurons, which causes adverse effects on the mind and body.
• High concentrations of
cannabinoid receptors exist in
the hippocampus, cerebellum
and basal ganglia.
• The hippocampus is located
within the temporal lobe and is
important for short-term
memory.
• When the THC binds with the
cannabinoid receptors inside the
hippocampus, it interferes with
the recollection of recent events.
•THC also affects coordination, which is controlled by the
cerebellum.
•The basal ganglia controls unconscious muscle movements,
which is another reason why motor coordination is impaired
when under the influence of marijuana
Cocaine (Crack)
Cocaine acts upon a part of the brain called the ventral
tegmental area (VTA).
It interferes with a chemical
messenger in the brain called
dopamine, which is involved in the
body's pleasure response.
Dopamine is released by cells of
the nervous system during
pleasurable activities such as eating
or having sex.
Once released, dopamine travels across a synapse, and
binds to a receptor on a post-synaptic neurone.
• This sends a signal to that
nerve cell, which produces
a good feeling. Under
normal conditions, once the
dopamine sends that signal
it is reabsorbed by the
neuron that released it. This
reabsorption happens with
the help of a protein called
the dopamine transporter.
Crack interrupts this cycle. It attaches to the dopamine
transporter, preventing the normal reabsorption process. As
dopamine builds up in the synapse, it continues to
stimulate the receptor, creating a lingering feeling of
exhilaration or euphoria in the user.
• Addictive drugs chemically alter a part of
the brain called the reward system.
Using Cocaine as an example of addiction:
The drug traps the chemical dopamine in the spaces between nerve cells.
Dopamine creates the feelings of pleasure we get from enjoyable activities
such as eating and having sex. But in cocaine users, dopamine keeps
stimulating those cells, creating a "high" -- a euphoric feeling that lasts
anywhere from five to 15 minutes. But then the drug begins to wear off, leaving
the person feeling let-down and depressed, resulting in a desire to smoke more
crack in order to feel good again.
The brain responds to the dopamine overload of the crack high by either
destroying some of it, making less of it or shutting down its receptors. The result
is that, after taking the drug for a while, crack users become less sensitive to it
and find that they must take more and more of it to achieve the desired effect.
Eventually, they cannot stop taking the drug because their brains have been
"rewired" -- they actually need it in order to function.
Sources
• Slide 2
http://www.mun.ca/biology/desmid/brian/BI
OL2060/BIOL2060-13/1322.jpg
• Slides 11 to 18 adapted from:
• http://health.howstuffworks.com/marijuana.
htm
• http://health.howstuffworks.com/crack3.ht
m