Summary
Nur 243 Neuropharmacology Summary
- Course
- NUR 243
- Institution
- University Of Rhode Island
This is a comprehensive and detailed summary Neuropharmacology from the book Pharmacology for Nursing Care by Richard A. Lehne.
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BACKGROUND KNOWLEDGE→the study of drugs that alter processes controlled by the nervous system; drugs
produce effects similar to excitation or suppression of neuronal activity;
The impact of a drug on a neuronally regulated process is dependent on the ability to
directly or indirectly influence receptor activity on target cells
Postsynaptic Cell:
can be another neuron, a muscle cell, or cell w/in secretory gland; if the postsynaptic
cell is another neuron it may increase or decrease firing rate; if it’s a muscle cell it
may contract or relax; if the cell is glandular it may decrease secretion
Receptors:
neurons alter receptor activity by releasing transmitter molecules which diffuse
across the synaptic gap and bind to receptors of the postsynaptic cell; neurons
depend on target cells to have a receptor that the neuron can alter activity
Process of neuron influencing behavior of postsynaptic cell→
1. Axonal conduction: the process of conducting an action potential down the
axon of the neuron; drugs that alter this process are NOT selective (all nerves
along axon will be affected)
→Local Anesthetics: drugs that work by decreasing axonal conduction; produce
non selective inhibition of axonal connection and thereby suppress
transmission in any nerve they reach; valuable but limited indications
***only neuropharmacological drug to not produce their effects by directly or
indirectly altering receptor activity through synaptic transmission
2. Synaptic transmission: the process by which information is carried across the
gap between the neuron and postsynaptic cell; most neuropharmacological
agents/drugs act by altering synaptic transmission; this makes the production
of effects much more selective than axonal conduction
→ axons don’t differ from each other but synapses do; synapses at different
sites have different transmitters
FIVE STEPS OF SYNAPTIC TRANSMISSION:
1. Transmitter Synthesis:
-for the whole process to take place molecules of transmitters must be
present in the nerve terminal; molecules in presynaptic nerve terminal
synthesize the transmitter
-drugs can increase transmitter synthesis (increasing receptor
activation), decrease it (decreasing receptor activation), or create super
transmitters (synthesis of transmitter molecules making it more
effective than transmitter itself)
, -in increased transmitter synthesis storage vesicles will store
abnormally high transmitter amounts; when action potential gets to
axon terminal more transmitters will be released allowing more of
them to be available to receptors at postsynaptic cell increasing
activation of those receptors)
-Some drugs can cause neurons to synthesize transmitter molecules
that have a different structure than normal- these drugs act as
substrates for enzymes in the axon terminal and convert into
→ molecules whose ability to activate receptors is greater
than that of a naturally occurring transmitter at a particular site
ultimately increasing receptor activation
Transmitter Storage:
-one transmitter is synthesized it must be stored until its time of
release; stored in vesicles in axon terminal
-drugs can decrease the storage of transmitters causing a decrease in
receptor activation by interfering with the transmitter storage
Transmitter Release:
-triggered by the arrival of an action potential at the axon terminal;
each action potential causes only a small fraction of all vesicles present
in the terminal to discharge their contents
-drugs can inhibit (decrease receptor activation) or promote (increases
receptor activation) transmitter release
-amphetamines (CNS stimulants) promote transmitter release
-Botulinum toxin inhibits transmitter release
2. Receptor Binding:
-following release, the transmitter molecules diffuse across the
synaptic gap and then undergo reversible binding to receptors of the
postsynaptic cell→ cascade of events altering behavior of postsynaptic
cell
-many drugs act directly at receptors- they can bind to receptors and
cause activation, bind to receptors and block activation, bind to receptor
components and enhance receptor activation by the natural transmitter
at the site
-agonists→ drugs that directly activate receptors (morphine-affects cns,
epinephrine-affects the cardiovascular system, insulin- affects diabetes)
-antagonists→ drugs that prevent receptor activation (naloxone-used to
treat overdose with morphine type drugs, antihistamines, propranolol-
used to treat htn, angina pectoris, and cardiac dysrhythmias)
, - drug that enhances receptor activation→ benzodiazepines: diazepam
and valium- used to treat anxiety, seizure disorders, muscle spasms
Termination of Transmission→ (Removal of transmitter from synaptic gap)
-transmission is terminated by dissociation of transmitter from its receptors then
the free transmitter is removed from the synaptic gap
-drugs can interfere with the termination of transmitter action by blockade of
transmitter reuptake or inhibition of transmitter degradation thereby increasing
receptor activation
1. Reuptake:axon terminals contain pumps that transport transmitter molecules
back into same neuron they were released
2. Enzymatic Degradation: synapse contains large quantities of
transmitter-inactivating enzymes
3. Diffusion: simple diffusion away from synaptic gap; very slow; little
significance
EFFECTS: Synaptic transmission:
-effect on receptor function equivalent to that produced by the natural
neurotransmitter at a particular synapse
-If a drug’s effects mimic effects of natural neurotransmitter the receptor activation
would be increased
-If a drug’s effects were equivalent to reducing the amount of natural transmitter
available for receptor binding the receptor activation would be decreased
-receptor activation can also make a process go slower
→ HR will decrease when the endogenous neurotransmitter acetylcholine
activates cholinergic receptors on the heart (drug that mimics acetylcholine
at receptors on heart will cause the heartbeat to slow)
THE PNS SUBDIVISIONS:
1. Somatic Motor System: controls voluntary movement of muscles
2. Autonomic Nervous System: controls involuntary processes; regulates the
heart, secretory glands (saliva, sweat, gastric, bronchial glands), and smooth
muscle (muscles of the bronchi, blood vessels, urogenital system, and GI tract)
a. Parasympathetic Nervous System:
-“housekeeping”; digestion of food and excretion of wastes, controls vision and
conserves energy by reducing CO
-Drugs used to affect PNS are for their effects on the GI Tract, bladder, and
eye,and occasionally the heart and lungs
-A variety of poisons act by mimicking blocking effects of parasympathetic
stimulation (insecticides, nerve gases, toxic compounds in certain mushrooms
and plants)
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