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NEUROTROPIC DRUGS
By CJEVC
MONOAMINES:
A group of structurally similar CNS neurotransmitters that
include the catecholamines (dopamine, norepinephrine)
and 5-hydroxytryptamine (serotonin).
Catecholamines: Dopamine and Norepinephrine
Serotonin - Another monoamine
PEPTIDES:
Substance -excitatory transmitter involved in spinal cord
pathways transmitting pain impulses
Endorphins, enkephalins, and dynorphins -endogenous
opioids,
Excitatory transmitters in certain brain synapses that
inhibit painful sensations
Substance P
1.
3. Storage of neurotransmitter
Example -antihypertensive drug
Reserpine (Serpalan, Serpasil) impairs the ability of adrenergic
terminals to sequester and store norepinephrine in
presynaptic vesicles.
4. Release
Either increase or decrease release of neurotransmitter from
the presynaptic terminal
Amphetamines increase presynaptic release of catecholamine
neurotransmitters (e.g., norepinephrine).
botulinum toxin (Botox) impair the release of acetylcholine
from the skeletal neuromuscular junction
5. Reuptake
Some chemical synapses terminate activity primarily by
transmitter reuptake.
7. Postsynaptic receptor
Antagonists can be used to block postsynaptic receptor to
decrease synaptic transmission.
Ex: beta blockers antagonists specific for the beta-adrenergic
receptors on the myocardium to treat hypertension
8. Presynaptic autoreceptors
There are also receptors on the Presynaptic terminal that
serve as a method of negative feedback in controlling
neurotransmitter release
The accumulation of neurotransmitter in the synaptic cleft
may allow binding to the presynaptic receptors and limit
further release of chemical transmitter
9. Membrane effects
Alter synaptic transmission by affecting membrane
organization and fluidity.
Sedative-Hypnotic and
Antianxiety Agents
Pharmacological Management
of Parkinson Disease
Levodopa
Dopamine does not cross the blood-brain barrier.
The immediate precursor to dopamine,
dihydroxyphenylalanine- dopa crosses the blood-brain
barrier quite readily.
Dopa, or levodopa (the L-isomer of dopa),
Upon entering the brain, levodopa is transformed into
dopamine by decarboxylation from the enzyme dopa
decarboxylase
The most effective single drug in the treatment of
Parkinson Disease
Most of the levodopa ends up as dopamine in the
peripheral circulation, and can cause gastrointestinal and
cardiovascular side effects
Behavioral Changes
Mental side effects have been reported; psychotic
symptoms, depression
Diminished Response to Levodopa
May be caused by a progressive increase in the severity of
Parkinson Disease rather than a decrease in drugs efficacy
Antihistamine drugs with anticholinergic properties are
also used
Less effective in treating parkinsonism, but have milder side
effects than their anticholinergic counterparts.
Amantadine (Symmetrel)
Originally developed as an antiviral drug
Ability to reduce parkinsonian symptoms discovered by
chance
Dantrolene Sodium
Only muscle relaxant available that exerts its effect
directly on the skeletal muscle
Impairs the release of calcium from the sarcoplasmic
reticulum within the muscle cell during excitation
Dantrolene is not prescribed to treat muscle spasms
caused by musculoskeletal injury.
Most common side effect of dantrolene - generalized
muscle
The use of dantrolene is sometimes counterproductive
because the increased motor function that occurs when
spasticity is reduced may be offset by generalized motor
weakness.
Can cause severe hepatotoxicity
Diazepam
Effective in reducing spasticity as well as muscle spasms
because this drug increases the inhibitory effects of GABA in
the CNS.
Adverse effects: sedation
patients with spasticity who do not want a decrease in mental
alertness will not tolerate diazepam therapy very well.
Extended use cause tolerance and physical dependence thus
long-term treatment should be avoided
Gabapentin
Developed originally as an antiseizure drug gabapentin
(Neurontin)
Decreases spasticity by inhibition in the spinal cord, thereby
decreasing excitation of the alpha motor neuron with
subsequent skeletal muscle relaxation.