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The monoamines are generally stored in vesicles until they are ready to be released into the nerve synapse. When they are released, they may bind with receptors on post synaptic neurons as would be expected causing an action potential in that neuron. After binding, the neurotransmitter is released from the receptor
into the synapse. Two enzymes are responsible for
the breakdown of monamines: monoamine oxidase (MAO) which breaks down serotonin, dopamine and norepinephrine and catechol-o-methyl tranferase which breaks down norepinephrine and dopamine. These enzymes are present in the nerve synapse and inside of the neuron. After release from binding into the nerve synapse, the monoamine neurotransmitter is taken
up into the nerve and re-manufactured to be stored in vesicles within the neuron ready to be released again.
Generally, antidepressants which are the most commonly used medication for the treatment of emotional disorders in animals involving impulsivity, aggression, anxiety and fear have their effect by blocking the reuptake of the neurotransmitter into the cell thus increasing the ratio of neurotransmitter to receptor or blocking the dissolution of the nerve transmitter itself by blocking the effect of the particular enzyme that breaks it down.
The most well accepted theory as to why antidepressants are effective involves the depletion of neurotransmitters in the brain of affected animals. An aggressive animal is presumed to have a depletion of serotonin, for example. The depletion of serotonin causes an upregulation of the postsynaptic neurotransmitter receptors. Think of this as an increase in the number
of receptors available for binding. Administration of selective serotonin reuptake inhibitors (SSRIs) such as  uoxetine and sertraline, cause an increase in the amount of serotonin available for binding increasing the ratio of serotonin to receptors in the nerve synapse. This causes the down regulation of the receptors on the post synaptic neuron increasing the ratio of serotonin to receptors.
Serotonin reuptake inhibitor/antagonists (SARI) inhibit
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the serotonin reuptake transporter and antagonize the serotonin 2A receptor on the postsynaptic neuron. SARIs, such as trazodone, block the serotonin reuptake inhibitor at the presynaptic neuron to a lesser extent than the SSRIs, however they have a powerful action in the blockade of the serotonin 2A receptor. The blockade
of the serotonin 2A receptor indirectly increases the stimulation of the presynaptic neuronal autoreceptor.
Monoamine oxidase inhibitors such as selegiline (Anipryl®) function by blocking the breakdown of dopamine by inhibition of MAO. Tricyclic antidepressants such as clomipramine (Clomicalm®) and amitriptylline (Elavil®) inhibit the reuptake of norepinephrine and serotonin. In addition, they cause a blockade of muscarinic cholinergic receptors, H1 histamine receptors and alpha1 adrenergic receptors. The multi-action of this class of medications causes many clinicians to avoid using them in older patients. Patients may experience dry mouth, and sedation among other side effects.
There are at least  ve benzodiazepine receptor subtypes. Different receptor subtypes are found in different
areas of the body. For example, the benzodiazepine 1 receptor is found primarily in the cerebellum. The GABA A receptor is allosterically modulated by multiple other receptors including the benzodiazepine receptor site. So, benzodiazepines have their effect primarily on GABA. When GABA and a benzodiazepine bind together at the GABA A receptor, the effect is greatly ampli ed. When
a benzodiazepine binds by itself, there is no effect on
the GABA A receptor. When GABA binds by itself to its own receptor, the effect is substantially less than when
a benzodiazepine is also bound to the benzodiazepine receptor site on the GABA receptor. Like many team efforts, the  nal outcome is much greater than the sum of its parts.
Acepromazine is a phenothiazine neuroleptic agent and a postsynaptic dopamine antagonist. Through it’s action on dopamine 2 receptors, it causes sedation. In veterinary medicine, it is used as a sedative. It is not used as an anxiolytic.
Clonidine is a centrally acting alpha 2 agonist affecting alpha 2, A, B and C receptors. It reduces in SNS arousal and nociceptive pain at lower dosages; and causes sedation at higher dosages. It can be used as a pre visit pharmaceutical or a short term arousal reliever. 3
Often, attempting to understand how a medication works can seem tedious. However, once you understand how a given medication affects the body, how it affects other neurotransmitters indirectly, or the requirement of one neurotransmitter for the other to cause an effect, it makes the selection of medications much more ef cient and effective.

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