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58413
Antidepressant Drugs
Description
Biological (Depression & Schizophrenia) Mind Map on Antidepressant Drugs, created by n.c.wetmore on 26/04/2013.
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biological
depression & schizophrenia
biological
depression & schizophrenia
Mind Map by
n.c.wetmore
, updated more than 1 year ago
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n.c.wetmore
over 11 years ago
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Resource summary
Antidepressant Drugs
Types of Antidepressants
Tricyclics
operate by blocking transporter proteins that reabsorb serotonin, dopamine & norepinephrine into presynaptic neurone after release
results in prolong the presence of NT in synaptic cleft, continue stimulating postsynaptic cell
Also block histamine receptors, acetycholine receptors & certain sodium channels
blocking histamine causes drowsiness
blocking acetycholine leads to dry mouth and hard to urinate
block sodium channels causes heart irregularities
Selective Serotonin Reuptake Inhibitors (SSRIs)
specific to NT serotonin
prozac blocks reuptake of serotonine
produce milder side effects than try but effectiveness is about the same
Serotonin Norepinephrine Reuptake Inhibitors (SNRIs)
block the reuptake of serotonin and norepinephrine
Monoamine Oxidase Inhibitors (MAOIs)
block enzyme monoaime oxidase (MASO
presynaptic terminal enzyme that metabolises catecholamines and serotonin into active forms.
when block this enzyme the presynaptic terminal has more of its transmitter available for release
last resort after try and SSRI
must avoid foods containing syramine (cheese etcs
combo of tyramine and MAOIs increases blood pressure
atypical antidepressant
buropion inhibits reuptake of dopamine and to some extent norepinephrine but not serotonin
St Johns Wort
advantage of being less expensive than anti depressants
advantage/disadvantage available without a prescription
can end up taking inappropriate amounts which is dangerous
all mammals have liver enzyme breaks down plant toxin
increases effectiveness of that enzyme
this also breaks down medicines and makes them ineffective
How do Antidepressants work
increase presence of serotonin or other NT at sun apse so problem is too little of the NT
blood metabolites, people with sep have approx normal levels of release of NT
some studies show people with dep have increase in serotonin release
BARTON ET AL 2008
possible to decrease serotonin levels suddenly by consuming all amino acids except tryptophan, procurer to serotonin
decrease in serotonin doesn't provoke any feelings of dep
NEUMEISTER ET AL 2004
would expect drugs to have diff effects but most have equal effects on NT
two studies, patients failed respond to antidep drug
one added second drug and other switched
patients who didn't respond to first, responded to second
RUSH ET AL 2006
neither did control group so no conclusions found
time course is threat in term of NT
antidep produce effects on NT in synapses within min-hrs depending on drug
takes 2 weeks for it to start working
delay of benefits suggests increase level of NT at synapses doesn't explain the benefits of drugs
focus on neurotophins
neurotophins aid in survival, growth and connections of neurons
most with deo have lower levels of neurotrophin called brain-derived neutotrophic factor BDNF
important for synaptic, plasticity,learning and proliferation of new neurones in hippo
low BDNF people with dep have smaller hippo, impaired learning, reduced production of new hippo neurons
prolonged use of antidep increases BDNF prod and improves learning and formation of new neurons
takes weeks
time course for BDNF and changes in hippo matches time course for behavioural recovery
procedures block neuron production also block behavioural benefits of antidep drugs
BDNF alone doesn't auto elevate mood but helps by facilitating new learning that builds new synapses and removes old ones
mode of action explains why antidep help people in dep but fail to elevate mood for normal people
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