All right, so today we're going to be talking about antidepressants. Thank you everybody who's supporting the

podcast, the really nice comments, everything I really appreciate it and thank you so much for today's sponsor

True Learn. So let's talk about antidepressants, SSRIs, SNRIs, TCA's, MAOIs, atypical

antidepressants. There's a lot to know here so I'll keep it as high yield as possible and

throwing a bunch of pneumotics to help you remember what you really need to know.

Before we get started, let's really quickly talk about a couple basic fundamental concepts that will help you better understand the meds.

We'll go over today, let's start with the monoamine hypothesis. So the

monamine hypothesis dates back to the 1950s, basically states that the

underlying pathophysologic basis of depression is essentially a depletion in levels of

serotonin or epinephrine or dopamine in the CNS. Now we've learned a lot over the years

and we know that's not all that's going on there's definitely more to it than just a

chemical imbalance but understanding this basic concept it's going to help you

better understand the meds will go over today and their proposed mechanism of

action so before we start with the first class of meds, let's really

quickly run down this whole neurotransmitter exchange in the brain. So we have two

neurons close together. One neuron is the pre-synaptic neuron, the other is the post-synaptic neuron.

They're separated by a teeny tiny space

called a synaptic cleft.

So the pre-synaptic neuron, it's got all the goodies,

depending on which type of neuron we're referring to,

serotonergic, etc.

It's stocked with either dopamine, serotonin, or epinephrine, and they're all stored in these

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