hey everyone right here welcome back to our last video in the pharmacology series and this one will be about central nervous system pharmacology so you may be thinking we already talked about the central nervous system when we did an autonomic nervous system pharmacology but remember the receptors that the autonomic nervous system drugs were influencing were cholinergic and adrenergic receptors both at the ganglion and at the target organ but central nervous system drugs act in the central nervous system and not peripherally so they target entirely different receptors within the brain and the spinal cord and therefore have entirely different effects and we have a brand new set of receptors that I'll talk about in this video now I will say that this is going to be a bit of an oversimplification because central nervous system pharmacology gets extremely complex with neuronal signaling circuits and synapses but luckily for the board exam we absolutely do not have to worry about any of those complexities but what we do need to understand is that there's a continuum of central nervous system excitability from completely no energy to way too much energy and we all operate along this continuum and drugs can modify we're on the continuum you are the most simplified way I can put it is that dopamine and serotonin receptors when activated generally caused the CNS to get more excited and gaba receptors when activated caused the CNS to get more depressed and just the opposite is true if you block those receptors our first category of CNS drugs are the antipsychotics antipsychotics are used to treat schizophrenia which is a chronic and severe mental disorder the brain is too active and it causes disorganized thought and speech so we need to come brain down now the receptors were concerned with our dopamine and serotonin receptors serotonin also sometimes known by its chemical name 5-hydroxytryptamine or 5-ht but let's start with the first generation antipsychotics they act by blocking the d2 receptor which is a specific subtype of the dopamine receptor haloperidol and phenothiazines are two examples of a first generation antipsychotic they have anticholinergic fighter flight side effects and also long-term use can cause extra pyramidal stimulation leading to what's known as tardive dyskinesia this stiff and jerky movements of your face and body that you can't control so they came out with second-generation antipsychotics that don't have as many side effects these antipsychotics block both dopamine receptors and serotonin receptors or 5ht receptors so both of these classes of drugs seek to decrease activity of the dopaminergic pathway and in the case of second generation the serotonergic pathways antipsychotics are also sometimes used as antiemetic drugs which means they help prevent nausea and vomiting our second group of CNS drugs are the antidepressants antidepressants are used to treat depression where the CNS generally needs to be stimulated and excited antidepressants do this by increasing the presence of mono amines which from our ans video includes dopamine norepinephrine epinephrine serotonin and histamine and we have have a couple of categories of antidepressants here so the first are the SSRIs or selective serotonin reuptake inhibitors this first category blocks the reuptake of serotonin meaning there's less recycling of the serotonin molecules and there's more serotonin left in the synapse to activate the serotonin receptors SNRIs or tricyclic antidepressants block the reuptake of both serotonin and norepinephrine meaning there's more both neurotransmitters in the synapse to activate their respective receptors and it makes sense that we're getting anticholinergic side effects because we're leaving mono amines around and we're getting these extra norepinephrine for instance that can activate those ANS receptors and cause anticholinergic or adrenergic side effects the last category here are the monoamine oxidase inhibitors monoamine oxidase is the enzyme that degrades and essentially cleans up neurotransmitters in your brain once they've completed their job but if you inhibit this enzyme there are more mono amines that stay active for a longer amount of time and so they can do their job longer and thus create a more excitatory effect in the central nervous system and lastly we have lithium which is the drug of choice for manic depression or bipolar disorder and this can come up as a simple recollection question on the board exam or you just have to know that lithium is used for treating mania or manic depression alright our third group of CNS drugs are the angle it ixora sedatives and they include both benzodiazepines and barbiturates so let's talk about each of these specifically benzodiazepines bind to sites on the GABA a receptor so here we have benzodiazepines binding to a specific site on the GABA subtype a receptor this increases the binding of the gaba neurotransmitter which in turn activates this whole receptor and promotes the influx of chloride ions into the cell so this ultimately inhibits and slows down the central nervous system if you're curious gaba stands for gamma amino butyric acid so benzodiazepines are the ideal drug for oral sedation in the dental clinic they're safer they have less addiction potential a larger therapeutic index or window and less respiratory depression as compared to their counterparts barbiturates one of the more commonly prescribed to relieve dental anxiety prior to an appointment is diazepam the trade name valium propylene glycol is commonly present in IV or intra benzodiazepines and served to or intravenous benzodiazepines and serves to make them more soluble and stable but they can also induce thrombophlebitis in large veins which are these blood clots that cause pain and inflammation barbiturates have the same mechanism of action as benzodiazepines but with more undesirable side effects barbiturates are specifically contraindicated in patients with intermittent porphyria which is a blood forming disease because they enhance porphyrin synthesis and will aggravate the disease barbiturate overdose also causes respiratory depression and thiopental is one of the specific barbiturates and it has a quick onset and short duration of action which is also undesirable because its effect ends as soon as it's redistributed out of the brain so it has quick onset short duration of action and a shorter window in order to have its effect remember benzodiazepines barbiturates are sedatives and Anzio lytx or anti-anxiety medications they are not analgesics so they provide no pain relief and the last group of CNS drugs are the general anesthetics these are used to induce a medically controlled coma for more in-depth surgeries so the onset of general anesthesia is inversely proportional to the solubility of the anesthetic in your blood in other words these drugs are leaky and they leak out of your blood and the more soluble they are the more you'll need to reach a level in your brain that triggers effective anesthesia so the more soluble the agent and blood the more you'll need to reach critical tension in the brain the four stages of general anesthesia that you may need to know for the board exam are analgesia or pain relief delirium surgical anesthesia which is the desirable stage and an overdose at medullary paralysis halothane is an example of a general anesthetic and it's associated with hepatotoxicity which means it can be toxic to the liver and sometimes they'll include a board exam question on Parkinson's disease so let's talk about it briefly Parkinson's is a result of dopamine deficiency in the brain so the remedy is to increase dopamine in the brain the problem is injected dopamine cannot pass the blood-brain barrier but it's precursor levodopa can the other problem is that levodopa is quickly converted to dopamine by this enzyme dopa decarboxylase so in order to keep levodopa in its desirable state it's administered along with carbidopa to block this enzyme allowing levodopa across the blood-brain barrier and then it can be converted to dopamine once in the brain where it can be used to treat Parkinson's so the combination of levodopa and carbidopa is required you should also know that levodopa is a sympathy mimetic which from our ans video we know will produce sympathetic stimulation in the periphery all right so that's it for this video thank you so much for watching if you're interested in supporting my channel please check out my patreon page a huge thank you to Michael Raja ion's Lao David Jayden Gannett and all of my patrons for their support you can unlock extras like access to my video slides to take notes on and practice questions for the board exam so go check that out the link is in the description thanks again for watching I'll see you in the next video