Neuropharmacology

When chemicals contact the surface of a neuron, they change the balance

of ions (electrically charged atoms) between the inside and outside of the cell membrane.

When this change reaches a threshold level, this effect runs across the cell's membrane to the axon.

When it reaches the axon, it initiates the action potential, which is a rapidly moving exchange of ions.

No. Bupropion (aka Wellbutrin) is known as an atypical antidepressant in that it prevents the reuptake of serotonin, norepinephrine, and dopamine (to a lesser extent). Typical tricyclic antidepressants only block reuptake of serotonin and norepinephrine. It's unique dopamine reuptake inhibition capability allows it to be used to treat nicotine addiction (marketed as Zyban) and, to some extent, attention deficit disorder. Furthermore, it lacks the classic three ring chemical structure of tricyclic antidepressants (TCAs).

Here are a list of some common TCAs:

imipramine (tofranil)

amitriptyline (Elavil/Endep)

doxepin (adapin)

nortrypyline (Pamelor), etc

The clearance of alcohol from the body is not affected by citalopram. SSRIs like citalopram work on serotonin- and norepinephrine- synthesizing neurons and slowly cause an increase in the synaptic availability of both of these neurotransmitters. The role of serotonin in the brain is modulatory, i.e., it facilitates the release of other neurotransmitters in cerebral cortex; whereas alcohol is a CNS depressant. It binds to and and opens GABA-gated channels enhancing inhibitory synaptic transmission. Alcohol is therefore counterproductive to the effects of SSRIs - but depending on the amount consumed this may not necessarily a bad thing during the acute phase of SSRI therapy when anxiety is often briefly exacerbated.

Since their discovery in the 1950s, tricyclic antidepressants have been used to treat mental depression.

By having fun! Massage, hugging, kissing, holding hands, controlled sex (like tantra), hanging with friends, cuddling, eye gazing, etc. A good book for reference is The Chemistry of Connection.

Selective serotonin reuptake inhibitors (SSRIs) achieve their therapeutic effect by modifying synaptic availability of the neurotransmitter serotinin. This is accomplished, first of all, by blocking the proteins that normally transport serotonin back into the cells that release them (presynaptic cell). In doing so, synaptic levels of serotonin are temporarily boosted. This phase is normally associated with an acute increase in anxiety. However, this subsides over several days as subtypes of postsynaptic5-HT receptors down-regulate in response to the excess serotonin. During this time another kind of protein called an autoreceptor (in this case 5-HT1 autoreceptors) located on the presynaptic cell begins to desensitize. Normally these types of receptor proteins provide a kind of feedback mechanism that limits the production of neurotransmitters.With these desensitized, the cell receives less feedback and the rate of serotonin synthesis and release increases. Since not all postsynaptic 5-HT receptors down-regulate in response to increased synaptic levels of serotonin - the ones that don't are able to bind more serotonin and this is thought to account for the longer term effects of SSRIs. Similar processes occur as 'secondary effects' on cells that release noradrenaline - as these express 5-HT2a heteroceptors - and this also is thought to contribute to their therapeutic efficacy. The reason serotonin is targeted by SSRIs in the first place is that the same regions of the brain that contain a high density of serotinin-releasing neurons (Raphe nuclei) are known to regulate mood directly as well as indirectly via interactions with other brain areas and neurotransmitter systems (like noradrenaline and dopamine in other parts of the limbic system as well as frontal cortex). However, because it's so complex, and no two brains are the same, responses to SSRIs can vary. In most cases of mild to moderate depression they offer a benefit .

nitrous oxide : lower solubility

halothane : higher solubility

The receptors are located primarily in the limbic system of the brain. The limbic system is a region in the brain containing structures such as the hippocampus and amygdala. The region plays a role in a variety of functions such as emotion and behavior, long-term memory and smell.

Yes. Anything that comes into our bodies MAY contain pathogens.

a central carbon, a hydrogen atom, an amino group, and a carboxyl group

Inhibitory neurotransmitters prevent the firing of neurons by binding with certain receptors, causing the influx of chloride ions to hyperpolarize the neuron. When this happens, it requires a much larger excitatory signal to override the inhibitory effects in order to allow the neuron to fire.

No. An amino group contains one nitrogen atom bonded to two hydrogen atoms, and are found in amino acids. Glycerol is a molecule that when bonded to three fatty acids, forms a triglyceride molecule.

When an acetylcholinesterase (AChE) inhibitor binds with acetylcholinesterase, regardless of whether it is reversible or irreversible, it prevents the ability of AChE to bind with acetylcholine (ACh) and break it down. Therefore, ACh accumulates in the synaptic gap, causing the postsynaptic neuron or muscle cell to fire/contract repeatedly. As this happens, a fatigue effect is reached due to depletion of chemical energy stores (ATP, etc.), and weakness results from the reduced ability of neurons/muscles to respond to further stimulation.

There are approximately 150 USP units in 1 mg of Heparin. The conversion factor between USP units and mg can vary based on the type of Heparin being used, so it is best to consult the specific product's labeling for an accurate conversion.

Clozapine is not a tricyclic antidepressant, but rather an atypical antipsychotic medication.

Atypical antipsychotics differ from typical antipsychotics by the range of receptors that are modulated or affected.

Typical antipsychotics primarily inhibit Dopamine 2 (DA2) receptors. Atypical antipsychotics block a host of receptors, namely serotonin and dopamine, but also including alpha and histamine receptors in varying proportions.

The benefit of Clozapine is that there is a lesser degree of dopamine inhibition that is aimed at reducing certain side effects.