Wellbutrin-sr Drug Uses

Wellbutrin SR (Anti Depressant) is a pharmaceutical prescription antidepressant, which acts directly on the brain and other nerve cells. It is also used to treat ADHD (Attention Deficit Disorder), bipolar depression, chronic fatigue syndrome, cocaine addiction, nicotine addiction, and lower back pain. Also, aids in quitting smoking (identical to Zyban). It is chemically unrelated to tricyclic, tetracyclic, selective serotonin re-uptake inhibitor, or other known antidepressant agents.

How Taken

Wellbutrin SR comes as a tablet to take it orally. It is usually taken one to three times a day and may be taken with or without food. Do not crush, chew, or divide Wellbutrin SR. Do not stop taking Wellbutrin SR without talking to your doctor, especially if you have taken large doses for a long time. Your doctor probably will want to decrease your dose gradually. This drug must be taken regularly for a few weeks before its full effect is felt.

Wellbutrin-sr Warnings/Precautions

Before taking Wellbutrin SR, tell your doctor if you have: history of seizures or head injury or brain tumor, heart disease, liver or kidney disease, eating disorder, diabetes, alcohol dependence, any allergies, the intent to quit smoking. Because of the possibility this drug will make you dizzy and affect coordination, do not drive or operate machinery until you get used to the drug's effects. Limit or avoid consumption of alcoholic beverages; alcohol can increase your risk of seizures. Chronic alcohol users who suddenly stop the intake of alcohol while taking Wellbutrin SR may increase the risk of having seizures. Suddenly stopping certain tranquilizers is not recommended because doing so may increase the risk of having seizures. If you are over 65 years old you may be more sensitive to the effects of this drug. Tell your doctor if you are pregnant or plan to become pregnant before taking this drug. This drug passes into breast milk. Because of the potential risk to the infant, breast-feeding while using this drug is not recommended. Consult your doctor before breast-feeding.

Wellbutrin-sr Missed Dose

Take any missed dose as soon as possible but not if it is within 4 hours of the next dose. If it is time for the next dose, skip the missed dose and resume your regular schedule. Do not "double-up" the dose.

Wellbutrin-sr Possible Side Effects

This medication is generally well tolerated. Dry mouth, headache, increased sweating, nausea/vomiting, constipation, anxiety, fatigue and blurred vision may occur. If these effects persist or worsen, notify your doctor. Report promptly: unusual weight loss or gain, palpitations, agitation, trouble sleeping. Unlikely but report promptly: tremor, dizziness, fainting, mood changes, slowed movements, difficulty urinating, decreased sex drive, and drowsiness. Very unlikely but report promptly: seizures, mental problems, fever, muscle aches, yellowing of the eyes or skin. In the unlikely event you have an allergic reaction to this drug, seek medical attention immediately. Symptoms may include trouble breathing, rash, itching, swelling, or severe dizziness. If you notice other effects not listed above, contact your doctor or pharmacist.

Wellbutrin-sr Storage

Store at controlled room temperature, 20° to 25°C (68° to 77°F). Dispense in a tight, light-resistant container.

Wellbutrin-sr Overdose

Seek emergency medical attention if an overdose is suspected. Symptoms of a Wellbutrin SR overdose include seizures, hallucinations, loss of consciousness, weakness, a fast heartbeat, and heart attack.

More Information

Dizziness may be more likely to occur when you rise from a sitting or lying position. Rise slowly to prevent dizziness and a possible fall. Too much of this medicine can increase the risk of a seizure. Limit the consumption of caffeine while taking Wellbutrin SR.

Disclaimer

This drug information is for your information purposes only, it is not intended that this information covers all uses, directions, drug interactions, precautions, or adverse effects of your medication. This is only general information, and should not be relied on for any purpose. It should not be construed as containing specific instructions for any particular patient. We disclaim all responsibility for the accuracy and reliability of this information, and/or any consequences arising from the use of this information, including damage or adverse consequences to persons or property, however such damages or consequences arise. No warranty, either expressed or implied, is made in regards to this information.

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A new study has revealed more about how the medication ketamine, when used experimentally for depression, relieves symptoms of the disorder in hours instead of the weeks or months it takes for current antidepressants to work. While ketamine itself probably won’t come into use as an antidepressant because of its side effects, the new finding moves scientists considerably closer to understanding how to develop faster-acting antidepressant medications — among the priorities of the National Institute of Mental Health (NIMH), part of the National Institutes of Health.
Ketamine blocks a receptor called NMDA on brain cells, an earlier NIMH study in humans had shown, but the new study in mice shows that this is an intermediate step. It turns out that blocking NMDA increases the activity of another receptor, AMPA, and that this boost in AMPA is crucial for ketamine’s rapid antidepressant actions. The study was reported online in Biological Psychiatry on July 23, by NIMH researchers Husseini K. Manji, MD, Guang Chen, MD, PhD, Carlos Zarate, MD, and colleagues.
“Our research is showing us how to develop medications that get at the biological roots of depression. This new finding is a major step toward learning how to improve treatment for the millions of Americans with this debilitating disorder; toward eliminating the weeks of suffering and uncertainty they have to endure while they wait for their medications to work,” said NIH Director Elias Zerhouni, M.D.
Almost 15 million American adults have a depressive disorder. During the long wait to begin feeling the effects of conventional medications, patients may worsen, raising the risk of suicide for some. Depressive disorders also affect children and adolescents.
By aiming new medications at more direct molecular targets, such as NMDA or AMPA, scientists may be able to bypass some of the steps through which current antidepressants indirectly exert their effects — a roundabout route that accounts for the long time it takes for patients to begin feeling better with the conventional medications.
While ketamine appears to achieve this, it is an unlikely candidate to become a new treatment for depression, because of the side effects it can cause in humans, including hallucinations. It is approved as an anesthetic by the Food and Drug Administration at much higher doses than those given in the study, but its use is limited because it may cause hallucinations during recovery from anesthesia.
Both NMDA and AMPA are receptors for the neurotransmitter glutamate, one of the chemical messengers that enable brain cells to communicate with each other. The glutamate system has been implicated in depression recently, leading to efforts to unravel its molecular machinery in search of abnormalities and of better targets for antidepressant medications.
This focus on the glutamate system is a departure from the thinking that led to currently available antidepressants, which are thought to relieve depression through a lengthy trickle-down process of biochemical reactions that affect the circuitry underlying depression.
The fact that NMDA and AMPA receptors are part of the glutamate system and that targeting them directly led to such rapid, sustained relief of depression-like behaviors in this study — and that a single dose of ketamine did the same in humans in the earlier study — suggests that they are probably the key targets for antidepressant medications.
“In any other illness of depression’s magnitude, patients aren’t expected to just accept that their treatments won’t start helping them for weeks or months. The value of our research on compounds like ketamine is that it tells us where to look for more precise targets for new kinds of medications that can close the gap,” said NIMH Director Thomas R. Insel, MD. “We’re making tremendous progress.”
To conduct the new study, researchers induced depression-like behaviors in mice; for example, the mice gave up after being forced to engage in hopeless tasks, such as prolonged swimming. A dose of ketamine reversed the depression-like behaviors for at least two weeks.
When the researchers gave the mice a substance that blocks the AMPA receptor beforehand, ketamine was not able to reverse the depression-like behaviors. The boost in AMPA thus appears to be a necessary ingredient for ketamine’s antidepressant effects.
In a related experiment, the scientists used two different compounds instead of ketamine to try to block just one part of the NMDA receptor, an even more precise target. These other compounds also reduced depressive behaviors, suggesting that it may be feasible to develop other fast-acting antidepressants without ketamine’s side effects.
“Today’s antidepressant medications eventually end up doing the same thing, but they go about it the long way around, with a lot of biochemical steps that take time. Now we’ve shown what the key targets are and that we can get at them rapidly,” said Zarate. “Ketamine probably can’t become the medication of choice, but this research is leading to some very real possibilities for a whole new generation of antidepressant medications.”

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