Interesting.
Perhaps some folks here may have some feedback about various antidepressants they may have tried that include the neurotransmitter norepinephrine. I believe those were the tricyclic category of antidepressants. I know that the only medication I have used in that category was imipramine- more than 25 years ago. There are now, more recently, also the SNRI class of antidepressants that affect the reuptake of norepinephrine as well as serotonin. The most recognized meds in that category would be effexor and/or cymbalta.
Remember not to mix with MAOIs.

From Wiki

"Serotonin–norepinephrine reuptake inhibitors (SNRIs) are a class of antidepressant drugs used in the treatment of major depression and other mood disorders. They are sometimes also used to treat anxiety disorders, obsessive-compulsive disorder (OCD), attention deficit hyperactivity disorder (ADHD), chronic neuropathic pain, fibromyalgia syndrome (FMS), and for the relief of menopausal symptoms.

SNRIs act upon, and increase, the levels of two neurotransmitters in the brain known to play an important part in mood: serotonin, and norepinephrine. These can be contrasted with the more widely-used selective serotonin reuptake inhibitors (SSRIs) which act upon serotonin alone.

Overview of SNRIs

Venlafaxine (Effexor) – The first and most commonly used SNRI. It was introduced by Wyeth in 1994. The reuptake effects of venlafaxine are dose-dependent. At low doses (<150 mg/day), it acts only on serotonergic transmission. At moderate doses (>150 mg/day), it acts on serotonergic and noradrenergic systems, whereas at high doses (>300 mg/day), it also affects dopaminergic neurotransmission.[1]

Desvenlafaxine (Pristiq)[2] – The active metabolite of venlafaxine. It is believed to work in a similar manner, though some evidence suggests lower response rates compared to venlafaxine and duloxetine. It was introduced by Wyeth in May 2008.

Duloxetine (Cymbalta, Yentreve)[3] – By Eli Lilly and Company, has been approved for the treatment of depression and neuropathic pain in August 2004. Duloxetine is contraindicated in patients with heavy alcohol use or chronic liver disease, as duloxetine can increase the levels of certain liver enzymes that can lead to acute hepatitis or other diseases in certain at risk patients. Currently, the risk of liver damage appears to be only for patients already at risk, unlike the antidepressant nefazodone, which, though rare, can spontaneously cause liver failure in healthy patients. [4] Duloxetine is also approved for Major Depressive Disorder (MDD), Generalized Anxiety Disorder (GAD), chronic musculoskeletal pain, including chronic osteoarthritis pain and chronic low back pain (as of October, 2010), and is one of the only three medicines approved by the FDA for Fibromyalgia [1].

Milnacipran (Dalcipran, Ixel, Savella)[5] – Shown to be significantly effective in the treatment of depression and fibromyalgia. The Food and Drug Administration (FDA) approved milnacipran for treatment of fibromyalgia in the United States of America in January 2009, however it is currently not approved for depression in that country. Milnacipran has been commercially available in Europe and Asia for several years.

Levomilnacipran (F2695) – The levo- isomer of milnacipran. Under development for the treatment of depression in the United States and Canada.

Sibutramine (Meridia, Reductil) – An SNRI, which, instead of being developed for the treatment of depression, was widely marketed as an appetite suppressant for weight loss purposes.

Bicifadine (DOV-220,075) – By DOV Pharmaceutical, potently inhibits the reuptake of serotonin and norepinephrine (and dopamine to a lesser extent), but rather than being developed for the already-crowded antidepressant market, it is being researched as a non-opioid, non-NSAID analgesic.


SNRIs are approved for treatment of the following conditions:

Major depressive disorder (MDD)
Generalized anxiety disorder (GAD)
Social anxiety disorder (SAD)
Panic disorder
Neuropathic pain
Fibromyalgia
Chronic musculoskeletal pain.

The disease for which SNRIs are mostly indicated, Major Depressive Disorder, is thought to be mainly caused by decreased levels of serotonin and norepinephrine in the synaptic cleft, causing erratic signaling. Due to the monoamine hypothesis of depression, which asserts that decreased concentrations of monoamine neurotransmitters leads to depression symptoms, the following relations were determined: "Norepinephrine may be related to alertness and energy as well as anxiety, attention, and interest in life; [lack of] serotonin to anxiety, obsessions, and compulsions; and dopamine to attention, motivation, pleasure, and reward, as well as interest in life."[6] SNRIs work by inhibiting the reuptake of the neurotransmitters serotonin and norepinephrine. This results in an increase in the extracellular concentrations of serotonin and norepinephrine and, therefore, an increase in neurotransmission. Most SNRIs including venlafaxine, desvenlafaxine, and duloxetine, are several fold more selective for serotonin over norepinephrine, while milnacipran is three times more selective for norepinephrine than serotonin. Elevation of norepinephrine levels is thought to be necessary for an antidepressant to be effective against neuropathic pain, a property shared with the older tricyclic antidepressants (TCAs), but not with the SSRIs.[7]
Main article: Reuptake inhibitor

Recent studies have shown that depression may be linked to increased inflammatory response[8], thus attempts at finding an additional mechanism for SNRIs have been made. Studies have shown that SNRIs as well as SSRIs have significant anti-inflammatory action on microglia[9] in addition to their effect on serotonin and norepinephrine levels. As such, it is possible that an additional mechanism of these drugs exists which acts in combination with the previously understood mechanism. The implication behind these findings suggests use of SNRIs as potential anti-inflammatories following brain injury or any other disease where swelling of the brain is an issue. It should be noted, however, that regardless of the mechanism, the efficacy of these drugs in treating the diseases for which they have been indicated has been proven, both clinically and in practice.
Pharmacodynamics

Most SNRIs function alongside primary metabolites and secondary metabolites in order to inhibit reuptake of serotonin, norepinepherine, and trace amounts of dopamine. For example, venlafaxine works alongside its primary metabolite O-desmethylvenlafaxine to strongly inhibit serotonin and norepinephrine reuptake in the brain while . Recent evidence suggests that dopamine and norepinepherine behave in a cotransportational manner, due to dopamine's inactivation by norepinephrine reuptake in the prefrontal cortex, which largely lacks dopamine transporters. Therefore, SNRIs can increase dopamine neurotransmission in this part of the brain.[10] Furthermore, because SNRIs are extremely selective, they have no measurable effects on unintended systems, such as on monoamine oxidase inhibition.[11] Furthermore, studies have shown that SNRIs as well as SSRIs have significant anti-inflammatory action on microglia[12][13][14][15][16][17]

And then the older tri-cyclic medications

Tricyclic antidepressants (TCAs) are heterocyclic chemical compounds used primarily as antidepressants. The TCAs were first discovered in the early 1950s and were subsequently introduced later in the decade.

In recent times, the TCAs have been largely replaced in clinical use in most parts of the world by newer antidepressants such as the selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs), which typically have more favorable side-effects profiles, though they are still sometimes prescribed for certain indications.


Pharmacology

The majority of the TCAs act primarily as serotonin-norepinephrine reuptake inhibitors (SNRIs) by blocking the serotonin transporter (SERT) and the norepinephrine transporter (NET), respectively, which results in an elevation of the synaptic concentrations of these neurotransmitters, and therefore an enhancement of neurotransmission.[16][17] Notably, the TCAs have negligible affinity for the dopamine transporter (DAT), and therefore have no efficacy as dopamine reuptake inhibitors (DRIs).[16] Both serotonin and norepinephrine have been highly implicated in depression and anxiety, and it has been shown that facilitation of their activity has beneficial effects on these mental disorders.[18]

In addition to their reuptake inhibition, many TCAs also have high affinity as antagonists at the 5-HT2[19] (5-HT2A[20] and 5-HT2C[20]), 5-HT6,[21] 5-HT7,[22] α1-adrenergic,[19] and NMDA receptors,[23] and as agonists at the sigma receptors[24] (σ1[24] and σ2[25]), some of which may contribute to their therapeutic efficacy, as well as their side effects.[26] The TCAs also have varying but typically high affinity for antagonising the H1[19] and H2[27][28] histamine receptors, as well as the muscarinic acetylcholine receptors.[19] As a result, they also act as potent antihistamines and anticholinergics. These properties are generally undesirable in antidepressants, however, and likely contribute to their large side effect profiles.[26]

Most, if not all, of the TCAs also potently inhibit sodium channels and L-type calcium channels, and therefore act as sodium channel blockers and calcium channel blockers, respectively.[29][30] The former property is responsible for the high mortality rate upon overdose seen with the TCAs via cardiotoxicity.[31]


Finally, and sorry,
this is so long and scattered- in reading about Imipramine (a tricyclic) there is mention of BDNF.

Mechanism of action

Imipramine, a tertiary amine, affects numerous neurotransmitter systems known to be involved in the etiology of depression, anxiety, ADHD, enuresis and numerous other mental and physical conditions. Imipramine is similar in structure to some muscle relaxants, and has a significant analgesic effect and, thus, is very useful in some pain conditions.

The mechanisms of Imipramine's medicinal action include, but are not limited to, effects on:

Serotonin (5-HT): Moderate to strong reuptake inhibition. Imipramine's serotonin reuptake inhibition is almost comparable but still less than its reuptake inhibition of norepinephrine. When compared to other tricyclic antidepressants (with the exception of clomipramine)iImipramine's strong serotonin reuptake inhibition make it more akin to the SSRI class of antidepressants than its metabolite desipramine, which has almost purely noradrenergic effects.

Norepinephrine (NE): Strong reuptake inhibition.

Dopamine (DA): Reuptake and release at D1 and D2 receptors. Similar but less potent than psychostimulants, dopamine agonists, and the atypical antidepressant bupropion on dopaminergic mechanisms (increase in release and blockade of reuptake inhibition). While this effect is much less than the primary effects on NE, SER and ACh, it is nonetheless significant and is partially responsible for the therapeutic benefits of treatment with Imipramine. Enhancement of brain dopamine activity has been implicated in Imipramine's ability to stimulate motor activity and prolong time spent in escape in mice. Regarding dopamine uptake, imipramine is far less potent than most other antidepressants (for example, it has only 5% of the potency of amitryptiline or paroxetine, see the table below).[citation needed]

Acetylcholine (ACh): Imipramine is an anticholinergic. Thus, it is prescribed with caution to the elderly and with extreme caution to those with psychosis, as the general brain activity enhancement in combination with the "dementing" effects of anticholinergics increases the potential of Imipramine to cause hallucinations, confusion and delirium in this population. Imipramine is an antagonist at M2 muscarinic acetylcholine receptors (see external links). The blockade of cholinergic (muscarine) receptors is known to cause euphoria, potentially contributing to the mood lifting effects of Imipramine as well. Antimuscarinic effect is also responsible for rapid heart rate (tachycardia).

Epinephrine: Imipramine antagonizes adreno-receptors (II), thus sometimes causing increased heart rate (contributed to by other effects as well), orthostatic hypotension, and a general decrease in the responsiveness of the central nervous system (hence, a contribution to its potent anti-anxiety properties).

σ receptor and Enkephalinase: Activity on σ-receptors is present, but it is very low (Ki of 520 nM on σ-receptors, see references) and it is about half the power of amitryptiline (300 nM).

Histamine: Imipramine is an antagonist at histamine H1 receptors. This contributes to the acute sedative effect that it has in most people. In turn, its anti-histaminergic and general calming effects take place immediately, and, thus, Imipramine is sometimes prescribed as a sleep aid in low doses.

BDNF: BDNF is implicated in neurogenesis in the hippocampus, and studies suggest that depressed patients have decreased levels of BDNF and reduced hippocampal neurogenesis. It is not clear how neurogenesis restores mood, as ablation of hippocampal neurogenesis in murine models do not show anxiety related or depression related behaviours. Chronic Imipramine administration results in increased histone acetylation (which is associated with transcriptional activation and decondensed chromatin) at the hippocampal BDNF promotor, and also reduced expression of hippocampal HDAC5.[5][6]

μ receptor: Imipramine has been shown to increase the expression of μ-opioid receptors in rat forebrain.[7]