M Briley’s research while affiliated with Centre de Recherche Pierre Fabre and other places

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Publications (65)


Milnacipran, a Well‐Tolerated Specific Serotonin and Norepinephrine Reuptake Inhibiting Antidepressant
  • Article

June 2006

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26 Reads

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11 Citations

CNS Drug Reviews

M. Briley

Where are the new therapies for anxiety and obsessive-compulsive disorders?

October 2001

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15 Reads

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2 Citations

IDrugs: the investigational drugs journal

The benzodiazepines have monopolized the acute anxiety market for about 40 years, but their potential for tolerance and dependency has stimulated an interest in alternative anxiolytics. Until recently, however, attention has focused on existing drugs such as monoamine oxidase inhibitors, tricyclic antidepressants, selective serotonin reuptake inhibitors. The 5-HT1A partial agonist, buspirone (Bristol-Myers-Squibb), is one of the few compounds developed principally as an anxiolytic since the benzodiazepines. The challenge for the future is not only to find efficacious treatments with a rapid onset of action and an acceptable side effect profile but also to determine the optimal compounds for each of the different anxiety disorders.




Pharmacodynamics of milnacipran in young and elderly volunteers Br

March 2000

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34 Reads

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50 Citations

To investigate the pharmacodynamics of milnacipran in healthy young and elderly volunteers. Randomized double-blind crossover designs were employed and a standardized psychometric battery was administered pre and post dose for both studies. In the first study 10 healthy young volunteers received milnacipran 12.5 mg, 25 mg, 50 mg, 100 mg as a single dose or matched placebo. The test battery was administered at baseline and at 1, 2, 4 and 6 h post dose. The second study compared the effects of milnacipran 75 mg (50 mg+25 mg) per day, amitriptyline 50 mg (25 mg+25 mg) per day and placebo for 3 days' dosing in healthy volunteers aged over 65 years. The test battery was administered at baseline and at 2, 10 and 24 h post dose. The psychometric battery included critical flicker fusion (CFF), choice reaction time (CRT), compensatory tracking (CTT) and tests of short-term memory (STM), subjective sedation (LARS) and subjective sleep (LSEQ). Milnacipran produced no significant dose related effects in the young volunteers. For the elderly, milnacipran significantly (P<0.05) raised CFF scores compared with placebo but had no significant effects on any of the other measures used. Amitriptyline, in contrast, significantly (P<0. 05) lowered CFF threshold, lengthened CRT and increased error on the CTT. On the subjective variables, LARS and LSEQ, amitriptyline increased ratings both of sedation and of difficulty in waking from sleep. The results showed that milnacipran at single doses of up to 100 mg in healthy young volunteers is free from disruptive effects on cognitive function and psychomotor performance. In addition, milnacipran 75 mg (50+25 mg) appears to be free of negative effects on cognitive function in elderly volunteers, where it seemingly improves performance on CFF. In contrast, the tricyclic antidepressant amitriptyline, used here as a positive internal control, significantly impaired performance in the elderly on the majority of psychometric measures used in this study. This finding not only validated the sensitivity of this current test battery but also indicates the potential behavioural toxicity of amitriptyline in clinical use in the elderly.


Functional Neuropharmacology of Compounds Acting at 5-HT1B/D Receptors

January 2000

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9 Reads

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26 Citations

Handbook of Experimental Pharmacology

The neuropharmacology of serotonin (5-HT) has been fundamentally revised in recent years with the discovery of multiple serotonin receptor subtypes. Detailed descriptions of the pharmacology of the various receptor subtypes are to be found elsewhere in this book. We review here the available data on the in vitro and in vivo neuropharmacology of the 5-HT1B/D group of receptor subtypes and attempt to identify their possible functions and potential implications in psychiatric disorders.



From Dirty Drugs to Hyperselectivity and Part Way Back Again

December 1998

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6 Reads

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1 Citation

Human Psychopharmacology Clinical and Experimental

Tricyclic antidepressants (TCAs) are effective in the treatment of depression, but their usefulness is limited by adverse effects resulting from binding to muscarinic, histaminergic and other receptors. Selective serotonin reuptake inhibitors (SSRIs) have a more favourable tolerability profile, but their selectivity for serotonin reuptake appears to be associated with some decrease in efficacy, particularly in severe depression. Milnacipran is a new serotonin and noradrenaline reuptake inhibitor that has been developed for the treatment of depression. It inhibits monoamine reuptake both in vitro and in vivo, but does not bind to neurotransmitter receptors. Furthermore, milnacipran has no effect on auto- or heteroreceptors, and no adaptive changes in receptor function occur during longterm treatment. Milnacipran has been shown to be effective in behavioural tests of noradrenergic or serotonergic activity, and in animal models of depression; no sedative, stimulant or anticholinergic effects have been observed. It has a favourable pharmacokinetic profile, as it does not accumulate during repeated administration, does not form active metabolites, and is unlikely to interact significantly with other drugs. Milnacipran, therefore, may offer therapeutic advantages, potentially combining the efficacy of TCAs with the good tolerability profile of SSRIs. © 1997 John Wiley & Sons, Ltd.


Boyer P, Briley M. Milnacipran, a new specific serotonin and noradrenaline reuptake inhibitor. Drugs Today (Barc) 34: 709-720

September 1998

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12 Reads

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22 Citations

Drugs of today (Barcelona, Spain: 1998)

Milnacipran is a new antidepressant which inhibits equipotently the reuptake of serotonin and noradrenaline both in vitro and in vivo with no effect on dopamine reuptake. Microdialysis studies have shown increased extracellular levels of both serotonin and noradrenaline after acute administration. Milnacipran is devoid of interactions at any known neurotransmitter receptor. In particular, and unlike tricyclic antidepressants (TCAs), it has no activity at noradrenergic, muscarinic or histaminergic receptors. Contrary to TCAs, chronic administration of milnacipran does not modify beta-adrenoceptor binding or second messenger function. Milnacipran is active on various animal models of depression such as the forced swimming test in the mouse, learned helplessness in the rat and the olfactory bulbectomized rat model. Milnacipran has a high bioavailability, low plasma protein binding, and is largely eliminated in the urine as the parent drug or as a glucuronide. These features suggest that interactions with other drugs given concurrently are unlikely. Studies in patients with liver dysfunction and in the elderly suggest that dose adjustment is not necessary. In patients with renal impairment, decreased elimination of milnacipran is correlated to the degree of renal impairment allowing an easy dosage adjustment. An intermediate half-life of approximately 8 h is compatible with twice-daily administration. Clinical studies comparing milnacipran, placebo and other antidepressants provide evidence of its efficacy in moderate to severe depression in both hospitalized and outpatient settings. Meta-analyses of the original data of controlled trials comparing milnacipran with imipramine or selective serotonin reuptake inhibitors (SSRIs) show that milnacipran provides antidepressant efficacy similar to that of TCAs and significantly superior to that of SSRIs. An analysis of a database of over 3300 patients shows that both the general and cardiovascular tolerability of milnacipran are superior to those of TCAs with notably less cholinergic side effects. The tolerance of milnacipran was comparable to that of SSRIs with a higher incidence of dysuria with milnacipran but a higher frequency of nausea and anxiety with the SSRIs. Milnacipran represents an interesting new therapeutic option in depression, being as well tolerated as the SSRIs but offering clinical efficacy similar to the TCAs.


Milnacipran, a new specific serotonin and noradrenaline reuptake inhibitor

August 1998

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9 Reads

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11 Citations

Drugs of today (Barcelona, Spain: 1998)

Milnacipran is a new antidepressant which inhibits equipotently the reuptake of serotonin and noradrenaline both in vitro and in vivo with no effect on dopamine reuptake. Microdialysis studies have shown increased extracellular levels of both serotonin and noradrenaline after acute administration. Milnacipran is devoid of interactions at any known neurotransmitter receptor. In particular, and unlike tricyclic antidepressants (TCAs), it has no activity at noradrenergic, muscarinic or histaminergic receptors. Contrary to TCAs, chronic administration of milnacipran does not modify beta-adrenoceptor binding or second messenger function. Milnacipran is active on various animal models of depression such as the forced swimming test in the mouse, learned helplessness in the rat and the olfactory bulbectomized rat model. Milnacipran has a high bioavailability, low plasma protein binding, and is largely eliminated in the urine as the parent drug or as a glucuronide. These features suggest that interactions with other drugs given concurrently are unlikely. Studies in patients with liver dysfunction and in the elderly suggest that dose adjustment is not necessary. In patients with renal impairment, decreased elimination of milnacipran is correlated to the degree of renal impairment allowing an easy dosage adjustment. An intermediate half-life of approximately 8 h is compatible with twice-daily administration. Clinical studies comparing milnacipran, placebo and other antidepressants provide evidence of its efficacy in moderate to severe depression in both hospitalized and outpatient settings. Meta-analyses of the original data of controlled trials comparing milnacipran with imipramine or selective serotonin reuptake inhibitors (SSRIs) show that milnacipran provides antidepressant efficacy similar to that of TCAs and significantly superior to that of SSRIs. An analysis of a database of over 3300 patients shows that both the general and cardiovascular tolerability of milnacipran are superior to those of TCAs with notably less cholinergic side effects. The tolerance of milnacipran was comparable to that of SSRIs with a higher incidence of dysuria with milnacipran but a higher frequency of nausea and anxiety with the SSRIs. Milnacipran represents an interesting new therapeutic option in depression, being as well tolerated as the SSRIs but offering clinical efficacy similar to the TCAs.


Citations (39)


... This test was performed according to the methods published by File (File and Briley, 1991;File, 1992). The rats were singly housed for 5 days prior to testing. ...

Reference:

Repeated forced swim stress has additive effects in anxiety behavior and in cathecolamine levels of adult rats exposed to deltamethrin
New Concepts in Anxiety
  • Citing Book
  • January 1991

... The optimal potency ratio for inhibiting these three monoamine transporters is unknown, but there is a wide variation in potency ratios among clinically active dual reuptake inhibitors (Briley and Moret, 1997). Most likely, the ideal rank order would be NϾDϾS, considering the balance among the three transporters and the potential adverse effects associated with the transporter blockade (Liang and Richelson, 2008). ...

Antidepressant Properties of Specific Serotonin—Noradrenaline Reuptake Inhibitors
  • Citing Chapter
  • January 1997

... However, the fact that electroconvulsive treatment, one of the most effective treatments for depression (Fink 1979), was shown after repeated administration not to reduce but to elevate 5-HT2 receptors (Kellar et al 1981) while down-regulation of 13-adrenoceptors occurred (Pandey et al 1979; Stanford and Nutt, 1982), led to the hypothesis that the down-regulation of ,B-adrenoceptors is a mandatory component to obtain antidepressant effects (Sulser 1979). More recently, however, several studies have shown that many clinically effective novel antidepressant compounds do not cause a significant down-regulation of brain 13- adrenoceptors following long-term treatment (ClemensJewery 1978; Mishra et al 1980; Sellinger-Barnette 1980; Ferris et al 1982; Suranyi-Cadotte et al 1985; see review by Assie et al 1988). For example, after 28 days of treatment with buspirone, a 5-HTIA agonist with both anxiolytic and antidepressant efficacy, no down-regulation of f3-adreno- ceptors labelled by [3H]DHA in rat cortex occurred as evaluated by saturation analysis of the binding data while, alternatively, down-regulation of 5-HT2 receptors labelled with [3H]spiperone was noted (Taylor and Hyslop, in press). ...

Is Down-regulation of β-Adrenoceptors Necessary for Antidepressant Activity?
  • Citing Chapter
  • January 1988

... Abrupt withdrawal of a benzodiazepine (12, 24 or 48 h) following prolonged administration (7-21 days) has been shown to induce anxiety in rats or mice, measured in different animal models: plus-maze (Assie´et al., 1991;Bhattacharya et al., 1995;File and Hitchcott, 1991;Fontanesi et al., 2007;Martijena et al., 1996;Pokk and Zharkovsky, 1998;Wright et al., 1991), social interaction (Andrews and File, 1993;Andrews et al., 1997) or in both (Begg et al., 2005), and light-dark test (Souza Pinto et al., 2007). Withdrawal for 24 h from chronic diazepam treatment (21 days) has been related to increased 5-HT release in the hippocampus (Andrews and File, 1993;Andrews et al., 1997). ...

Effects of Repeated Administration of Diazepam to Rats on Locomotor Activity, Elevated Plus-maze and Various Brain Receptors
  • Citing Chapter
  • January 1991

... use and effect relationship (see Fig. 2; Morgan 2000;Kish 2002;Cole & Sumnall, 2002). In addition, some results are the exact opposite of what these theories would predict. For example, reduced serotonin function should make ecstasy users less anxious, as serotonergic neurotoxins reduce anxiety-related behaviour in animals (e.g. Briley et al . 1990Briley et al . , 1991 and drugs that release serotonin cause anxiety (e.g. Kahn et al . 1988;Murphy et al . 1989). Several reports, however, indicate that they are more anxious (e.g. Parrott et al . 2000Parrott et al . , 2001. ...

The Role of Serotonin in Anxiety: Behavioural Approaches
  • Citing Chapter
  • January 1991

... Pharmacological studies have suggested an involvement of 5-HT 1B , 5-HT 1A and 5-HT 2C receptors in the control of locomotor activity [8,30]. Thus, we should take under consideration the role of serotoninergic neurotransmission in behavioral changes observed in CRI. ...

Functional Neuropharmacology of Compounds Acting at 5-HT1B/D Receptors
  • Citing Chapter
  • January 2000

Handbook of Experimental Pharmacology

... Milnacipran hydrochloride is a serotonin and norepinephrine reuptake inhibitor (SNRI), with a balanced potency for the inhibition of serotonin and noradrenaline reuptake (Boyer & Briley, 1998;Forest Laboratories Inc., 2009;Papakostas & Fava, 2007). In view of the variations in drug response due to genetic differences and the lack of local evidencebased treatment guidelines, a consensus meeting was organized to develop a local consensus to guide medical practitioners and psychiatrists on the use of milnacipran in different psychiatric conditions. ...

Milnacipran, a new specific serotonin and noradrenaline reuptake inhibitor
  • Citing Article
  • August 1998

Drugs of today (Barcelona, Spain: 1998)

... The liposterolic extract of saw palmetto has antiandrogenic activity in human prostatic cell lines [3]. Furthermore, it inhibits binding of dihydrotestosterone (DHT) to its receptor [4] and prevents the conversion of testosterone into DHT by inhibiting the activity of 5-alpha-reductase [5], exhibiting a similar mechanism to the Food and Drug Administration (FDA)-approved medication finasteride. In vitro studies have shown that it also inhibits cyclooxygenase and 5-lipoxygenase pathways, thereby preventing the biosynthesis of inflammation-producing prostaglandins and leukotrienes [6]. ...

Permixon, a new treatment for benign prostatic hyperplasia, acts directly at the cytosolic androgen receptor in rat prostate
  • Citing Article
  • January 1983

... 3. Equip the baseplate with protrusions to connect a grid of equally spaced holes in the punching board (the protrusion diameter is 6 mm) ( Figure 2B). 4. Use the holes to connect components such as feeders, movable walls, and treadmills (see Table of Materials) equipped with towers with baseplates. ...

Validation of open:closed arm entries in an elevated plus-maze: A novel test of anxiety in the rat
  • Citing Article
  • January 1985

Journal of Neuroscience Methods