No description available.

No description available.

<p>Den här uppsatsen analyserar informationssajten om depression Depressionslinjen, som ges ut av läkemedelsföretaget Pfizer. Analysen görs enligt Fairclough (2001a; 2001b; 2002). Analysen visar att läsaren/patienten konstitueras som passiv medan SSRI och läkaren konstitueras som aktiva och handlande. Terapi och andra alternativ till läkemedel nämns, men olika diskursiva grepp används som ger intrycket av att dessa kommer i andra hand. Lågt Serotonin framstår som orsak till depression. Med utgångspunkt från texter av Filip Kotler (1991) visar uppsatsen att Depressionslinjen har åtskilliga inslag av marknadsföring. Tre alternativa sätt att se på depression föreslås: Depression som samhällsproblem, depression som existensiell utmaning och depression som minne. Slutsatsen är att Depressionslinjen har en idologisk roll i och med att sidan för fram en professionell lösning på depression där serotoninet får skulden till problemet.</p>

Antidepressants are generally believed to exert their clinical efficacy by enhancing 5-HT transmission. Interestingly, sustained administration of selective serotonin (5-HT) reuptake inhibitors (SSRIs) strongly suppresses in the first few days the firing activity of 5-HT neurons in the dorsal raphe nucleus (DRN), thereby severely hampering the increase of 5-HT in target regions. Remarkably, the firing activity of 5-HT neurons gradually recovers over the time course of treatment and this recovery is believed to be accounted for by the desensitization of 5-HT1A somatodendritic autoreceptors. Here, we sought to investigate whether additional mechanisms might contribute to the dynamic regulation of excitability of 5-HT neurons during the course of SSRI treatments. Borrowing from the well-described homeostatic strengthening of glutamatergic synapses onto cortical pyramidal neurons following prolonged periods of inactivity, we hypothesized that a similar homeostatic-like regulation of synaptic strength might be operant on 5-HT cells during an SSRI treatment. To test this possibility, we used whole-cell electrophysiological recordings on acute midbrain slices to monitor glutamatergic synapses onto 5-HT neurons. We found that a two-day treatment with the SSRI citalopram induced a robust reduction in both the amplitude and frequency of AMPAR-mediated mEPSCs. We also show that this depression in synaptic strength, induced by an SSRI, is transient since excitatory drive onto 5-HT neurons was enhanced by 7 days of treatments. Altogether, these results document a dynamic regulation of glutamatergic synaptic transmission during the time course of a prolonged treatment with an SSRI. Further elucidation of the cellular and molecular mechanisms driving this synaptic plasticity might identify novel pharmacological target to shorten the delay of antidepressant action.

Den här uppsatsen analyserar informationssajten om depression Depressionslinjen, som ges ut av läkemedelsföretaget Pfizer. Analysen görs enligt Fairclough (2001a; 2001b; 2002). Analysen visar att läsaren/patienten konstitueras som passiv medan SSRI och läkaren konstitueras som aktiva och handlande. Terapi och andra alternativ till läkemedel nämns, men olika diskursiva grepp används som ger intrycket av att dessa kommer i andra hand. Lågt Serotonin framstår som orsak till depression. Med utgångspunkt från texter av Filip Kotler (1991) visar uppsatsen att Depressionslinjen har åtskilliga inslag av marknadsföring. Tre alternativa sätt att se på depression föreslås: Depression som samhällsproblem, depression som existensiell utmaning och depression som minne. Slutsatsen är att Depressionslinjen har en idologisk roll i och med att sidan för fram en professionell lösning på depression där serotoninet får skulden till problemet.

Antidepressants are generally believed to exert their clinical efficacy by enhancing 5-HT transmission. Interestingly, sustained administration of selective serotonin (5-HT) reuptake inhibitors (SSRIs) strongly suppresses in the first few days the firing activity of 5-HT neurons in the dorsal raphe nucleus (DRN), thereby severely hampering the increase of 5-HT in target regions. Remarkably, the firing activity of 5-HT neurons gradually recovers over the time course of treatment and this recovery is believed to be accounted for by the desensitization of 5-HT1A somatodendritic autoreceptors. Here, we sought to investigate whether additional mechanisms might contribute to the dynamic regulation of excitability of 5-HT neurons during the course of SSRI treatments. Borrowing from the well-described homeostatic strengthening of glutamatergic synapses onto cortical pyramidal neurons following prolonged periods of inactivity, we hypothesized that a similar homeostatic-like regulation of synaptic strength might be operant on 5-HT cells during an SSRI treatment. To test this possibility, we used whole-cell electrophysiological recordings on acute midbrain slices to monitor glutamatergic synapses onto 5-HT neurons. We found that a two-day treatment with the SSRI citalopram induced a robust reduction in both the amplitude and frequency of AMPAR-mediated mEPSCs. We also show that this depression in synaptic strength, induced by an SSRI, is transient since excitatory drive onto 5-HT neurons was enhanced by 7 days of treatments. Altogether, these results document a dynamic regulation of glutamatergic synaptic transmission during the time course of a prolonged treatment with an SSRI. Further elucidation of the cellular and molecular mechanisms driving this synaptic plasticity might identify novel pharmacological target to shorten the delay of antidepressant action.

This article presents a study conducted on data containing drug concentrations. The data was obtained from femoral venous blood samples collected at medico legal autopsies in Sweden. Cases positive for antidepressant drugs were scrutinized and divided in to two groups for 15 antidepressant drugs: B‑cases, where the cause of death was intoxication with more than one drug detected in the blood sample. C‑cases, where the cause of death was NOT intoxication and at least one drug (the antidepressant) was detected in the blood sample. This data was then processed to find frequencies of concomitant drugs taken together with the antidepressant drugs. Frequencies of the most common concomitant drugs were then compared between B-cases and C-cases for each antidepressant drug. This revealed that the drugs dextropropoxyphene, ethanol, codeine, flunitrazepam, paracetamol, propiomazine and alimemazine were signifcantly more common as concomitant drugs in B-cases (intoxications) than in C‑cases (non‑intoxications). With regards to unknown interactions the most interesting combinations were: Propiomazine with mirtazapine, venlafaxine, citalopram or fluoxetine; Paracetamol with paroxetine; Flunitrazepam with mirtazapine, venlafaxine or citalopram; Codeine with mirtazapine or sertraline. These combinations should be further investigated.

Post partum depression (PPD) drabbar mellan 10 – 15 % av nyförlösta mödrar. Att drabbas av en PPD kan orsaka känslomässiga och kognitiva besvär för hela familjen. Kvinnan löper också en större risk att drabbas av en depression senare i livet, vilket är en faktor som kan påverka mammans relation till barnet och sin omgivning. En tidig korrekt behandling är viktig för mammans framtida välbefinnande. Bland möjliga orsaker till post partum depression nämns hormonförändring, förändrad nivå av neurotransmittorer, nutritionella orsaker och sömnbrist. Behandlingen av PPD är inriktad mot psykoterapi, antidepressiv behandling och elektrokonvulsiv behandling (ECT). Syftet med denna litteraturstudie var att titta på effekten av det antidepressiva läkemedlet serotoninåterupptagshämmare (SSRI). Studierna som granskades i detta arbete hämtades från Pubmed. Fem studier valdes och samtliga var randomiserade kliniska prövningar. Tre av studierna visade ingen signifikant skillnad mellan SSRI och placebo/psykoterapi/tricykliskt antidepressiva (Nortriptylin). I två av studierna hittades en signifikant skillnad, med en bättre effekt för SSRI i jämförelse med placebo respektive samtal. I studie 2 erhölls en signifikant skillnad med avseende på remission efter 8 veckor (p=0.04) och i studie 3 var det en signifikant skillnad mellan andelen som nådde behandlingsmålet &lt;13 på Edinburgh Postnatal Depression Scale (EPDS) efter 4 veckor. Vad gäller förbättringen av den kliniska sjukdomsbilden nådde fler lägre poäng på mätskalorna i de grupper där SSRI var inkluderat. Samtliga behandlingar som inkluderades i studierna nådde goda resultat. Sammanfattningsvis är SSRI ett bra alternativ för behandling av PPD, men i den inledande fasen kan det dock inte ses som bättre än psykoterapi eller behandling med nortriptylin. I den framtida forskningen skulle det vara intressant att se fler och framförallt större studier för att klargöra effekten av SSRI vid PPD.

No description available.

Antidepressants are generally believed to exert their clinical efficacy by enhancing 5-HT transmission. Interestingly, sustained administration of selective serotonin (5-HT) reuptake inhibitors (SSRIs) strongly suppresses in the first few days the firing activity of 5-HT neurons in the dorsal raphe nucleus (DRN), thereby severely hampering the increase of 5-HT in target regions. Remarkably, the firing activity of 5-HT neurons gradually recovers over the time course of treatment and this recovery is believed to be accounted for by the desensitization of 5-HT1A somatodendritic autoreceptors. Here, we sought to investigate whether additional mechanisms might contribute to the dynamic regulation of excitability of 5-HT neurons during the course of SSRI treatments. Borrowing from the well-described homeostatic strengthening of glutamatergic synapses onto cortical pyramidal neurons following prolonged periods of inactivity, we hypothesized that a similar homeostatic-like regulation of synaptic strength might be operant on 5-HT cells during an SSRI treatment. To test this possibility, we used whole-cell electrophysiological recordings on acute midbrain slices to monitor glutamatergic synapses onto 5-HT neurons. We found that a two-day treatment with the SSRI citalopram induced a robust reduction in both the amplitude and frequency of AMPAR-mediated mEPSCs. We also show that this depression in synaptic strength, induced by an SSRI, is transient since excitatory drive onto 5-HT neurons was enhanced by 7 days of treatments. Altogether, these results document a dynamic regulation of glutamatergic synaptic transmission during the time course of a prolonged treatment with an SSRI. Further elucidation of the cellular and molecular mechanisms driving this synaptic plasticity might identify novel pharmacological target to shorten the delay of antidepressant action.