Psychedelia.dk

Er der nogen der kan give en forståelig beskrivelse af de funktioner ethanol har i hjernen?

Så vidt jeg ved, påvirker det GABA-receptorerne? Som antagonist eller agonist? Og har det ingen indvirkning på dopamin-receptorerne, som jeg svagt genkalder at have læst i en undersøgelse? ("Husker" at have læst at en promille på 0,6 udløser/påvirker dopamin receptorerne så meget som ethanol kan)

ethanol Binder sig som antagonist til de glutaminerge Kainat- og NMDA-receptorerer og øger frigivelsen af GABA.

Der er en animation på dette site som bl.a. viser ethanols virkning i hjernen:

http://www.netstof.dk/site/Drugs_in_the_brain/Drug_in_the_brain/

_________________
Bagsidens gule sider - Giftlinjen, rådgivning om misbrug mm.

Den er fandme godt animeret og meget pædagogisk!

Så er netstof.dk da ikke helt tåbeligt.

Udemærket at animationen er forklaret på et plan hvor de fleste kan være med.

Jeg er helt enig, meget god og pædagogisk animation - og på et passende plan. Jeg vidste ikke at alkohol også bandt til glutamat-receptoren, men det giver meget godt mening.
Så vidt jeg ved, virker alkohol faktisk på benzodiazepin-receptorkomplekset på GABA-A, og benzodiazepin antagonister kan vist nok virke hæmmende på ethanols virkninger.

Nix. Alkohol binder til BK-kanalen som styrer calcium-influx. Indirekte aktiverer/potentierer dette GABA. Flumazenil kan ikke redde en fra alkoholoverdoser.

Fra Rang, Dale & Ritter - Pharmacology - Fourth edition: "The benzodiazepine antagonist, flumazenil, reverses the central depressant actions of ethanol (see Lister & Nutt 1987), but this appears to result from physiological antagonism, rather than from a direct pharmacological interaction. The use of flumazenil to reverse ethanol intoxication and treat dependance has not found favour for several reasons. It carries a risk of causing seisures, and could cause an increase in ethanol consumption and thus increase long-term toxic manifestations".
Ifølge den bog ER det altså muligt at bruge flumazenil, om ikke ligefrem anbefalelsesværdig praksis - men post det gerne hvis du har nyere information.

Tak for linket, kopfka - Det var lige hvad jeg eftersøgte.

Flumazenil acts as an antidote for pharmacological and toxic effects due to benzodiazepines. Several isolated observations and short uncontrolled series have also suggested a possible effect against the impairment of consciousness induced by pure alcohol intoxication. Patients admitted in the emergency department with coma related to acute alcohol (ALC) or pure benzodiazepine (BZD) intoxication were randomized and treated blindly with either placebo or 1 mg flumazenil. A modified Glasgow score was used to observe the evolution of consciousness. In the 18 ALC patients, 1 mg flumazenil was not more effective than placebo, whereas it appeared to be very active in the BZD group. However, an open administration of higher doses of flumazenil (2-5 mg) in 11 ALC patients, whose condition had not initially improved, was followed by clear improvement of consciousness in five of them. Flumazenil, administered at a dose usually active against BZD sedation, does not improve CNS depression induced by ALC intoxication. Higher doses could be more effective in some patients, but it should also be verified in a placebo-controlled trial.

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

Levose> Jeg synes da det abstract du citerer tyder på at flumazenil har en vis effekt, selv om der skal højere doser til end for at modvirke benzodiazepiner? Blot er det ikke verificeret ved placebokontrolleret studie. Siden artiklen er fra 1991, skulle man tro at nogen havde forsøgt det. Min version af Rang, Dale & Ritter's "Pharmacology" er skrevet i '99. Det plejer at være en ret troværdig lærebog. Uden at vide specielt meget om emnet, kunne jeg forestille mig at ethanol var en forholdsvist uselektiv påvirkning, som påvirkede adskillige receptorer.

Jeg fandt en artikel som når frem til at flumazenil hæmmer i hvert fald de aggressionsfremmende sider af alkohol:

1: Psychopharmacology (Berl). 1993;111(2):144-52. Links
Prevention of the pro-aggressive effects of alcohol in rats and squirrel monkeys by benzodiazepine receptor antagonists.Weerts EM, Tornatzky W, Miczek KA.
Department of Psychology, Tufts University, Medford, MA 02155.

Pharmacological manipulations at the benzodiazepine-GABAA-chloride ionophore receptor complex modify some of the behavioral and physiological actions of alcohol (ethanol). The interactions between alcohol, benzodiazepines and aggression were examined in similar ethopharmacological studies in squirrel monkeys and in rats in confrontations with conspecifics. Dominant male squirrel monkeys were tested (1) within their social groups, and (2) in dyadic confrontations with "rival" males from a different social group, and resident male rats were tested in their home cage in confrontations with an inexperienced male intruder. Low doses of alcohol (0.1-0.3 g/kg) increased aggressive behaviors in dominant squirrel monkeys and a subgroup of resident rats, whereas high doses of alcohol (1-3 g/kg) decreased aggression and produced marked motor incoordination. Individuals that showed alcohol-enhanced aggression were selected, and pretreated with benzodiazepine antagonists (flumazenil, ZK 93426) prior to alcohol administration. Both ZK 93426 (3 mg/kg) and flumazenil (10 mg/kg) blocked the aggression-enhancing effects of alcohol in dominant squirrel monkeys and resident rats in confrontations with conspecifics. Neither compound altered the reductions in aggression and increases in inactivity produced by high doses of alcohol. Interestingly, agonist-like increased feeding and inverse agonist-like reductions in social behaviors were observed simultaneously at the same dose of flumazenil, in the same individual and testing situation. ZK 93426 did not alter feeding but also reduced social behaviors. The two antagonists were also not equipotent in their interactions with alcohol. ZK 93426 reduced alcohol-induced motor incoordination in squirrel monkeys, whereas flumazenil did not. In fact, flumazenil potentiated the effects of low doses of alcohol.