1. Dear Drugs-Forum readers: We are a small non-profit that runs one of the most read drug information & addiction help websites in the world. We serve over 4 million readers per month, and have costs like all popular websites: servers, hosting, licenses and software. To protect our independence we do not run ads. We take no government funds. We run on donations which average $25. If everyone reading this would donate $5 then this fund raiser would be done in an hour. If Drugs-Forum is useful to you, take one minute to keep it online another year by donating whatever you can today. Donations are currently not sufficient to pay our bills and keep the site up. Your help is most welcome. Thank you.
    PLEASE HELP

In vivo electrophysiological effects of methylphenidate in the prefrontal cortex: involvement of dop

In vivo electrophysiological effects of methylphenidate in the prefrontal cortex: involvement of dop

  1. testodan
    Attention deficit hyperactivity disorder (ADHD) is the most commonly diagnosed psychiatric disorder
    in children. Psychostimulants such as methylphenidate (MPH) are used as first line treatment. The prefrontal cortex (PFC) has a proven role in the expression of ADHD. Previous studies from our laboratory have demonstrated that MPH activates the firing activity of medial PFC neurones in
    anaesthetised rats. The aim of the present study was to determine the respective contribution and
    location of the different types of catecholamine receptors inmediating these excitatory effects and to
    compare these effects with those induced by other selective dopamine or noradrenaline uptake
    blockers. Single unit activity of presumed pyramidal PFC neurones was recorded in rats anaesthetised
    with urethane. The activation of firing elicited by an iv administration of MPH (1 or 3 mg/kg) was
    partially reduced or prevented by the selective D1 receptor antagonist SCH 23390 administered
    systemically (0.5 mg/kg, iv), or locally by passive diffusion through the recording electrode. On the
    other hand, administration of the alpha 2 receptor antagonist yohimbine (1 mg/kg, iv) significantly
    potentiated the excitatory effect of MPH and activated PFC neurones previously treated with a low
    inactive dose of MPH (0.3 mg/kg, iv). Local administration of MPH (1 mM through the recording
    electrode) significantly increased the firing of PFC neurones in a D1 receptor-dependent manner. In
    addition, the response of PFC neurones to MPH, administered at a low dose (0.3 mg/kg, iv), is greatly
    potentiated by dopamine (1 mM), but not by noradrenaline (1 mM), diffusing passively through the
    recording electrode, and this effect is reversed by D1 receptor blockade. Finally, the selective
    dopamine uptake inhibitor GBR 12909 (6 mg/kg, iv) and desipramine (6 mg/kg, iv) only activate a
    subset of PFC neurones. These results demonstrate the involvement of cortical dopamine D1 and
    noradrenergic alpha 2 receptors in the in vivo electrophysiological effects of MPH on PFC neurones.