Effects of milnacipran on the inhibitory postsynaptic potential in neurons of the rat locus coeruleus.

Effects of milnacipran (MIL), a serotonin and noradrenaline reuptake inhibitor (SNRI), on synaptic transmission were examined in the rat locus coeruleus (LC). Bath-application of MIL produced a hyperpolarization associated with a decrease in input resistance of LC neurons. The MIL-induced hyperpolarization reversed polarity near the equilibrium potential of K+.

[Effects of milnacipran on neuronal excitability and synaptic transmission in neurons of the rat locus coeruleus].

Effects of milnacipran (MIL), a selective serotonin and noradrenaline (NA) reuptake inhibitor, on the neuronal excitability and synaptic transmission in the rat locus coeruleus (LC) were examined by intracellular and whole-cell patch-clamp recording techniques. We compared MIL and methylphenidate (MPH), a selective NA and dopamine reuptake inhibitor, as a therapeutic agent for attention deficit/hyperactivity disorder. Application of MPH (1-100 microM) and MIL (1-100 microM) to artificial cerebrospinal fluid (ACSF) produced a hyperpolarizing response in LC neurons in a concentration-dependent manner.

Effects of adenosine and ATP on the membrane potential and synaptic transmission in neurons of the rat locus coeruleus.

Effects of adenosine (Ado) and adenosine 5'-triphosphate (ATP) on the membrane potential and synaptic transmission in neurons of the rat locus coeruleus (LC) were examined, in vitro. Ado (30-300 microM) produced a hyperpolarizing response and inhibited spontaneous firing activity in neurons of the rat LC. Ado decreased input resistance of LC neurons.

Effects of methylphenidate on the inhibitory postsynaptic potential in rat locus coeruleus neurons.

Effects of methylphenidate (MPH), an agent used clinically for the treatment of children presenting the attention-deficit/hyperactivity disorder (AD/HD), on synaptic transmission in the rat locus coeruleus (LC) were examined by intracellular recording methods. Bath-application of MPH (30 nM-3 microM) increased the amplitude of the inhibitory postsynaptic potential (IPSP), while it did not change the amplitude of the excitatory postsynaptic potential (EPSP). MPH increased the time-to-peak and the half-decay time of the IPSP in LC neurons.