Noradrenaline modulates glutamate-mediated neurotransmission in the rat basolateral amygdala in vitro

The entorhinal cortex and the amygdala are interconnected structures of the limbic system in which paroxysmal activity occurs during temporal robe epilepsy. Conflicting evidence shows that noradrenaline (i) inhibits the spreading to other parts of the limbic system of paroxysmal activity generated in the amygdala or the entorhinal cortex, but also (ii) increases glutamatergic transmission in the basolateral amygdala. Given our previous work on the inhibitory effect of noradrenaline on entorhinal cortex neurons, we developed an in vitro slice preparation to study the synaptic transmission in the basolateral amygdala and its modulation by noradrenaline. Noradrenaline reduced the fast excitatory postsynaptic potential (EPSP) by similar to 40% at 100 mu M and the slow EPSP by similar to 50% at 50 mu M. A similar effect was obtained with the alpha(2)-agonist UK 14304 at 100 and 50 mu M respectively. In contrast, the beta-agonist isoproterenol increased the fast EPSP by similar to 40% at 100 mu M and the slow EPSP by similar to 20% at 50 mu M. Accordingly, the effect of noradrenaline on the EPSPs was blocked by the alpha(2)-antagonist yohimbine (10 mu M) but not by the alpha(1)-antagonist prazosine (10 mu M) and the beta-antagonist propranolol (10 mu M). Noradrenaline (50-100 mu M) was ineffective on most (14/16) of the isolated inhibitory postsynaptic potentials (IPSPs). These experiments provide evidence that noradrenaline inhibits the excitatory synaptic response of basolateral amygdala neurons. A pharmacological analysis revealed that the noradrenergic modulation of the excitatory transmission in the basolateral amygdala can be dissected into a predominant alpha(2)-adrenoreceptor-mediated inhibition and a beta-adrenoreceptor-mediated excitation.