The lateral nucleus of the amygdala (LA), a key component of the fear conditioning circuitry, receives a rapid but relatively impoverished auditory input from the auditory thalamus and a slower but richer input from the auditory cortex. We examined in urethane anesthetized rats whether individual cells in the LA receive convergent inputs from these two areas, and whether different postsynaptic receptors contribute to the temporally separated excitations over the two pathways. With both extracellular and intracellular recordings, individual cells could be activated by stimulation of each pathway. In extracellular recordings iontophoretic application of the N-methyl-D-aspartate (NMDA) receptor antagonist APV and the L-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor antagonist CNQX demonstrated that synaptic transmission in both pathways depends on AMPA receptors, whereas transmission in the thalamic pathway also depends on the involvement of NMDA receptors. The involvement of NMDA receptors in synaptic activation of the LA from the thalamus but not the cortex was confirmed in intracellular recordings using systemic injections of the NMDA antagonist MK-801. The slow time course of NMDA currents could provide LA cells with a mechanism to integrate the inputs arriving rapidly from the thalamus and somewhat later from the cortex, thus allowing the LA to integrate signals in the two pathways during the acquisition and expression of conditioned fear reactions.

Amygdala↗

PubMedDate not supplied

Effects of pertussis and cholera toxins on alpha-adrenoceptor function in rat tail artery: differences in hypertension.

The alpha 1- and alpha 2-adrenoceptor-stimulated contractile responses of rat tail artery rings were compared in Sprague-Dawley (SD), spontaneously hypertensive (SHR), and Wistar-Kyoto (WKY) rats that were untreated, treated with pertussis toxin, or treated with cholera toxin. The maximal responses, expressed as milligrams of tension, induced by clonidine (an alpha 2-adrenoceptor agonist) and cirazoline (a selective alpha 1-adrenoceptor agonist) were significantly greater in SHR than in SD or WKY, and the tissues were more sensitive to the agonists in SHR or SD than in WKY. Yohimbine (0.1 microM), a selective alpha 2-adrenoceptor antagonist, shifted the dose-response curves for clonidine to the right. The effects of yohimbine were greater in SD than in WKY or SHR, but not different between WKY and SHR. Prazosin (0.05 microM), a selective alpha 1-adrenoceptor antagonist, shifted the dose-response curves of cirazoline to the right, but the effects of prazosin were not different among these three strains of rats. Nifedipine (0.05 microM) completely blocked the response to clonidine in SD and WKY; however, in SHR, approximately one-third of the response to clonidine was resistant to nifedipine. Nifedipine, at 0.05 microM, only partially inhibited responses to cirazoline in SD, SHR, and WKY, and no differences were noted between the strains. Pertussis toxin pretreatment (50 micrograms/kg, 3 days before experiment) almost completely blocked the responses to clonidine, but only partially inhibited those to cirazoline. After pertussis toxin pretreatment, the responses (maximal effects and EC50s) to clonidine and cirazoline were not significantly different in arteries from the three strains of rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-1 Receptor Antagonists↗