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Cholinergic receptors in the inferior colliculus influence the acoustic response of nucleus of the brachium of the inferior colliculus in chinchillas.
The nucleus of the brachium of the inferior colliculus (NIC) receives topographical and tonotopic input from the cochlear nucleus of the midbrain. Previous studies have shown that local injection of carbachol or histamine into the cochlear nucleus increases the spontaneous rate of firing of NIC neurons by an excitatory process mediated by a cholinergic receptor (ChR). The current experiments were designed to determine whether this excitatory effect was mediated by muscarinic (M) receptors, since they are the receptors believed to mediate excitatory effects of cholinergic stimulation in the central nervous system. Evoked potentials in the NIC in response to ipsilateral stimulation of the cochlear nucleus were recorded in urethane-anesthetized, paralyzed chinchillas. A population of NIC neurons responded to ipsilateral stimulation with an inhibitory volley. Exogenous application of the muscarinic receptor agonist, carbachol, or the M1 receptor antagonist, pirenzepine, into the cochlear nucleus decreased the amplitude of the recorded inhibitory response. In contrast, the M2 receptor antagonist, AF-DX 116, had no effect. Co-administration of the M1 and M2 receptor antagonists, pirenzepine and AF-DX 116, had no effect, indicating that the muscarinic receptors on NIC neurons are of the M1 type. These results suggest that muscarinic stimulation of cochlear nucleus neurons can influence the activity of NIC neurons through an excitatory pathway.Selective inhibition of mitochondrial respiration by amphotericin B.
Amphotericin B is a cell-permeable, lipid-soluble polyene antibiotic which is commonly used in the treatment of infections caused by molds. The toxicity of amphotericin B is thought to be associated with its interaction with mitochondrial inner membranes. Since this interaction is not known in detail, we have characterized this interaction in rat liver mitochondria using two spectrophotometric techniques: incubation with radiolabeled amphotericin B, with the mitochondrial swelling technique. The binding of amphotericin B to rat liver mitochondria causes the loss of inner membrane integrity indicated by an increase
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