Journal of neurophysiology
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Neurons can display sexual dimorphism in receptor expression, neurotransmitter release, and synaptic plasticity. We have detected sexual dimorphism in functional tachykinin receptors in vagal afferents (nodose ganglion neurons, NGNs) by studying the effects of hormonal variation on the depolarizing actions of substance P (SP) in female guinea pig NGNs. Using conventional "sharp" microelectrode recording plus measurement of serum 17beta-estradiol values, we examined SP responses in NGNs isolated from 1) ovariectomized females (OVX), 2) OVX females treated with 17beta-estradiol (OVX + E2), 3) pregnant females, and 4) males. ⋯ The percentage of SP-sensitive NGNs from OVX females (19%, 21/109; 15 +/- 1.9 mV) was not significantly different (P = 0.361) from that of control males (13%, 11/83; 13 +/- 2.0 mV). The serum 17beta-estradiol values for OVX + E2, pregnant, and OVX females were 23.9 +/- 3.3 pg/ml (n = 8), 16.0 +/- 2.4 pg/ml (n = 4), and 3.9 +/- 0.3 pg/ml (n = 8), respectively. These data indicate that there is a gender difference in NK-1 receptor expression in guinea pig nodose neurons, and they suggest that estrogen may modulate SP responsiveness in these neurons.
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Mammalian vestibular organs have two types of hair cell, type I and type II, which differ morphologically and electrophysiologically. Type I hair cells alone express an outwardly rectifying current, I(K, L), which activates at relatively negative voltages. We used whole cell and patch configurations to study I(K,L) in hair cells isolated from the sensory epithelia of rat semicircular canals. ⋯ Ca(2+)-dependent NO synthase is reported to be in hair cells and nerve terminals in the vestibular epithelium. Excitatory input to vestibular organs may lead, through Ca(2+) influx, to NO production and inhibition of I(K,L). The resulting increase in R(m) would augment the receptor potential, a form of positive feedback.
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Time-varying envelopes are a common feature of acoustic communication signals like human speech and induce a variety of percepts in human listeners. We studied the responses of 109 single neurons in the inferior colliculus (IC) of the anesthetized Mongolian gerbil to contralaterally presented sinusoidally amplitude-modulated (SAM) tones with a wide range of parameters. Modulation transfer functions (MTFs) based on average spike rate (rMTFs) showed regions of enhancement and suppression, where spike rates increased or decreased respectively as stimulus modulation depth increased. ⋯ The results suggest various possible mechanisms that could create IC MTFs, and strongly support the idea that inhibitory inputs shape the rMTF by sharpening regions of enhancement and creating a suppressive region. The paucity of BMFs above 100 Hz argues against simple rate-coding schemes for pitch. Finally, any labeled line or topographic representation of modulation frequency is unlikely to be independent of SPL.
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The effects of dopamine (DA) on a persistent Na(+) current (I(NaP)) in layer V-VI prefrontal cortical (PFC) pyramidal cells were studied using whole cell voltage-clamp recordings in rat PFC slices. After blocking K(+) and Ca (2+) currents, a tetrodotoxin-sensitive I(NaP) was activated by slow depolarizing voltage ramps or voltage steps. DA modulated the I(NaP) in a voltage-dependent manner: increased amplitude of I(NaP) at potentials more negative than -40 mV, but decreased at more positive potentials. ⋯ This was associated with a shift in the start of nonlinearity in the slope resistance to more negative membrane potentials. We proposed that this effect is due to a D1/D5 agonist-induced leftward shift in the activation of I(NaP). This enables DA to facilitate the firing of PFC neurons in response to depolarizing inputs.
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Saccadic eye movements are thought to be influenced by blinking through premotor interactions, but it is still unclear how. The present paper describes the properties of blink-associated eye movements and quantifies the effect of reflex blinks on the latencies, metrics, and kinematics of saccades in the monkey. In particular, it is examined to what extent the saccadic system accounts for blink-related perturbations of the saccade trajectory. ⋯ These data strongly support the idea that blinks interfere with the saccade premotor circuit, presumably upstream from the neural eye-position integrator. They also indicated that a neural mechanism, rather than passive elastic restoring forces within the oculomotor plant, underlies the compensatory behavior. The tight latency coupling between saccades and blinks is consistent with an inhibition of omnipause neurons by the blink system, suggesting that the observed changes in saccade kinematics arise elsewhere in the saccadic premotor system.