Journal of neurophysiology
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Blinks are known to change the kinematic properties of horizontal saccades, probably by influencing the saccadic premotor circuit. The neuronal basis of this effect could be explained by changes in the activity of omnipause neurons in the nucleus raphe interpositus or in the saccade-related burst neurons of the superior colliculus. Omnipause neurons cease discharge during both saccades and vergence movements. ⋯ The blink effect was time dependent with respect to saccade and vergence onset: the greatest effect occurred 100 ms prior to saccade onset, whereas there was no effect when the blink started after saccade onset. The effects of blinks on saccades and vergence, which are tightly coupled to latency, support the hypothesis that blinks cause profound spatiotemporal perturbations of the eye movements by interfering with the normal saccade/vergence premotor circuits. However, the measured effect may to a certain degree but not exclusively be explained by mechanical interference.
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During early neuronal development, GABA functions as an excitatory neurotransmitter, triggering membrane depolarization, action potentials, and the opening of plasma membrane Ca(2+) channels. These excitatory actions of GABA lead to a number of changes in neuronal structure and function. Although the effects of GABA on membrane biophysics during early development have been well documented, little work has been done to examine the possible mechanisms underlying GABA-regulated plastic changes in the developing brain. ⋯ BDNF (100 ng/ml) dramatically increased the frequency of excitatory GABAergic spontaneous postsynaptic currents. Together, these data suggest a positive excitatory feedback loop between GABA and BDNF expression during early development, where GABA facilitates BDNF expression, and BDNF facilitates the synaptic release of GABA. Signaling via the MAPK cascade and the transcription factor CREB appear to play a substantial role in this process.
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Uninjured C-type rat dorsal root ganglion (DRG) neurons predominantly express slowly inactivating TTX-resistant (TTX-R) and slowly repriming TTX-sensitive (TTX-S) Na(+) currents. After peripheral axotomy, TTX-R current density is reduced and rapidly repriming TTX-S currents emerge and predominate. The change in TTX-S repriming kinetics is paralleled by an increase in the level of transcripts and protein for the Na(v)1.3 sodium channel alpha-subunit, which is known to exhibit rapid repriming. ⋯ We observed parallel effects of GDNF and NGF on the Na(v)1.3 sodium channel transcript levels in axotomized DRG. Both GDNF and NGF were able to partially reverse the axotomy-induced increase in Na(v)1.3 mRNA, with GDNF plus NGF producing the largest effect. Our data indicate that both GDNF and NGF can partially reverse an important effect of axotomy on the electrogenic properties of sensory neurons and that their effect is additive.
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This research was guided by the working hypothesis that the aging auditory system progressively loses its ability to process rapid acoustic transients efficiently, and in elderly listeners, this results in difficulties in speech perception. Neural correlates of age-related deficits in temporal processing were investigated by recording from inferior colliculus (IC) neurons from young adult and old CBA mice. Single-unit responses were recorded to sinusoidally amplitude-modulated (SAM) noise carriers, presented at 65-80 dB SPL, having modulation frequencies (MFs) that ranged from 10 to 800 Hz. ⋯ The magnitude of the differences between the young adult and the old spike median responses was greatest at low MFs and then declined as MF increased. Finally, the young adult distribution of rBMFs extends to higher MFs than the old, with 36.0% of units having rBMFs >100 Hz as compared with only 12.5% of the old unit sample. We postulate that this age-related difference in rate coding of SAM noise carriers is consistent with a loss, or imbalance, of excitatory and inhibitory neural mechanisms known to shape encoding of envelope periodicities in the IC.
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Cisplatin causes both acute and chronic forms of tinnitus as well as increases in spontaneous neural activity (hyperactivity) in the dorsal cochlear nucleus (DCN) of hamsters. It has been hypothesized that the induction of hyperactivity in the DCN may be a consequence of cisplatin's effects on cochlear outer hair cells (OHCs); however, systematic studies testing this hypothesis have yet to appear in the literature. In the present investigation, the relationship between hyperactivity and OHC loss, induced by cisplatin, was examined in detail. ⋯ In several of the animals with severe OHC loss and hyperactivity, there was no significant damage to IHC stereocilia nor any observable irregularities of the reticular lamina that might have interfered with normal IHC function. Hyperactivity was also observed in the DCN of animals showing severe losses of OHCs accompanied by damage to IHCs, although the degree of hyperactivity in these animals was less than in animals with severe OHC loss but intact IHCs. These results support the view that loss of OHC function may be a trigger of tinnitus-related hyperactivity in the DCN and suggest that this hyperactivity may be somewhat offset by damage to IHCs.