PubMed Health⌕ Search

PubMed · 9729628

Frequency-dependent synaptic depression modifies postsynaptic firing probability in cats.

Abstract

1. The influence of stimulus trains applied to single I a axons on the firing behaviour of single motoneurones was assessed in anaesthetized cats. The change in motoneurone firing probability associated with a single I a afferent spike was measured from short-latency peaks in peristimulus time histograms or cross-correlograms. Some synapses showed frequency-dependent depression of the short-latency peak, which is consonant with the frequency-dependent depression reported for the I a-motoneurone excitatory postsynaptic potential (EPSP). 2. Where they could be measured, EPSPs superimposed on the depolarizing ramps of potential recorded from motoneurones as they fired repetitively showed frequency-dependent changes in amplitude that parallelled those of the simultaneously recorded histograms. 3. Thus it appears that at synapses with small EPSPs, which are typical in the mammalian CNS, modulation of the EPSP should result in similar modulation of cell firing.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B D Clark, T C Cope. 1998-10-01. Frequency-dependent synaptic depression modifies postsynaptic firing probability in cats.. https://doi.org/10.1111/j.1469-7793.1998.189bf.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Calcium channel subtypes on single GABAergic presynaptic terminal projecting to rat hippocampal neurons.

High voltage-activated Ca(2+) channel subtypes triggering GABA release from nerve terminals (boutons) projecting to rat hippocampal CA1 pyramidal neurons were studied. Evoked GABAergic inhibitory postsynaptic currents (eIPSCs) were recorded in response to focal stimulation of single boutons in mechanically dissociated neurons and in response to stimulation of nerve bundle in slice preparations. Nilvadipine (3 micro M), an L-type Ca(2+) channel blocker, completely inhibited eIPSCs evoked by stimulation of single boutons, but had no effect on eIPSCs evoked by stimulation of nerve bundle at low frequencies. Nilvadipine (3 micro M) did, however, prevent the potentiation of eIPSC amplitude following high-frequency stimulation of nerve bundles in the slice preparation. omega-Conotoxin-GVIA (3 micro M), an N-type Ca(2+) channel blocker, and omega-agatoxin-IVA (0.3 micro M), a P/Q-type Ca(2+) channel blocker, completely inhibited single bouton evoked eIPSCs in 33.3 and 83.3% of recordings, respectively. In response to low-frequency nerve bundle stimulation in the slice preparation, omega-conotoxin-GVIA (3 micro M), omega-agatoxin-IVA (0.1 micro M) both partially reduced eIPSC amplitude, with the residual component being abolished by Cd(2+) (0.1 mM). From these results, the following hypotheses could be drawn. (1). The distribution of P/Q- and N-type channels at a single bouton is nonuniform. (2. When a focal stimulation is applied to a single bouton, L-type channels play a significant role in a generation of an action potential which subsequently activates P/Q- and N-type channels at GABA release sites. (3). Action potentials conducted through axons in the slice preparation are sufficient to depolarize the bouton membrane, even when L-type channels are suppressed.

Afferent Pathways↗

Target-independent specification of proprioceptive sensory neurons.

Previous studies in the chick embryo have shown that sensory neurons fail to innervate muscle in the absence of motor neurons. Instead, motor neuron deletion causes more sensory axons to project to the skin. We used this experimental paradigm to determine when sensory neurons are specified to become proprioceptive afferents. Experimental embryos were treated with either saline or exogenous neurotrophin-3 (NT-3) to promote the survival of proprioceptive afferents. In saline-treated embryos, motor neuron deletion caused an increase in sensory neuron apoptosis on the deleted side, an effect reversed by NT3. Motor neuron deletion also eliminated the sartorious muscle nerve, as previously reported. In NT3-treated embryos, this altered nerve pattern was accompanied by the enlargement of the adjacent cutaneous nerve. These embryos were further analyzed by using immunohistochemistry for trkC (a receptor for NT3) retrograde and transganglionic labeling. Our results show that, following motor neuron deletion, more trkC+ afferents project in cutaneous nerves on the deleted side of NT3-treated embryos. Transganglionic labeling demonstrated that at least some of these neurons made spinal projections that are typical of proprioceptive afferents. These results therefore indicate that the proprioceptive phenotype is specified prior to target innervation and that these neurons can retain their identity despite projecting to inappropriate (cutaneous) targets.

Afferent Pathways↗

Avian brainstem neurogenesis is stimulated during cochlear hair cell regeneration.

Unlike mammals, adult avians are able to regenerate cochlear sensory hair cells following injury. Brainstem auditory neurons in chicken nucleus magnocellularis (NM), which receive their sole excitatory afferent input from the cochlea, were examined for evidence of mitosis during ototoxin-induced loss and regeneration of cochlear hair cells. Using tritiated thymidine as a mitotic marker in tissue processed for autoradiography and counterstained with thionin, labeled NM neurons and glia were counted from chickens killed 16 days after gentamicin or saline injections. Newly generated NM neurons were observed during cochlear hair cell regeneration. More labeled neurons were observed in the experimental chickens, but a few were also seen in the control chickens. We predicted labeled NM neurons would be found solely in the rostral high frequency region, given the gentamicin-induced high frequency cochlear hair cell loss and regeneration. However, the labeled NM neurons were located throughout the tonotopic axis of the nucleus. The total number of labeled neurons was lower than predicted. Many labeled NM glia were observed in experimental and control chickens. Labeled cells were also observed throughout the chicken brainstem and cerebellum in both experimental and control chickens, indicating great potential for CNS plasticity. Results in NM indicate the avian auditory system is capable of regenerating brainstem auditory neurons in addition to the previously well-established capability of regenerating cochlear hair cells in response to ototoxic injury. Recovery of both central and peripheral auditory components will be necessary to restore hearing damaged by noise or ototoxic drugs.

Afferent Pathways↗