Slow and persistent postinhibitory rebound acts as an intrinsic short-term memory mechanism.
نویسندگان
چکیده
Many neurons exhibit postinhibitory rebound (PIR), in which neurons display enhanced excitability following inhibition. PIR can strongly influence the timing of spikes on rebound from an inhibitory input. We studied PIR in the lateral pyloric (LP) neuron of the stomatogastric ganglion of the crab Cancer borealis. The LP neuron is part of the pyloric network, a central pattern generator that normally oscillates with a period of approximately 1 s. We used the dynamic clamp to create artificial rhythmic synaptic inputs of various periods and duty cycles in the LP neuron. Surprisingly, we found that the strength of PIR increased slowly over multiple cycles of synaptic input. Moreover, this increased excitability persisted for 10-20 s after the rhythmic inhibition was removed. These effects are considerably slower than the rhythmic activity typically observed in LP. Thus this slow postinhibitory rebound allows the neuron to adjust its level of excitability to the average level of inhibition over many cycles, and is another example of an intrinsic "short-term memory" mechanism.
منابع مشابه
Leading role of thalamic over cortical neurons during postinhibitory rebound excitation.
The postinhibitory rebound excitation is an intrinsic property of thalamic and cortical neurons that is implicated in a variety of normal and abnormal operations of neuronal networks, such as slow or fast brain rhythms during different states of vigilance as well as seizures. We used dual simultaneous intracellular recordings of thalamocortical neurons from the ventrolateral nucleus and neurons...
متن کاملClustering through postinhibitory rebound in synaptically coupled neurons.
Postinhibitory rebound is a nonlinear phenomenon present in a variety of nerve cells. Following a period of hyperpolarization this effect allows a neuron to fire a spike or packet of spikes before returning to rest. It is an important mechanism underlying central pattern generation for heartbeat, swimming and other motor patterns in many neuronal systems. In this paper we consider how networks ...
متن کاملMechanism of Postinhibitory Rebound in Molluscan Neurons1
SYNOPSIS. Postinhibitory rebound (PIR) is an intrinsic property of many neurons but the underlying mechanism is not well understood. We studied PIR and its relationship to spike adaptation in B-cells isolated from the buccal ganglia of Aplysia. These neurons exhibit PIR following inhibitory synaptic input and following direct membrane hyperpolarization. Hyperpolarizing and depolarizing voltage ...
متن کاملThe mechanism of postinhibitory rebound increases in plasma gh in acromegalic patients.
The mechanism of postinhibitory rebound increase in GH secretion was studied in 5 normal and 7 acromegalic subjects. Both normal and acromegalic subjects showed prompt GH decreases during the infusion of somatostatin (500 micrograms/75 min) (% decrease: 69.1 +/- 10.4 vs. 73.9 +/- 6.5) and rebound rises after its termination. The rebound rises occurred more promptly and markedly in normal contro...
متن کاملProtective Effect of Short-term Administration of Ethanolic Saffron Extract on improvement of Cognitive Deficits and Decrement of Lipid Peroxidation induced by Ethidium Bromide in Experimental Models of MS
Introduction: Cognitive dysfunction is recognized as a significant feature of multiple sclerosis (MS). Oxidative stress plays an important role in the pathogenesis of MS. Toxic demyelination by ethidium bromide (EB) is one of the common methods for induction of MS, which leads to neuronal death by production of free radicals and enhancement of oxidative stress burden. According to previous p...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- The Journal of neuroscience : the official journal of the Society for Neuroscience
دوره 30 13 شماره
صفحات -
تاریخ انتشار 2010