Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CEREBELLAR CORTEX”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,081 records · Page 60Linked to original sources
PubMed1996

Neural mechanisms of blood flow regulation during synaptic activity in cerebellar cortex.

1. We investigated the neural mechanisms of the increases in blood flow produced by synaptic activity using the parallel fiber (PF) system of the cerebellum as a model. The midline cerebellum was exposed in anesthetized rats and the PFs were stimulated with tungsten microelectrodes. Cerebellar blood flow (BFcrb) was recorded using a laser-Doppler probe, whereas field potentials were recorded using glass micropipettes. PF stimulation produced increases in BFcrb that were related to the frequency and intensity of stimulation (+60 +/- 9%, mean +/- SE, at 100 microA and 30 Hz; n = 6). The greatest increases were confined to a band stretching along the major axis of the stimulated folium and corresponding to the beam of activated PFs. The increase in evoked by PF stimulation was associated with a corresponding increase in glucose utilization, assessed by the 2-deoxyglucose method. The increases in BFcrb and the field potentials evoked by PF stimulation were abolished by tetrodotoxin (1 microM; n = 6). Ringer solution containing 12 mM Mg2+ and 0 mM Ca2+ blocked synaptic activity in the PFs and abolished the increases in flow (P > 0.05 from baseline; n = 5). The broad-spectrum glutamate receptor antagonist kynurenate (5 mM) prevented depolarization of Purkinje cells and interneurons and abolished the increase in BFcrb evoked by PF stimulation (P > 0.05; n = 6). Treatment with tetrodotoxin, Mg2+, or kynurenate did not affect the increase in BFcrb elicited by systemic hypercapnia or by topical application of the nitric oxide donor 3-morpholino sydnonimine (P > 0.05 from Ringer solution). We conclude that the increases in flow produced by synaptic activity are linked to glutamate-induced depolarization of Purkinje cells and interneurons. These findings provide evidence that activation of glutamate receptors participates in the mechanisms of functional hyperemia, and they support the validity of the PF system as a model for study of the relationship between synaptic activity and blood flow in the CNS.

Animals↗
PubMed2004

Local field potential oscillations in primate cerebellar cortex: synchronization with cerebral cortex during active and passive expectancy.

Many brain regions, such as the cerebellum, primary somatosensory cortex (SI), and primary motor cortex (MI), interact to produce coordinated actions. Synchronization of local field potentials (LFPs) in sensorimotor cerebral areas has been related to motor performance, often through 10- to 25-Hz oscillatory LFPs. The macaque cerebellar paramedian lobule (PM) also shows 10- to 25-Hz LFP oscillations, which are modulated in a stimulus-response lever press task to get reward (active condition), but also, albeit differently, in a similarly timed stimulus-reward relation (passive condition). This study focuses on simultaneous LFP activity in primate SI or MI and the PM cerebellum during the active (left- or right-hand lever presses) and passive conditions. Results show a similar modulation pattern of 10- to 25-Hz oscillations in the cerebellum, MI, and SI during the active condition (left or right hand), decreasing after stimulus onset, returning, and again decreasing after movement onset. In the passive condition, when the monkey did not move but got reward, all 3 areas show an oscillatory profile where oscillations increase after stimulus onset and last until reward, denoting a role for these oscillations in passive expectancy. However, synchronization between cerebellar LFPs and SI LFPs is higher during the active condition than during the passive condition, and highest for the interested hand. This greater PM-SI synchronization, when the monkey had to press the lever, could represent a form of cerebro-cerebellar communication, perhaps to serve somatosensory processing to accomplish the task; PM-MI synchronization was less selective for the hand used and might carry a more general type of information.

Animals↗
PubMed2004

Long-term synaptic changes induced in the cerebellar cortex by fear conditioning.

To better understand learning mechanisms, one needs to study synaptic plasticity induced by behavioral training. Recently, it has been demonstrated that the cerebellum is involved in the consolidation of fear memory. Nevertheless, how the cerebellum contributes to emotional behavior is far from known. In cerebellar slices at 10 min and 24 hr following fear conditioning, we found a long-lasting potentiation of the synapse between parallel fibers and Purkinje cells in vermal lobules V-VI, but not in the climbing fiber synapses. The mechanism is postsynaptic, due to an increased AMPA response. In addition, in hotfoot mice with a primary deficiency of the parallel fiber to Purkinje cell synapse, cued (but not contextual) fear conditioning is affected. We propose that this synapse plays an important role in the learned fear and that its long-term potentiation may represent a contribution to the neural substrate of fear memory.

Animals↗
PubMed1989

[Effect of electro-acupuncture (EA) on response of cerebellar cortex to slow pain].

Experiments were performed on cats under chloralose anaesthesia and immobilized by Flaxedil. The right saphenous nerve was stimulated with single rectangular electric pulse of 30V and A-fibers were blocked selectively by the anodal current so as to elicic the C-fiber input only. The cerebellar cortical field potential evoked by C-fiber input (C-CEP) was recorded on the contralateral vermian VI lobule surface. C-CEP can be inhibited obviously by injecting the morphine (0.5 mg/kg) intravenously. It indicated that C-CEP had the close concern with the slow pain information and might be regarded as the index of the slow pain. The effects of the EA at the "Zusanli" point on C-CEP were observed. The results as following: 1. The amplitude of C-CEP decreased obviously after the EA at the ipsilateral "Zusanli" (strength: 10V, duration: 0.2 ms, frequency: 5 Hz). 2. From 5V-30V the more the strength of the EA was, the more the inhibitory efficiency was. 3. The inhibitory efficiency of the EA at the ipsilateral "Zusanli" point on C-CEP was stronger than at the contralateral, and the strongest at the bilateral.

Animals↗