Home  About us  Contact
 

Synaptic Integration (synaptic + integration)

Distribution by Scientific Domains
Life Sciences100%

Selected Abstracts

Soluble guanylyl cyclase appears in a specific subset of periglomerular cells in the olfactory bulb

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2005
Maria Gutičrrez-Mecinas
Abstract In the brain, nitric oxide acts as an atypical messenger in cellular nonsynaptic transmission. In the olfactory bulb, this gas is produced at the level of the olfactory glomeruli by a subpopulation of periglomerular cells that participates in the first synaptic relay of the olfactory information between the olfactory nerve and the dendritic tufts of principal cells. It has been proposed that nitric oxide modulates intraglomerular synaptic integration of sensory inputs, but its specific role in the glomerular circuitry remains to be understood. In this article, we demonstrate that, in the glomerular circuits, a specific subset of periglomerular cells, most of them expressing the calcium binding protein calbindin D-28 k, expresses the ,1 subunit of the soluble guanylyl cyclase. These cells could be the targets for the action of nitric oxide at the glomerular level via activation of soluble guanylyl cyclase and production of cGMP. [source]

Effects of variability in anatomical reconstruction techniques on models of synaptic integration by dendrites: a comparison of three internet archives

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2004
Tibor Szilágyi
Abstract The first step in building a realistic computational neuron model is to produce a passive electrical skeleton on to which active conductances can be grafted. For this, anatomically accurate morphological reconstructions of the desired cell type are required. In this study compartmental models were used to compare from a functional perspective three on-line archives of rat hippocampal CA1 pyramidal cell morphologies. The topological organization of cells was found to be similar for all archives, but several morphometric differences were observed. The three-dimensional size of the cells, the diameter and tortuosity of dendrites, and the electrotonic length of the main apical dendrite and of the branches in stratum lacunosum moleculare were dissimilar. The experimentally measured kinetics of somatically recorded inhibitory postsynaptic currents evoked in the stratum lacunosum moleculare (data from the literature) could be reproduced only using the archives that contained cells with an electrotonically short main apical dendrite. In the amplitude attenuation of the simulated postsynaptic currents and the voltage escape from the command potential under voltage clamp conditions, a two- to three-fold difference was observed among archives. Upon activation of a single model synapse on distal branches, cells with low dendritic diameter showed a voltage escape larger than 15 mV. The diameter of the dendrites influenced greatly the results, emphasizing the importance of methods that allow an accurate measurement of this parameter. Our results indicate that there are functionally significant differences in the morphometric data available in different archives even if the cell type, brain region and species are the same. [source]

Active properties of motoneurone dendrites: diffuse descending neuromodulation, focused local inhibition

THE JOURNAL OF PHYSIOLOGY, Issue 5 2008
C. J. Heckman
The dendrites of spinal motoneurones are highly active, generating a strong persistent inward current (PIC) that has an enormous impact on processing of synaptic input. The PIC is subject to regulation by descending neuromodulatory systems releasing the monoamines serotonin and noradrenaline. At high monoaminergic drive levels, the PIC dominates synaptic integration, generating an intrinsic dendritic current that is as much as 5-fold larger than the current entering via synapses. Without the PIC, motoneurone excitability is very low. Presumably, this descending control of the synaptic integration via the PIC is used to adjust the excitability (gain) of motoneurones for different motor tasks. A problem with this gain control is that monoaminergic input to the cord is very diffuse, affecting many motor pools simultaneously, probably including both agonists and antagonists. The PIC is, however, exquisitely sensitive to the reciprocal inhibition mediated by length sensitive muscle spindle Ia afferents and Ia interneurones. Reciprocal inhibition is tightly focused, shared only between strict mechanical antagonists, and thus can act to ,sculpt' specific movement patterns out of a background of diffuse neuromodulation. Thus it is likely that motoneurone gain is set by the interaction between diffuse descending neuromodulation and specific and focused local synaptic inhibitory circuits. [source]

Synaptic release of dopamine in the subthalamic nucleus

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2004
Stephanie J. Cragg
Abstract The direct modulation of subthalamic nucleus (STN) neurons by dopamine (DA) neurons of the substantia nigra (SN) is controversial owing to the thick caliber and low density of DA axons in the STN. The abnormal activity of the STN in Parkinson's disease (PD), which is central to the appearance of symptoms, is therefore thought to result from the loss of DA in the striatum. We carried out three experiments in rats to explore the function of DA in the STN: (i) light and electron microscopic analysis of tyrosine hydroxylase (TH)-, dopamine ,-hydroxylase (D,H)- and DA-immunoreactive structures to determine whether DA axons form synapses; (ii) fast-scan cyclic voltammetry (FCV) to determine whether DA axons release DA; and (iii) patch clamp recording to determine whether DA, at a concentration similar to that detected by FCV, can modulate activity and synaptic transmission/integration. TH- and DA-immunoreactive axons mostly formed symmetric synapses. Because D,H-immunoreactive axons were rare and formed asymmetric synapses, they comprised the minority of TH-immunoreactive synapses. Voltammetry demonstrated that DA release was sufficient for the activation of receptors and abolished by blockade of voltage-dependent Na+ channels or removal of extracellular Ca2+. The lifetime and concentration of extracellular DA was increased by blockade of the DA transporter. Dopamine application depolarized STN neurons, increased their frequency of activity and reduced the impact of ,-aminobutyric acid (GABA)-ergic inputs. These findings suggest that SN DA neurons directly modulate the activity of STN neurons and their loss may contribute to the abnormal activity of STN neurons in PD. [source]