BDNF and NT-3 increase excitatory input connectivity in rat hippocampal cultures

2009 ◽  
Vol 30 (6) ◽  
pp. 998-1010 ◽  
Author(s):  
Shimshon Jacobi ◽  
Jordi Soriano ◽  
Menahem Segal ◽  
Elisha Moses
2010 ◽  
Vol 104 (6) ◽  
pp. 2932-2939 ◽  
Author(s):  
Shimshon Jacobi ◽  
Jordi Soriano ◽  
Elisha Moses

Neurotrophins are known to promote synapse development as well as to regulate the efficacy of mature synapses. We have previously reported that in two-dimensional rat hippocampal cultures, brain-derived neurotrophic factor (BDNF) and neurotrophin-3 significantly increase the number of excitatory input connections. Here we measure the effect of these neurotrophic agents on propagating fronts that arise spontaneously in quasi-one-dimensional rat hippocampal cultures. We observe that chronic treatment with BDNF increased the velocity of the propagation front by about 30%. This change is attributed to an increase in the excitatory input connectivity. We analyze the experiment using the Feinerman–Golomb/Ermentrout–Jacobi/Moses–Osan model for the propagation of fronts in a one-dimensional neuronal network with synaptic delay and introduce the synaptic connection probability between adjacent neurons as a new parameter of the model. We conclude that BDNF increases the number of excitatory connections by favoring the probability to form connections between neurons, but without significantly modifying the range of the connections (connectivity footprint).


2020 ◽  
Author(s):  
Karen A Bell ◽  
Rayne Delong ◽  
Priyodarshan Goswamee ◽  
A Rory McQuiston

Abstract The entorhinal cortex alvear pathway is a major excitatory input to hippocampal CA1, yet nothing is known about its physiological impact. We investigated the alvear pathway projection and innervation of neurons in CA1 using optogenetics and whole cell patch clamp methods in transgenic mouse brain slices. Using this approach, we show that the medial entorhinal cortical alvear inputs onto CA1 pyramidal cells (PCs) and interneurons with cell bodies located in stratum oriens were monosynaptic, had low release probability, and were mediated by glutamate receptors. Optogenetic theta burst stimulation was unable to elicit suprathreshold activation of CA1 PCs but was capable of activating CA1 interneurons. However, different subtypes of interneurons were not equally affected. Higher burst action potential frequencies were observed in parvalbumin-expressing interneurons relative to vasoactive-intestinal peptide-expressing or a subset of oriens lacunosum-moleculare (O-LM) interneurons. Furthermore, alvear excitatory synaptic responses were observed in greater than 70% of PV and VIP interneurons and less than 20% of O-LM cells. Finally, greater than 50% of theta burst-driven inhibitory postsynaptic current amplitudes in CA1 PCs were inhibited by optogenetic suppression of PV interneurons. Therefore, our data suggest that the alvear pathway primarily affects hippocampal CA1 function through feedforward inhibition of select interneuron subtypes.


1983 ◽  
Vol 49 (3) ◽  
pp. 674-685 ◽  
Author(s):  
L. Z. Wise ◽  
D. R. Irvine

1. The auditory responses of 207 single neurons in the intermediate and deep layers of the superior colliculus (SC) of barbiturate -or chloralose-anesthetized cats were recorded extracellularly. Sealed stimulating systems incorporating calibrated probe microphone assemblies were employed to present tone- and noise-burst stimuli. 2. All acoustically activated neurons responded with onset responses to noise bursts. Of those neurons also tested with tonal stimuli, approximately 30% were unresponsive over the frequency range tested (0.1-40 kHz), while the others had higher thresholds to tones than to noise. 3. Details of frequency responsiveness were obtained for 55 neurons; 21 were broadly tuned, while 34 were sharply tuned with clearly defined characteristic frequencies (CFs). All sharply tuned neurons had CFs greater than or equal to 10 kHz. 4. The majority of neurons (81%) responded with latencies in the range 8-20 ms; only 11% of neurons had latencies greater than 30 ms. 5. Binaural response properties were examined for 165 neurons. The great majority (79%) received monaural excitatory input only from the contralateral ear (EO). However, most EO cells were binaurally influenced, the contralateral response being either inhibited (EO/I; 96 of 131 units) or facilitated (EO/F; 33 of 131 units) by simultaneous ipsilateral stimulation. Small subgroups were monaurally excited by either ear (EE cells; 8%) or were unresponsive monaurally but responded strongly to binaural stimulation (OO/F cells; 7%). 6. EO/I, EO/F, and OO/F neurons showed characteristic forms of sensitivity to interaural intensity differences (IIDs). The IID functions of EO/I neurons would be expected to produce large contralateral spatial receptive fields with clearly defined medial borders, such as have been described in studies of deep SC neurons employing free-field stimuli. 7. Preliminary evidence suggests a possible topographic organization of IID sensitivity in deep SC, such that the steeply sloping portion of the function (corresponding to the medial edge of the receptive field) is shifted laterally for EO/I neurons located more caudally in the nucleus. 8. The auditory properties of deep SC neurons are compared with previous reports and implications for the organization of auditory input are considered. The binaural properties and auditory spatial fields of deep SC neurons suggest that any representation of auditory space in this structure is unlikely to be based on restricted spatial fields.


2007 ◽  
Vol 28 (9) ◽  
pp. 1388-1395 ◽  
Author(s):  
Daniela Tardito ◽  
Massimo Gennarelli ◽  
Laura Musazzi ◽  
Raffaella Gesuete ◽  
Stefania Chiarini ◽  
...  

1985 ◽  
Vol 53 (1) ◽  
pp. 252-265 ◽  
Author(s):  
L. A. Miller ◽  
G. Hagiwara ◽  
J. J. Wine

We have used electrophysiological techniques to document segmental differences in the pathways between the giant, escape command axons, lateral giants (LG) and medial giants (MG), and the nongiant, fast flexor (FF) motoneurons. We found no difference in the input from LG and MG axons to FF motoneurons in the posterior (4th and 5th) ganglia. Since flexor motor output in these segments would be inconsistent with the LG-evoked behavior pattern, this finding was puzzling. Electromyographic (EMG) recordings during escape responses by intact unrestrained animals confirm that the FF muscles innervated by the posterior ganglia are not excited during LG-mediated tailflips, but are excited during MG-mediated tailflips. In the 2nd and 3rd ganglia, the command axons fire the FF motoneurons with high probability, in part via electrical excitatory postsynaptic potentials (EPSPs) from premotor neurons, the segmental giants (SG). In the 4th and 5th ganglia, the equivalent pathway is much less effective. Single, directly elicited impulses in SGs in ganglia 2 and 3 fire their respective FF motoneurons with high probability, while those in ganglia 4 and 5 rarely fire FF motoneurons. The command axons fire the SGs reliably in all segments. The amplitude of the SG-evoked EPSP in FF motoneurons is significantly smaller in posterior vs. anterior ganglia. For technical reasons, we are unable to present conclusive evidence on ganglionic variations in FF-motoneuron thresholds. The FF motoneurons receive additional excitatory input from intersegmental interneurons recruited by the command neurons. Motoneurons in ganglia 4 and 5 are excited by large interneurons that do not synapse on motoneurons in ganglia 2 and 3, but this additional input is not sufficient to compensate for the weaker effect of SG input. Unlike the all-or-none segmental differences demonstrated previously for the LG-to-motor giant pathway (24), the SG-to-FF pathway changes gradually, retains significant though subthreshold strength in posterior ganglia, and is common to both LGs and MGs. These features provide opportunities for variation in the spatial patterning of flexion and in the resulting escape trajectories.


2012 ◽  
Vol 107 (4) ◽  
pp. 1241-1246 ◽  
Author(s):  
Gary Marsat ◽  
Leonard Maler

To interact with the environment efficiently, the nervous system must generate expectations about redundant sensory signals and detect unexpected ones. Neural circuits can, for example, compare a prediction of the sensory signal that was generated by the nervous system with the incoming sensory input, to generate a response selective to novel stimuli. In the first-order electrosensory neurons of a gymnotiform electric fish, a negative image of low-frequency redundant communication signals is subtracted from the neural response via feedback, allowing unpredictable signals to be extracted. Here we show that the cancelling feedback not only suppresses the predictable signal but also actively enhances the response to the unpredictable communication signal. A transient mismatch between the predictive feedback and incoming sensory input causes both to be positive: the soma is suddenly depolarized by the unpredictable input, whereas the neuron's apical dendrites remain depolarized by the lagging cancelling feedback. The apical dendrites allow the backpropagation of somatic spikes. We show that backpropagation is enhanced when the dendrites are depolarized, causing the unpredictable excitatory input to evoke spike bursts. As a consequence, the feedback driven by a predictable low-frequency signal not only suppresses the response to a redundant stimulus but also induces a bursting response triggered by unpredictable communication signals.


2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Nikolaos Andreakos ◽  
Shigang Yue ◽  
Vassilis Cutsuridis

AbstractMemory, the process of encoding, storing, and maintaining information over time to influence future actions, is very important in our lives. Losing it, it comes with a great cost. Deciphering the biophysical mechanisms leading to recall improvement should thus be of outmost importance. In this study, we embarked on the quest to improve computationally the recall performance of a bio-inspired microcircuit model of the mammalian hippocampus, a brain region responsible for the storage and recall of short-term declarative memories. The model consisted of excitatory and inhibitory cells. The cell properties followed closely what is currently known from the experimental neurosciences. Cells’ firing was timed to a theta oscillation paced by two distinct neuronal populations exhibiting highly regular bursting activity, one tightly coupled to the trough and the other to the peak of theta. An excitatory input provided to excitatory cells context and timing information for retrieval of previously stored memory patterns. Inhibition to excitatory cells acted as a non-specific global threshold machine that removed spurious activity during recall. To systematically evaluate the model’s recall performance against stored patterns, pattern overlap, network size, and active cells per pattern, we selectively modulated feedforward and feedback excitatory and inhibitory pathways targeting specific excitatory and inhibitory cells. Of the different model variations (modulated pathways) tested, ‘model 1’ recall quality was excellent across all conditions. ‘Model 2’ recall was the worst. The number of ‘active cells’ representing a memory pattern was the determining factor in improving the model’s recall performance regardless of the number of stored patterns and overlap between them. As ‘active cells per pattern’ decreased, the model’s memory capacity increased, interference effects between stored patterns decreased, and recall quality improved.


Sign in / Sign up

Export Citation Format

Share Document