scholarly journals GABAB Presynaptic Inhibition Has an In Vivo Time Constant Sufficiently Rapid to Allow Modulation at Theta Frequency

2002 ◽  
Vol 87 (3) ◽  
pp. 1196-1205 ◽  
Author(s):  
Bradley J. Molyneaux ◽  
Michael E. Hasselmo
Keyword(s):  
Receptor Antagonist ◽  
Time Constant ◽  
Presynaptic Inhibition ◽  
Time Course ◽  
Theta Rhythm ◽  
Hippocampal Formation ◽  
Gabaergic Interneurons ◽  
Glutamatergic Synaptic Transmission ◽  
Theta Frequency

Cyclical activity of GABAergic interneurons during theta rhythm could mediate phasic changes in strength of glutamatergic synaptic transmission in the hippocampal formation if presynaptic inhibition from activation of GABAB receptors is sufficiently rapid to change within a theta cycle. The experiments described here analyzed the time course of GABABmodulation using a heterosynaptic depression paradigm in anesthetized rats at physiological temperatures. Heterosynaptic depression of the slope of evoked potentials decayed with a time constant that would allow significant changes in transmission across different phases of the theta cycle. This heterosynaptic depression was significantly reduced by local infusion of the GABAB receptor antagonist CGP55845A.

Relation between venous pressure and blood volume in the intestine

1963 ◽  
Vol 204 (1) ◽  
pp. 31-34 ◽  
Author(s):  
Paul C. Johnson ◽  
Kenneth M. Hanson
Keyword(s):  
Blood Volume ◽  
Time Constant ◽  
Time Course ◽  
Venous Pressure ◽  
High Viscosity ◽  
Exponential Process ◽  
Pressure Volume Relationship ◽  
Venous Volume ◽  
Volume Characteristics

The pressure volume characteristics of the intestinal venous vasculature were studied in vivo by a weight technique. The pressure-volume relationship was linear over the range 0–20 mm Hg. In a few experiments the volume increment appeared to be reduced at venous pressures above 30 mm Hg. The average compliance of the intestinal veins was 0.34 ml/mm Hg 100 g tissue. The time course of the blood volume change was also examined. Rapid elevation of venous pressure to a higher level caused blood volume to increase at an exponentially declining rate. Therefore, the phenomenon of creep in the intestinal veins appears to be a simple exponential process. The half time of the increase in venous volume averaged 7.5 sec while the time constant was 10.9 sec. The magnitude of the time constant suggests the presence of elements of rather high viscosity in the venous wall.

The effect of carbenoxolone on hippocampal formation theta rhythm in rats: In vitro and in vivo approaches

2009 ◽  
Vol 78 (6) ◽  
pp. 290-298 ◽  
Author(s):  
Renata Bocian ◽  
Anna Posłuszny ◽  
Tomasz Kowalczyk ◽  
Henryk Gołębiewski ◽  
Jan Konopacki
Keyword(s):  
Theta Rhythm ◽  
Hippocampal Formation

scholarly journals Endocannabinoids regulate mAChR-evoked theta rhythm IPSCs in hippocampus

2015 ◽  
Author(s):  
Ai-Hui Tang ◽  
Daniel A Nagode ◽  
Bradley E Alger
Keyword(s):  
Theta Rhythm ◽  
Cannabinoid Receptor ◽  
Spectral Power ◽  
Hippocampal Slices ◽  
Ionotropic Glutamate Receptors ◽  
Frequency Range ◽  
Neuronal Oscillations ◽  
Theta Frequency ◽  
Endogenous Cannabinoids

Exogenous cannabinoids can affect behaviorally relevant neuronal oscillations, but there is little evidence that endogenous cannabinoids (endocannabinoids, eCBs) can affect them, although it is unknown whether eCBs were generated during oscillations investigated in previous studies. In rat hippocampal slices, muscarinic receptor (mAChR) agonists stimulate the occurrence of persistent, rhythmic inhibitory post-synaptic currents (IPSC) activity and mobilize eCBs. We tested the hypothesis that mAChR-induced IPSCs would be modulated by concomitantly produced eCBs. With ionotropic glutamate receptors inhibited, mAChR agonist application triggered eCB-sensitive IPSCs that were enhanced in amplitude and frequency when a cannabinoid receptor antagonist was also present. There was also a highly significant increase in IPSC spectral power in the theta-frequency range. The data show that eCBs released by mAChRs modulate rhythmic IPSCs, and suggest that eCBs are candidate regulators of neuronal oscillations associated with eCB production in vivo.

Orexinergic theta rhythm in the rat hippocampal formation: In vitro and in vivo findings

Hippocampus ◽  
2015 ◽  
Vol 25 (11) ◽  
pp. 1393-1406 ◽  
Author(s):  
Renata Bocian ◽  
Paulina Kazmierska ◽  
Paulina Kłos-Wojtczak ◽  
Tomasz Kowalczyk ◽  
Jan Konopacki
Keyword(s):  
Theta Rhythm ◽  
Hippocampal Formation

scholarly journals Differences in Time Course of ACh and GABA Modulation of Excitatory Synaptic Potentials in Slices of Rat Hippocampus

2001 ◽  
Vol 86 (4) ◽  
pp. 1792-1802 ◽  
Author(s):  
Michael E. Hasselmo ◽  
Brian P. Fehlau
Keyword(s):  
Presynaptic Inhibition ◽  
Acetylcholine Receptors ◽  
Time Course ◽  
Onset Time ◽  
Afferent Input ◽  
Muscarinic Acetylcholine Receptors ◽  
Time Constants ◽  
Synaptic Potentials ◽  
Extracellular Potentials

Activation of muscarinic receptors and GABABreceptors causes presynaptic inhibition of glutamatergic synaptic potentials at excitatory feedback connections in cortical structures. These effects may regulate dynamics in cortical structures, with presynaptic inhibition allowing extrinsic afferent input to dominate during encoding, while the absence of presynaptic inhibition allows stronger excitatory feedback during retrieval or consolidation. However, proposals for a functional role of such modulatory effects strongly depend on the time course of these modulatory effects; how rapidly can they turn off and on? In brain slice preparations of hippocampal region CA1, we have explored the time course of suppression of extracellularly recorded synaptic potentials after pressure pulse application of acetylcholine and GABA. Acetylcholine causes suppression of extracellular potentials with onset time constants between 1 and 2 s, and decay constants ranging between 10 and 20 s, even with very brief injection pulses. GABA causes suppression of extracellular potentials with onset time constants between 0.2 and 0.7 s, and decay time constants that decrease to values shorter than 2 s for very brief injection pulses. These techniques do not give an exact measure of the physiological time course in vivo, but they give a notion of the relative time course of the two modulators. The slow changes due to activation of muscarinic acetylcholine receptors may alter the dynamics of cortical circuits over longer intervals (e.g., between different stages of waking and sleep), setting dynamics appropriate for encoding versus consolidation processes. The faster changes in synaptic potentials caused by GABA could cause changes within each cycle of the theta rhythm, rapidly switching between encoding and retrieval dynamics during exploration.

Differential Effects of a Novel Non-Peptide Endothelin Receptor Antagonist (Bosentan) in Rat Liver and Vasculature

1995 ◽  
Vol 89 (6) ◽  
pp. 575-579 ◽  
Author(s):  
Paddy A. Phillips ◽  
John Risvanis ◽  
Kathryn Aldred ◽  
Louise M. Burrell ◽  
Briony Bartholomeusz
Keyword(s):  
Receptor Antagonist ◽  
Time Course ◽  
Competitive Inhibition ◽  
Ex Vivo ◽  
Female Rat ◽  
Endothelin Receptor ◽  
Binding Characteristics ◽  
Orally Active

1. We studied the effects of the non-selective, non-peptide, orally active endothelin (ET) receptor antagonist bosentan (Ro 47–0203) on rat hepatic and mesenteric vascular membrane 125I-ET-1 binding characteristics in vitro and ex vivo (after bosentan by gavage in vivo). 2. Bosentan caused a concentration-dependent competitive inhibition of 125I-ET-1 binding to female rat mesenteric vascular (predominantly ETA receptors) and hepatic (predominantly ETB receptors) membranes in vitro and ex viva 3. The time course of the inhibition of binding ex vivo after administration of bosentan in vivo was 1–4 h for mesenteric vascular (predominantly ETA receptors) binding and 1–16 h for hepatic (predominantly ETB receptors) binding. 4. The time course of displacement of 125I-ET-1 binding from mesenteric vascular and hepatic membranes by bosentan in vitro was similar. 5. Since bosentan is significantly excreted by the liver, the prolonged hepatic 125I-ET-1 binding by bosentan presumably represents hepatic accumulation of bosentan, which may have implications for bosentan antagonizing the actions of ET in the liver.

Mechanisms of Dopamine Activation of Fast-Spiking Interneurons That Exert Inhibition in Rat Prefrontal Cortex

2002 ◽  
Vol 88 (6) ◽  
pp. 3150-3166 ◽  
Author(s):  
Natalia Gorelova ◽  
Jeremy K. Seamans ◽  
Charles R. Yang
Keyword(s):  
Prefrontal Cortex ◽  
Receptor Antagonist ◽  
Pyramidal Neurons ◽  
Sch 23390 ◽  
Membrane Depolarization ◽  
Inward Rectifier ◽  
Repetitive Firing ◽  
Gabaergic Interneurons ◽  
Fast Spiking

Prefrontal cortical dopamine (DA) modulates pyramidal cell excitability directly and indirectly by way of its actions on local circuit GABAergic interneurons. DA modulation of interneuronal functions is implicated in the computational properties of prefrontal networks during cognitive processes and in schizophrenia. Morphologically and electrophysiologically distinct classes of putative GABAergic interneurons are found in layers II-V of rat prefrontal cortex. Our whole cell patch-clamp study shows that DA induced a direct, TTX-insensitive, reversible membrane depolarization, and increased the excitability of fast-spiking (FS) interneurons. The DA-induced membrane depolarization was reduced significantly by D1/D5 receptor antagonist SCH 23390, but not by the D2 receptor antagonist (−)sulpiride, D4 receptor antagonists U101958 or L-745870, α1-adrenoreceptor antagonist prazosin, or serotoninergic receptor antagonist mianserin. The D1/5 agonists SKF81297 or dihydrexidine, but not D2 agonist quinpirole, also induced a prolonged membrane depolarization. Voltage-clamp analyses of the voltage-dependence of DA-sensitive currents, and the effects of changing [K+]O on reversal potentials of DA responses, revealed that DA suppressed a Cs+-sensitive inward rectifier K+ current and a resting leak K+ current. D1/D5, but not D2 agonists mimicked the suppressive effects of DA on the leak current, but the DA effects on the inward rectifier K+ current were not mimicked by either agonist. In a subgroup of FS interneurons, the slowly inactivating membrane outward rectification evoked by depolarizing voltage steps was also attenuated by DA. Collectively, these data showed that DA depolarizes FS interneurons by suppressing a voltage-independent ‘leak’ K+ current (via D1/D5 receptor mechanism) and an inwardly rectifying K+ current (via unknown DA mechanisms). Additional suppression of a slowly inactivating K+ current led to increase in repetitive firing in response to depolarizing inputs. This D1-induced increase in interneuron excitability enhances GABAergic transmission to PFC pyramidal neurons and could represent a mechanism via which DA suppresses persistent firing of pyramidal neurons in vivo.

scholarly journals Linking minimal and detailed models of CA1 microcircuits reveals how theta rhythms emerge and how their frequencies are controlled

2020 ◽  
Author(s):  
Alexandra P Chatzikalymniou ◽  
Melisa Gumus ◽  
Anton R Lunyov ◽  
Scott Rich ◽  
Jeremie Lefebvre ◽  
...  
Keyword(s):  
Pyramidal Cell ◽  
Theta Rhythm ◽  
Computational Models ◽  
Pyramidal Cells ◽  
Cell Types ◽  
Minimal Models ◽  
Detailed Model ◽  
Theta Frequency ◽  
Hippocampal Theta

AbstractThe wide variety of cell types and their inherent biophysical complexities pose a challenge to our understanding of oscillatory activities produced by cellular-based computational models. This challenge stems from the high-dimensional and multi-parametric nature of these systems. To overcome this issue, we implement systematic comparisons of minimal and detailed models of CA1 microcircuits that generate intra-hippocampal theta rhythms (3-12 Hz). We leverage insights from minimal models to guide detailed model explorations and obtain a cellular perspective of theta generation. Our findings distinguish the pyramidal cells as the theta rhythm initiators and reveal that their activity is regularized by the inhibitory cell populations, supporting an ‘inhibition-based tuning’ mechanism. We find a strong correlation between the pyramidal cell input current and the resulting LFP theta frequency, establishing that the intrinsic pyramidal cell properties underpin network frequency characteristics. This work provides a cellular-based foundation from which in vivo theta activities can be explored.

Pharmacological analysis of components of the change in transmural potential difference evoked by distension of rat proximal small intestine in vivo

2008 ◽  
Vol 294 (1) ◽  
pp. G165-G173 ◽  
Author(s):  
Marie H. Larsson ◽  
Maria Sapnara ◽  
Evan A. Thomas ◽  
Joel C. Bornstein ◽  
Erik Lindström ◽  
...  
Keyword(s):  
Small Intestine ◽  
Receptor Antagonist ◽  
Time Course ◽  
Slow Component ◽  
Chloride Secretion ◽  
Rapid Response ◽  
Sustained Response ◽  
Potential Difference ◽  
Reflex Response

The reflex response to distension of the small intestine in vivo is complex and not well understood. The aim of this study was to characterize the neural mechanisms contributing to the complex time course of the intestinal secretory response to distension. Transmucosal potential difference (PD) was used as a marker for mucosal chloride secretion, which reflects the activity of the secretomotor neurons. Graded distensions (5, 10, and 20 mmHg) of distal rat duodenum with saline for 5 min induced a biphasic PD response with an initial peak (rapid response) followed by a plateau (sustained response). The rapid response was significantly reduced by the neural blockers tetrodotoxin and lidocaine (given serosally) and by intravenous (iv) administration of the ganglionic blocker hexamethonium and the NK1 receptor antagonist SR-140333. Serosal TTX and iv SR-140333 significantly reduced the sustained response, which was also reduced by the NK3 receptor antagonist talnetant and by the vasoactive intestinal polypeptide (VPAC) receptor antagonist [4Cl-d-Phe6, Leu17]-VIP. Serosal lidocaine and iv hexamethonium had no significant effect on this component. Inhibition of nitric oxide synthase had no effect on any of the components of the PD response to distension. The PD response to distension thus seems to consist of two components, a rapidly activating and adapting component operating via nicotinic transmission and NK1 receptors, and a slow component operating via VIP-ergic transmission and involving both NK1 and NK3 receptors.

scholarly journals In Vivo Calcium Accumulation in Presynaptic and Postsynaptic Dendrites of Visual Interneurons

1999 ◽  
Vol 82 (6) ◽  
pp. 3327-3338 ◽  
Author(s):  
Volker Dürr ◽  
Martin Egelhaaf
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Visual Motion ◽  
Direction Selectivity ◽  
Calcium Signal ◽  
Spatial Integration ◽  
Lobula Plate ◽  
Calcium Accumulation ◽  
Low Pass

In this comparative in vivo study of dendritic calcium accumulation, we describe the time course and spatial integration properties of two classes of visual interneurons in the lobula plate of the blowfly. Calcium accumulation was measured during visual motion stimulation, ensuring synaptic activation of the neurons within their natural spatial and temporal operating range. The compared cell classes, centrifugal horizontal (CH) and horizontal system (HS) cells, are known to receive retinotopic input of similar direction selectivity, but to differ in morphology, biophysics, presence of dendrodendritic synapses, and computational task. 1) The time course of motion-induced calcium accumulation was highly invariant with respect to stimulus parameters such as pattern contrast and size. In HS cells, the rise of [Ca2+]i can be described by a single exponential with a time constant of 5–6 s. The initial rise of [Ca2+]i in CH cells was much faster (τ ≈ 1 s). The decay time constant in both cell classes was estimated to be at least 3.5 times longer than the corresponding rise time constant. 2) The voltage-[Ca2+]i relationship was best described by an expansive nonlinearity in HS cells and an approximately linear relationship in CH cells. 3) Both cell classes displayed a size-dependent saturation nonlinearity of the calcium accumulation. Although in CH cells calcium saturation was indistinguishable from saturation of the membrane potential, saturation of the two response parameters differed in HS cells. 4) There was spatial overlap of the calcium signal in response to nonoverlapping visual stimuli. Both the area and the amplitude of the overlap profile was larger in CH cells than in HS cells. Thus calcium accumulation in CH cells is spatially blurred to a greater extent than in HS cells. 5) The described differences between the two cell classes may reflect the following computational tasks of these neurons: CH cells relay retinotopic information within the lobula plate via dendritic synapses with pronounced spatial low-pass filtering. HS cells are output neurons of the lobula plate, in which the slow, local calcium accumulation may be suitable for local modulatory functions.

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