Hemodynamic responses in the rat hippocampus are simultaneously controlled by at least two independently acting neurovascular coupling mechanisms.

We combined electrical perforant pathway stimulation with electrophysiological and fMRI recordings in the hippocampus to investigate the effects of neuronal afterdischarges (nAD) on subsequent fMRI BOLD signals in the presence of isoflurane and medetomidine. These two drugs already alter basal hemodynamics in the hippocampus, with isoflurane being mildly vasodilatory and medetomidine being mildly vasoconstrictive. The perforant pathway was stimulated once for 8 seconds with either continuous 20 Hz pulses () or 8 bursts of 20 high-frequency pulses ().

Brief neuronal afterdischarges in the rat hippocampus lead to transient changes in oscillatory activity and to a very long-lasting decline in BOLD signals without inducing a hypoxic state.

The effects of hippocampal neuronal afterdischarges (nAD) on hemodynamic parameters, such as blood-oxygen-level-dependent (BOLD) signals) and local cerebral blood volume (CBV) changes, as well as neuronal activity and metabolic parameters in the dentate gyrus, was investigated in rats by combining in vivo electrophysiology with functional magnetic resonance imaging (fMRI) or H-nuclear magnetic resonance spectroscopy (H-NMRS). Brief electrical high-frequency pulse-burst stimulation of the right perforant pathway triggered nAD, a seizure-like activity, in the right dentate gyrus with a high incidence, a phenomenon that in turn caused a sustained decrease in BOLD signals for more than 30 min. The decrease was associated with a reduction in CBV but not with signs of hypoxic metabolism.

The cholinergic system modulates negative BOLD responses in the prefrontal cortex once electrical perforant pathway stimulation triggers neuronal afterdischarges in the hippocampus.

Repeated high-frequency pulse-burst stimulations of the rat perforant pathway elicited positive BOLD responses in the right hippocampus, septum and prefrontal cortex. However, when the first stimulation period also triggered neuronal afterdischarges in the hippocampus, then a delayed negative BOLD response in the prefrontal cortex was generated. While neuronal activity and cerebral blood volume (CBV) increased in the hippocampus during the period of hippocampal neuronal afterdischarges (h-nAD), CBV decreased in the prefrontal cortex, although neuronal activity did not decrease.

Electrical Stimulation of the Lateral Entorhinal Cortex Causes a Frequency-Specific BOLD Response Pattern in the Rat Brain.

Although deep brain stimulation of the entorhinal cortex has recently shown promise in the treatment of early forms of cognitive decline, the underlying neurophysiological processes remain elusive. Therefore, the lateral entorhinal cortex (LEC) was stimulated with trains of continuous 5 Hz and 20 Hz pulses or with bursts of 100 Hz pulses to visualize activated neuronal networks, i.e.

Low frequency pulse stimulation of Schaffer collaterals in Trpm4 knockout rats differently affects baseline BOLD signals in target regions of the right hippocampus but not BOLD responses at the site of stimulation.

Electrical stimulation of right Schaffer collateral in Trpm4 knockout and wild type rats were used to study the role of Trpm4 channels for signal processing in the hippocampal formation. Stimulation induced neuronal activity was simultaneously monitored in the CA1 region by in vivo extracellular field recordings and in the entire brain by BOLD fMRI measurements. In wild type and Trpm4 knockout rats, consecutive 5 Hz pulse trains elicited similar neuronal responses in the CA1 region and similar BOLD responses in the stimulated right hippocampus.

Disentangling the role of TRPM4 in hippocampus-dependent plasticity and learning: an electrophysiological, behavioral and FMRI approach.

Hippocampal long-term potentiation (LTP) has been extensively studied as a cellular model of learning and memory. Recently, we described a central function of the Transient Receptor Potential M4 (TRPM4) channel in hippocampal LTP in mice in vitro. Here, we used Trpm4 knock-out (Trpm4) rats to scrutinize TRPM4's role in the intact brain in vivo.

Synchronized electrical stimulation of the rat medial forebrain bundle and perforant pathway generates an additive BOLD response in the nucleus accumbens and prefrontal cortex.

To study how a synchronized activation of two independent pathways affects the fMRI response in a common targeted brain region, blood oxygen dependent (BOLD) signals were measured during electrical stimulation of the right medial forebrain bundle (MFB), the right perforant pathway (PP) and concurrent stimulation of the two fiber systems. Repetitive electrical stimulations of the MFB triggered significant positive BOLD responses in the nucleus accumbens (NAcc), septum, anterior cingulate cortex/medial prefrontal cortex (ACC/mPFC), ventral tegmental area/substantia nigra (VTA/SN), right entorhinal cortex (EC) and colliculus superior, which, in general, declined during later stimulation trains. At the same time, negative BOLD responses were observed in the striatum.

Perforant pathway stimulation as a conditioned stimulus for active avoidance learning triggers BOLD responses in various target regions of the hippocampus: a combined fMRI and electrophysiological study.

Functional magnetic resonance imaging and electrophysiology were combined to monitor blood oxygen level dependent (BOLD) signals in the entire rat brain and neuronal activities in the dentate gyrus during electrical stimulation of the right perforant pathway. In naïve, medetomidine sedated animals, stimulation of the fiber bundle with 15 trains (i.e.

NMDA-dependent mechanisms only affect the BOLD response in the rat dentate gyrus by modifying local signal processing.

The role of N-methyl-D-aspartate (NMDA) receptor-mediated mechanisms in the formation of a blood oxygen level-dependent (BOLD) response was studied using electrical stimulation of the right perforant pathway. Stimulation of this fiber bundle triggered BOLD responses in the right hippocampal formation and in the left entorhinal cortex. The perforant pathway projects to and activates the dentate gyrus monosynaptically, activation in the contralateral entorhinal cortex is multisynaptic and requires forwarding and processing of signals.

Low frequency stimulation of the perforant pathway generates anesthesia-specific variations in neural activity and BOLD responses in the rat dentate gyrus.

To study how various anesthetics affect the relationship between stimulus frequency and generated functional magnetic resonance imaging (fMRI) signals in the rat dentate gyrus, the perforant pathway was electrically stimulated with repetitive low frequency (i.e., 0.

Effects of transient global ischaemia on freezing behaviour and activity in a context-dependent fear conditioning task--implications for memory investigations.

Transient global ischaemia induces cell death in the CA1 layer of the hippocampus. To evaluate the functional consequences, we performed context-dependent fear conditioning. Ischaemia was induced by 2-vessel-occlusion (2VO) in gerbils.

The current functional state of local neuronal circuits controls the magnitude of a BOLD response to incoming stimuli.

The purpose of this study was to determine how the history-dependent activation state of neuronal networks controls fMRI signals to incoming stimuli. Simultaneous electrophysiological and blood oxygen level-dependent (BOLD) responses were monitored during stimulation of the perforant pathway with low, high, and again low intensity but, otherwise identical pulse trains. Under three different anesthetics (alpha-chloralose, medetomidine, isoflurane) consecutive low intensity stimulation trains, set just below the threshold for population spike generation to single pulses, yielded a stable BOLD response, although at different magnitudes.

Distinct H2O2 concentration promotes proliferation of tumour cells after transient oxygen/glucose deprivation.

A solid tumour undergoes ischemia/reperfusion due to deficient vascularization and subsequent formation of new blood vessels. This study investigated the effect of transient oxygen and glucose deprivation (OGD) on proliferation of C6 glioma cells. The cells were subjected to 18 h of OGD followed by reoxygenation in the presence of glucose and different extra-cellular H(2)O(2) concentrations since H(2)O(2) affects cell proliferation.