An MRI time course of 512 echo-planar images (EPI) in resting human brain obtained every 250 ms reveals fluctuations in signal intensity in each pixel that have a physiologic origin. Regions of the sensorimotor cortex that were activated secondary to hand movement were identified using functional MRI methodology (FMRI). Time courses of low frequency (< 0.1 Hz) fluctuations in resting brain were observed to have a high degree of temporal correlation (P < 10(-3)) within these regions and also with time courses in several other regions that can be associated with motor function. It is concluded that correlation of low frequency fluctuations, which may arise from fluctuations in blood oxygenation or flow, is a manifestation of functional connectivity of the brain.

Functional connectivity in the motor cortex of resting human brain using echo-planar MRI.

The reverse transcription polymerase chain reaction (RT-PCR) is the most sensitive method for the detection of low-abundance mRNA, often obtained from limited tissue samples. However, it is a complex technique, there are substantial problems associated with its true sensitivity, reproducibility and specificity and, as a quantitative method, it suffers from the problems inherent in PCR. The recent introduction of fluorescence-based kinetic RT-PCR procedures significantly simplifies the process of producing reproducible quantification of mRNAs and promises to overcome these limitations. Nevertheless, their successful application depends on a clear understanding of the practical problems, and careful experimental design, application and validation remain essential for accurate quantitative measurements of transcription. This review discusses the technical aspects involved, contrasts conventional and kinetic RT-PCR methods for quantitating gene expression and compares the different kinetic RT-PCR systems. It illustrates the usefulness of these assays by demonstrating the significantly different levels of transcription between individuals of the housekeeping gene family, glyceraldehyde-3-phosphate-dehydrogenase (GAPDH).

/pdf/absolute-quantification-of-mrna-using-real-time-reverse-2kyvkvy0jn.pdf

Absolute quantification of mRNA using real-time reverse transcription polymerase chain reaction assays.

In response to stress, the brain activates several neuropeptide-secreting systems. This eventually leads to the release of adrenal corticosteroid hormones, which subsequently feed back on the brain and bind to two types of nuclear receptor that act as transcriptional regulators. By targeting many genes, corticosteroids function in a binary fashion, and serve as a master switch in the control of neuronal and network responses that underlie behavioural adaptation. In genetically predisposed individuals, an imbalance in this binary control mechanism can introduce a bias towards stress-related brain disease after adverse experiences. New candidate susceptibility genes that serve as markers for the prediction of vulnerable phenotypes are now being identified.

Stress and the brain: from adaptation to disease

LTP and LTD: an embarrassment of riches.

Developmental and regional expression in the rat brain and functional properties of four NMDA receptors.

A variety of experimental techniques have been used to investigate the tolerance/dependence liability of opiate-like peptides. 1 Microelectrophoretically applied enkephalin was found to inhibit the activity of cortical neurons, an effect which was largely abolished in morphine-tolerant/dependent rats, indicating the development of cross-tolerance between morphine and enkephalin. 2 Experiments were performed on the myenteric plexus/longitudinal muscle preparation from the ileum of morphine-tolerant/dependent guinea pigs. In this preparation enkephalin was found to substitute for morphine in preventing the loss of a naloxone-induced withdrawal contracture. Enkephalin was also able to substitute for morphine in reestablishing the ability of naloxone to precipitate a withdrawal contracture after washout of opiate from these preparations. 3 Repeated intracerebroventricular injection of endorphin-induced tolerance and physical dependence in the rat. Endorphin administered in this way was also found to suppress the naloxone-precipitated withdrawal signs of morphine tolerant/dependent rats. In summary, there appear to be no apparent differences between the dependence liabilities of morphine and opiate-like peptides.

Dependence liability of opiate-like peptides

Differential effects of visually induced analgesia and attention depending on the pain stimulation site.

A wealth of evidence from neurochemical studies suggests that GABA (y-aminobutyric acid) analogues may modulate the release of GABA. Most of these investigations used fairly crude procedures such as high K + induced transmitter release (see Reference 13 for review), but whether this phenomenon occurs under physiological conditions remains unclear. A conclusive link to the well-established reduction of inhibitory postsynaptic potentials (IPSPs) at higher frequencies of stimulation in hippocampal pyramidal cells2.” is lacking. Establishment of this connection is hampered by the problem of separating the relative contribution of several conceivable mechanisms to IPSP depression. For instance, any decline of inhibition may be brought about by a postsynaptic desensitization of GABA receptors as demonstrated in isolated hippocampal neurones.” In addition, shifts of the C1equilibrium potential reduced the postsynaptic response even before the onset of desensitization.’” In neurones of the hippocampal slice the decline of IPSPs at higher frequencies of stimulation was associated with a significant elevation of extracellular K’ concentration,’ ’ which may indirectly affect inhibition. Increases of extracellular Kconcentration were shown to diminish the inhibitory driving force,’ as recently confirmed in neocortical n e u r o n e ~ . ’ ~ Furthermore, the reduction of inhibition may be related to GABA uptake. In some hippocampal neurones nipecotic acid, a blocker of GABA uptake, slightly prolonged IPSPs.’ But nipecotic acid virtually abolished IPSPs in the majority of neurones8 Similar observations had led to the proposal of a negative feedback control of GABA release.’ Here we briefly review electrophysiological data of IPSPs from neocortical neurones that provide evidence for a negative feedback of GABA on its own release. Orthodromic stimulation of the neocortex in vitro evokes a complex synaptic Two temporally distinct inhibitory postsynaptic potentials (IPSP, and IPSP,) were analyzed from current voltage relationships, revealing different conductances of about 200 nS and 24 nS and reversal potentials of -73 mV and -89 mV, respectively (see References 7 and 9 for details of the methods). The conductances of IPSP, and IPSP, were fairly stable a t a stimulus frequency of 0.1 Hz. At higher frequencies both IPSPs were rapidly attenuated, and after about 5 stimuli a steady state was reached. The average decrease in synaptic conductance between 0.1 and 1 Hz was 80% for the IPSP, and 60% for the IPSP,. At these frequencies the reversal potentials decreased marginally. Membrane potential (Em) and input resistance (R,,,) were not affected.’ Application of nipecotic acid (50 to 500 pM) reduced the conductance of both IPSPs evoked at low frequencies, but had no effects a t higher stimulation rates. Em and R,, were not consistently affected by nipecotic acid. Local application of GABA i n the presence of nipecotic acid revealed a slightly cnhanced postsynaptic response.’ The behavior of the conductance versus frequency

GABAB Receptors Control GABA Release of Neocortical Neurones

The taurine analog acamprosate (calcium acetylhomotaurinate) has received considerable attention in Europe for its ability to prevent relapse in abstained alcoholics [(1); Chapter 28] and has been suggested to act by reducing craving associated with conditioned withdrawal (2,3).

Mechanism of Action of Acamprosate Focusing on the Glutamatergic System

Semicarbazide modulates cortical excitation in mouse brain slices

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