抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Interneurons of the hippocampus

Introduction to synaptic circuits, Gordon M.Shepherd and Christof Koch membrane properties and neurotransmitter actions, David A.McCormick peripheral ganglia, Paul R.Adams and Christof Koch spinal cord - ventral horn, Robert E.Burke olfactory bulb, Gordon M.Shepherd, and Charles A.Greer retina, Peter Sterling cerebellum, Rodolfo R.Llinas and Kerry D.Walton thalamus, S.Murray Sherman and Christof Koch basal ganglia, Charles J.Wilson olfactory cortex, Lewis B.Haberly hippocampus, Thomas H.Brown and Anthony M.Zador neocortex, Rodney J.Douglas and Kevan A.C.Martin Gordon M.Shepherd. Appendix: Dendretic electrotonus and synaptic integration.

The synaptic organization of the brain

Muscle fatigue is an exercise-induced reduction in maximal voluntary muscle force. It may arise not only because of peripheral changes at the level of the muscle, but also because the central nervous system fails to drive the motoneurons adequately. Evidence for “central” fatigue and the neural mechanisms underlying it are reviewed, together with its terminology and the methods used to reveal it. Much data suggest that voluntary activation of human motoneurons and muscle fibers is suboptimal and thus maximal voluntary force is commonly less than true maximal force. Hence, maximal voluntary strength can often be below true maximal muscle force. The technique of twitch interpolation has helped to reveal the changes in drive to motoneurons during fatigue. Voluntary activation usually diminishes during maximal voluntary isometric tasks, that is central fatigue develops, and motor unit firing rates decline. Transcranial magnetic stimulation over the motor cortex during fatiguing exercise has revealed focal cha...

Spinal and Supraspinal Factors in Human Muscle Fatigue

1. In ten normal volunteers, a transcranial magnetic or electric stimulus that was subthreshold for evoking an EMG response in relaxed muscles was used to condition responses evoked by a later, suprathreshold magnetic or electric test shock. In most experiments the test stimulus was given to the lateral part of the motor strip in order to evoke EMG responses in the first dorsal interosseous muscle (FDI). 2. A magnetic conditioning stimulus over the hand area of cortex could suppress responses produced in the relaxed FDI by a suprathreshold magnetic test stimulus at interstimulus intervals of 1-6 ms. At interstimulus intervals of 10 and 15 ms, the test response was facilitated. 3. Using a focal magnetic stimulus we explored the effects of moving the conditioning stimulus to different scalp locations while maintaining the magnetic test coil at one site. If the conditioning coil was moved anterior or posterior to the motor strip there was less suppression of test responses in the FDI. In contrast, stimulation at the vertex could suppress FDI responses by an amount comparable to that seen with stimulation over the hand area. With the positions of the two coils reversed, conditioning stimuli over the hand area suppressed responses evoked in leg muscles by vertex test shocks. 4. The intensity of both conditioning and test shocks influenced the amount of suppression. Small test responses were more readily suppressed than large responses. The best suppression was seen with small conditioning stimuli (0.7-0.9 times motor threshold in relaxed muscle); increasing the intensity to motor threshold or above resulted in less suppression or even facilitation. 5. Two experiments suggested that the suppression was produced by an action on cortical, rather than spinal excitability. First, a magnetic conditioning stimulus over the hand area failed to produce any suppression of responses evoked in active hand muscles by a small (approximately 200 V, 50 microsecond time constant) anodal electric test shock. Second, a vertex conditioning shock had no effect on forearm flexor H reflexes even though responses in the same muscles produced by magnetic cortical test shocks were readily suppressed at appropriate interstimulus intervals. 6. Small anodal electric conditioning stimuli were much less effective in suppressing magnetic test responses than either magnetic or cathodal electric conditioning shocks.(ABSTRACT TRUNCATED AT 400 WORDS)

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1993.sp019912

Corticocortical inhibition in human motor cortex.

Chemical Nature of Synaptic Transmission in Vertebrates

1. The muscarinic depolarizing action of ACh on cortical neurones is associated with an increase in membrane resistance (mean DeltaV/DeltaR = 3.16 mV/MOmega).2. ACh also promotes repetitive firing by slowing repolarization after spikes.3. The depolarizing effect has a mean reversal level of -86.7 mV (with mean resting potential -56 mV).4. It is concluded that as a muscarinic excitatory agent, ACh probably acts by reducing the resting K(+) conductance of cortical neurones, and also the delayed K(+) current of the action potential.5. These results are discussed in relation to the possible role of ACh in cortical function.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1971.sp009467

The mechanism of excitation by acetylcholine in the cerebral cortex

In cats under pentobarbitone anaesthesia, GABA was tested on cortical, pericruciate neurones and its action compared with IPSPs evoked by surface stimulation. GABA was applied to individual cells by microiontophoresis, while recording the membrane potential and resistance. When K citrate-recording electrodes were used, GABA always hyperpolarized the cell and lowered its resistance, like the synaptic inhibitory effect. By adequate polarization both the action of GABA and the IPSP could be reversed, at a similar level of membrane potential. Both could also be reversed by injecting Cl− into a cell from a KCl recording electrode and the new reversal potentials also did not differ significantly from each other: after this treatment, some cells could be excited with GABA. All these effects of GABA were only seen when it was applied outside the neurones; intracellular injections were ineffective. Since the reversal potentials for the action of GABA and the IPSP are approximately similar, it is concluded that GABA could be the main cortical inhibitory transmitter.

The action of γ-Aminobutyric acid on cortical neurones

eIF2α Phosphorylation Bidirectionally Regulates the Switch from Short- to Long-Term Synaptic Plasticity and Memory

The cerebral cortex is well provided with the enzymes required for the synthesis and destruction of ACh (Hebb, 1957) and it can be shown that large quantities of ACh are liberated in it continuously if precautions are taken to inactivate cerebral cholinesterases (Elliott, Swank & Henderson, 1950; MacIntosh & Oborin, 1953; Mitchell, 1963). Since this release of ACh is apparently related to the functional state of the brain as indicated by the electrocorticogram (MacIntosh & Oborin, 1953; Mitchell, 1963) it may come from the activity of cholinergic synapses, or as a by-product of cellular metabolism. If we consider the first of these two possibilities, we must expect to find cortical neurones which are clearly either excited or inhibited by ACh (at certain junctions ACh is known to excite, as it does in vertebrate muscle and ganglia, or it may inhibit activity, as in the heart and in certain molluscs (Tauc & Gerschenfeld, 1962)). With regard to the second possibility, ACh released by metabolic processes may or may not affect the excitability of surrounding neurones. In view of the profuse output ofACh in the cortex it is clearly of interest to find out whether ACh does alter neuronal activity. Many earlier observations have suggested that cortical neurones are excited by ACh (see reviews by Feldberg, 1945, 1950; Stone, 1957), but the evidence has often been conflicting (e.g. Nakao, Ballin & Gellhorn, 1956; Schlag, 1956) and at best indirect. In a previous paper (Krnjevic & Phillis, 1963a) we have shown, using the iontophoretic method of direct application to single cells, that cortical neurones are readily excited by L-glutamate and some related amino acids, and that a certain number of cells can also be made to discharge with ACh. We now present further evidence about the identity and distribution of these cholinoceptive neurones. Some of the results given here have been presented in brief reports (Krnjevic & Phillis, 1961, 1962).

Krešimir Krnjević

Papers

Chemical Nature of Synaptic Transmission in Vertebrates

The mechanism of excitation by acetylcholine in the cerebral cortex

The action of γ-Aminobutyric acid on cortical neurones

eIF2α Phosphorylation Bidirectionally Regulates the Switch from Short- to Long-Term Synaptic Plasticity and Memory

Acetylcholine-sensitive cells in the cerebral cortex.