Functional magnetic resonance imaging (fMRI) has revolutionized investigations of brain functions. Increases in fMRI signals

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BackgroundAlthough the mechanisms of short- and long-term potentiation of nociceptive-evoked responses are well known in the spinal cord, including central sensitization, there has been a growing body of information on such events in the cerebral cortex. In view of the importance of anterior cingulate cortex (ACC) in chronic pain conditions, this review considers neuronal plasticities in the thalamocingulate pathway that may be the earliest changes associated with such syndromes.ResultsA single nociceptive electrical stimulus to the sciatic nerve induced a prominent sink current in the layer II/III of the ACC in vivo, while high frequency stimulation potentiated the response of this current. Paired-pulse facilitation by electrical stimulation of midline, mediodorsal and intralaminar thalamic nuclei (MITN) suggesting that the MITN projection to ACC mediates the nociceptive short-term plasticity. The short-term synaptic plasticities were evaluated for different inputs in vitro where the medial thalamic and contralateral corpus callosum afferents were compared. Stimulation of the mediodorsal afferent evoked a stronger short-term synaptic plasticity and effectively transferred the bursting thalamic activity to cingulate cortex that was not true for contralateral stimulation. This short-term enhancement of synaptic transmission was mediated by polysynaptic pathways and NMDA receptors. Layer II/III neurons of the ACC express a short-term plasticity that involves glutamate and presynaptic calcium influx and is an important mechanism of the short-term plasticity.ConclusionThe potentiation of ACC neuronal activity induced by thalamic bursting suggest that short-term synaptic plasticities enable the processing of nociceptive information from the medial thalamus and this temporal response variability is particularly important in pain because temporal maintenance of the response supports cortical integration and memory formation related to noxious events. Moreover, these modifications of cingulate synapses appear to regulate afferent signals that may be important to the transition from acute to chronic pain conditions associated with persistent peripheral noxious stimulation. Enhanced and maintained nociceptive activities in cingulate cortex, therefore, can become adverse and it will be important to learn how to regulate such changes in thalamic firing patterns that transmit nociceptive information to ACC in early stages of chronic pain.

Compound action potentials of both myelinated (A) and non-myelinated (C) fibres in the common peroneal nerve of rabbits were studied during and after acute, graded compression of the nerve at 200 or 400 mmHg applied for 2 h or during ischaemia created by nitrogen inhalation or aortic occlusion. Compression of the nerve at 200 mmHg blocked the AI component (large myelinated fibres) after about 23 min, while compression at 400 mmHg shortened this time to 11 min. The A2 component (thinner myelinated fibres) had a lower conduction velocity and a higher resistance to compression. There was just a slight decrease in conduction velocity of the non-myelinated fibres when the nerves were compressed at 200 mmHg for 2 h. However, compression at 400 mmHg for 2 h induced a marked deterioration of amplitude and conduction velocity of the C-fibres. There was an incomplete restitution of function of A- and C-fibres during 2 h of recovery. The thinner myelinated fibres were more susceptible to deprivation of oxygen than the thicker ones, while non-myelinated fibres differed in response according to method of ischaemia induction. It is concluded that non-myelinated fibres are very resistant to compression and a very high pressure (greater than 400 mmHg) is needed to affect these fibres.

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