Extracellular single unit activity in the intralaminar thalamic nuclei (ncl. centralis lateralis, CL, n = 77 and ncl. parafascicularis, Pf, n = 163) and in the pretectal area (Pt, n = 75) was examined following chronic electrolytic lesions of the nucleus reticularis thalami (nRT) in ketamine-anaesthetized rats after single electrical stimuli to the ventrobasal complex (VB). Extensive alterations of either the ongoing ("spontaneous") activity or the pattern of VB evoked responses were observed. Four major changes were observed in the activity of these intralaminar or pretectal neurones: 1) many neurones were silent, two times more frequently than in a parallel study with control intact rats; 2) the firing pattern of all the other neurones was in the form of tonic (stationary-like) discharge, without burst discharges as previously described in intact animals. They were ranked into classes according to their spontaneous discharge: class I, silent (no resting discharge) 12 %, class II (1-15 Hz), 54 % and class III (> 16 Hz), 34 %. Class III neurones were never found in intact rats; 3) electrical stimulation of the VB evoked a short latency orthodromic excitatory response in these neurones but this response was not followed by any slowing or depression of the spontaneous activity in more than 40 % of recorded cells. When it occurred, this pause was shorter than that always observed in intact rats by more than 35 % and longer in 7 % of the responsive cells. All these changes were correlated with the extent of damage to the ipsilateral nRT; 4) VB stimulation evoked prolonged excitatory responses lasting more than 150 ms in 13 % of the responsive cells, and nRT stimulation led to a short latency response followed by a pause of activity. These findings suggest that the nRT is involved in sensory integration and modulation.
The regeneration of the sciatic nerve after microsuture was compared with the connection of transected nerve with a coagulum of autologous blood plasma in 20 rabbits. The epineuroperineural suture was performed in 10 rabbits (group A). The severed nerve was approximated with fibrin glue of autologous blood plasma in 10 rabbits (group B). Their skin sensation margin during a 3-month-period of regeneration was examined, 90 days after surgery the connection was inspected and the nerve conduction velocity was measured across the site of the anastomosis. The microsuture was found to be firm in all 10 animals of group A. On the other hand, in 2 animals of group B, the glue failed to keep the nerve stumps approximated (dehiscence occurred in 20 % of the animals). There were no significant differences found on clinical and electrophysiological testing of regenerated nerves of both groups. The method of autologous fibrin glue in the repair of peripheral nerve transection does not provide a sufficiently firm connection. This procedure with the preparation of the centrifuged plasma is a more time-consuming method in comparison with the microsuture. Epineuroperineural microsuture with maximal effort to adapt the corresponding nerve fibres remains the method of choice for peripheral nerve reconstruction.
In recent years, epidemiological data has shown an increasing number of young people who deliberately self-injure. There have also been parallel increases in the number of people with tattoos and those who voluntarily undergo painful procedures associated with piercing, scarification, and tattooing. People with self-injury behaviors often say that they do not feel the pain. However, there is no information regarding pain perception in those that visit tattoo parlors and piercing studios compared to those who don’t. The aim of this study was to compare nociceptive sensitivity in four groups of subjects (n=105, mean age 26 years, 48 women and 57 men) with different motivations to experience pain (i.e., with and without multiple body modifications) in two different situations; (1) in controlled, emotionally neutral conditions, and (2) at a "Hell Party" (HP), an event organized by a piercing and tattoo parlor, with a main event featuring a public demonstration of painful techniques (burn scars, hanging on hooks, etc.). Pain thresholds of the fingers of the hand were measured using a thermal stimulator and mechanical algometer. In HP participants, information about alcohol intake, self-harming behavior, and psychiatric history were used in the analysis as intervening variables. Individuals with body modifications as well
as without body modifications had higher thermal pain thresholds at Hell Party, compared to thresholds measured at control neutral conditions. No such differences were found relative to mechanical pain thresholds. Increased pain threshold in all HP participants, irrespectively of body modification, cannot be simply explained by a decrease in the sensory component of pain; instead, we found that the environment significantly influenced the cognitive and affective component of pain.
We evaluated the effects of 2.5xlO-10 M or 5xlO-10 M concentrations of human pituitary prolactin (pPRL), human recombinant non-glycosylated (NG-PRL) and glycosylated (GL-PRL) prolactin on the proliferation of normal human lymphocytes with or without coactivation by interleukin-2 (IL-2). None of the PRL forms alone affected the lymphocyte proliferation in a serum-free medium, however, the stimulatory activity of IL-2 was significantly potentiated with all 3 PRL variants. Since the 5xlO~10 M concentrations of individual PRLs exerted the same effects, this result suggests that GL-PRL in primary lymphocyte culture is not a less mitogenic form, if sufficient amounts of IL-2 are available.
Unilateral dorsal rhizotomy of brachial plexus nerves (C5-Th1) performed under general anesthesia is known to induce self-mutilation in rats. The aim of this study was to determine the effect of different anesthetic agents, and of pre-rhizotomy nociceptive stimulation on the appearance of self-mutilation. Self-mutialtion appeared in 78 % of animals after rhizotomy had been performed under pentobarbital anesthesia. When ketamine was used as the general anesthetic, self-mutilation was almost suppressed (13 %) and consisted of superficial erosions. Mechanical nociceptive stimulation, when applied just before the induction of ketamine anesthesia and subsequent rhizotomy, provoked self-mutilation in 91 % of rats. Furthermore, a serious type of self-mutilation consisting of total amputation of the distal part of the forepaw was present in 28 % of all self-mutilating animals after previous nociceptive stimulation. In terms of self-mutilation, these results suggest 1) the crucial role of anesthesia, especially that which involved NMDA receptors (ketamine), and 2) the need of an additional factor to chronic deafferentation, formed either by activity of nociceptive pathways just before rhizotomy (nociceptive stimulation preceding ketamine anesthesia) or by injury discharges (pentobarbital anesthesia).
Electrode migration is the most common complication of spinal
cord stimulation (SCS). The problem of longitudinal migration has
already been solved, but lateral migration remains the most
common current complication. The present article describes new
electrodes fixation opportunities for the reduction of lateral
migration in SCS. The pig was chosen as an animal model to
illustrate a new protocol of electrode fixation for the control of
lateral and longitudinal migration. The displacement of the
electrode was measured using two different optical methods: the
digital image stereo-correlation and the digital image processing
methods. Fixation with two anchors has always considerably
reduced electrode displacement and when fixation is done with two
anchors and a loop then lateral migration is reduced by 62.5 %
and longitudinal migration is reduced by 94.1 %. It was shown that
the results are significantly different at the α=0.001 significance
level. Based on a statistical evaluation it is possible to state that the
differences between experimental results obtained for three
different protocols of lead fixation are statistically significant and
we can recommend the new fixation method for common practice.
Baclofen, which is a specific agonist of the metabotropic GABAB receptor, is used in clinical practice for the treatment of spasticity of skeletal muscles. It also exerts an analgesic effect, but this effect is still not clear and especially controversial in neuropathic pain. In this work, we studied the antinociceptive effects of baclofen in a model of chronic peripheral neuropathic pain – loose ligation of the sciatic nerve (chronic constriction injury, CCI). As controls we used sham-operated animals. The changes of thermal pain threshold were measured using the plantar test 15-25 days after the operation. The obtained results suggest that baclofen increases pain threshold in both groups. The antinociceptive effect of baclofen was dose-dependent and the maximum response without motor deficits was observed at a dose of 15 mg/kg s.c. In the rats with CCI, significant differences between affected (ipsilateral) and contralateral hind paw were present. This difference was dose-dependent, the highest value (6.2±1.37 s) was found at the dose of 20 mg/kg. Based on our results and previous findings it could be summarized that baclofen has antinociceptive action, which is attenuated in the model of chronic neuropathic pain probably due to the degeneration of GABA interneurons after chronic constriction injury.
An anterograde biocytin and a retrograde WGA-colloidal gold study in the rat can provide information about reciprocal communication pathways between the red nucleus and the trigeminal sensory complex. No terminals were found within the trigeminal motor nucleus, in contrast with the facial motor nucleus. A dense terminal field was observed in the parvicellular reticular formation ventrally to the trigeminal motor nucleus. The parvicellular area may be important for the control of jaw movements by rubrotrigeminal inputs. On the other hand, the contralateral rostral parvicellular part of the red nucleus receives terminals from the same zone in the rostral part of the trigeminal sensory complex, where retrogradely labelled neurones were found after tracer injections into the red nucleus. Such relationships could be part of a control loop for somatosensory information from the orofacial area.
Reciprocal interactions between intralaminar thalamic nuclei (ncl. centralis lateralis, CL, and ncl. parafascicularis, Pf), the pretectal area (Pt) and lateral thalamic nuclei (ventrobasal complex, VB, ncl. anterior ventralis, AV, and ncl. ventralis anterior, VA) have been observed in ketamine-anaesthetized rats. Extracellular single unit activity has been recorded after single electrical stimuli. Electrical stimulation of the VB evoked a short latency orthodromic response followed by a pause in spontaneous activity in neurones of medial thalamic nuclei. Lateral thalamic neurones responded to electrical stimulation of the intralaminar nuclei or the pretectal area with the same pattern of response. Striatal, sensorimotor cortical or peripheral electrical stimulation also evoked similar responses. The pauses in spontaneous activity were shown to be the result of inhibition since the responsiveness of the intralaminar nuclei or the lateral thalamic neurones to all inputs was abolished or reduced after a conditioning electrical singleshock stimulation in the VB or in the intralaminar nuclei, respectively. The two components of the response were of a different origin, since most of the short latency responses disappeared after medullary, upper cervical sections or large decortications, while the inhibitions persisted. These inhibitions were shown to be of thalamic origin since their duration was decreased after extensive decortications increased after medullary section. It is concluded that the neuroneal properties studied in this report are probably broadly represented throughout the thalamus and that thalamic neurones are under inhibitory control elicited by afferent volleys. This inhibitory control includes a relay in the nucleus reticularis thalami (nRT). The mechanisms of sensory interaction can be purely thalamic, but they can be modulated by suprathalamic and/or mesencephalic loops.