Relative afferent pupillary defect with normal visual function.

The origin of the dopaminergic innervation of the central extended amygdala (EAc; i.e., the lateral bed nucleus of the stria terminalis [BSTl]-central amygdaloid nucleus [Ce] continuum) and accumbens shell (AcSh) was studied in the rat by combining retrograde transport of Fluoro-Gold (FG) with tyrosine hydroxylase (TH) immunofluorescence. Perikaryal profiles (PP) immunoreactive to FG and to both FG and TH were counted in A8-A14 dopaminergic districts. Our results suggest that dopaminergic inputs to the EAc and AcSh arise from the ventral tegmental area-A10, substantia nigra, pars compacta-A9, and retrorubral nucleus-A8 groups as well as from the dorsal raphe nucleus and periaqueductal gray substance, housing the dorsocaudal part of A10 group (A10dc). Quantitative estimates reveal that the A10dc group contains approximately half of the total number of FG/TH double-labeled PP projecting to Ce and BSTl. By using an anti-dopamine serum, DR/PAG projections to Ce were confirmed to be in part dopaminergic. In contrast, modest numbers of FG/TH double-labeled PP were seen in the A10dc group after injections in the sublenticular extended amygdala, interstitial nucleus of the posterior limb of the anterior commissure or AcSh. Ventral mesencephalic projections to the EAc display a crude mediolateral topographic organization, whereas those to the AcSh are topographically organized along a mediolateral and an inverted dorsoventral dimension. The diencephalic dopaminergic groups do not innervate the EAc or AcSh, except for the periventricular gray-A11 which sends light dopaminergic projections to Ce and BSTl. Overall, the present results provide additional details on the organization of the mesolimbic dopaminergic system that critically controls behavioral responsiveness to salient environmental stimuli.

Afferent Pathways↗

PubMed2002

Potentiation of local field potentials in the anterior cingulate cortex evoked by the stimulation of the medial thalamic nuclei in rats.

The limbic thalamus and cingulate cortex are essential components in mediating the affective component of pain responses. In the present study, we examined the excitatory properties of medial thalamus (MT)-evoked field potentials in the anterior cingulated cortex (ACC). We also examined the effects of paired pulses and brief tetanic stimuli of the MT. The aim of this study was to determine whether nociceptive inputs to medial thalamic afferents cause plastic changes in the ACC. In alpha-chloralose (50 mg/kg, i.v.) anaesthetized rats, tungsten microelectrodes were used to stimulate the MT and to record field potentials in the ACC. The locations of MT were identified by searching and examining their responses to peripheral noxious stimuli. Early negative (about 4.7 ms latency) and late positive (about 11.7 ms) potentials could be evoked in the ACC by MT stimuli. The evoked field potentials were potentiated by prepulse stimulation. Maximal paired pulse facilitation (509+/-51%) was produced in 80-150 ms interpulse intervals. Evoked field potentials were also potentiated (28.8+/-6.3% and 29.6+/-5.9%, respectively) by low (10 Hz/10 s) and high (100 Hz/2s/2x) frequency tetanic stimulation of the MT, with a duration maintained for about 90 s and 120 min, respectively. The potentiation of MT-evoked ACC potentials provides a neural basis for synaptic plasticity, which may be essential for the establishment of pain-initiated conditioning behavior and affective responses to noxious stimuli.

Afferent Pathways↗

PubMed2002

[Prostaglandin inhibitor indomethacin inhibits afferent activities of Adelta and C units in the saphenous nerve of diabetic hyperalgesic rats].

The effects of a non-selective inhibitor of cyclo-oxygenase (COX) indomethacin, and exogenous prostaglandin E(2) (PGE(2)) on A(delta) units and C units in the saphenous nerve of diabetic hyperalgesic rats were studied. The results showed that the conduction velocity of A(delta) units and C units and their mechanical threshold in diabetic hyperalgesic rats were obviously decreased, and a small number of A(delta) units (4/24) and C units (2/18) produced increased spontaneous activities. Intraperitoneal injection of indomethacin in diabetic hyperalgesic rats significantly relieved mechanical hyperalgesia, and resulted in a decrease in spontaneous afferent activities of the A(delta) units and C units. Subcutaneous injection of exogenous PGE(2) into the diabetic hyperalgesic and control rats produced a significant decrease in mechanical threshold of the A(delta) units and C units, and elicited discharge from 3 A(delta) units (3/24) and 1 C unit (1/18) in diabetic hyperalgesic rats and from 2 A(delta) units (2/13) in control rats. The present data suggest that the synthesis and release of PGs are increased in diabetic neuropathy, PGs can sensitize and /or activate A(delta) units and C units and elicit hyperalgesia and allodynia in diabetic rats.

Afferent Pathways↗