Correlation of primate superior colliculus and reticular formation discharge with proximal limb muscle activity.
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We studied the discharge of neurons from both the superior colliculus (SC) and the underlying mesencephalic reticular formation (MRF) and its relation to the simultaneously recorded activity of 11 arm muscles. The 242 neurons tested with a center-out reach task yielded 2,586 pairs of neuron/muscle cross-correlations (normalized, such that perfect correlations are +/-1.0). Of these, 43% had peaks with magnitude as large as 0.15, a value that corresponds to the 5% level of significance, and 16% were as large as 0.25. The great majority of peaks in this latter group was positive. The median lag time within this group was 52 ms, indicating that the neuronal discharge tended to precede the correlated muscle activity. We found a small but significantly higher proportion of cells with these relatively strong correlations in the MRF than in the SC. For both areas, these occurred most frequently with muscles of the shoulder girdle and became less frequent for axial as well as for increasingly distal arm musculature. The results support a role for the SC and MRF in guiding the arm during reach movements via the control of proximal limb musculature. (+info)
Clonidine evokes vasodepressor responses via alpha2-adrenergic receptors in gigantocellular reticular formation.
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The gigantocellular depressor area (GiDA) is a functionally defined subdivision of the medullary gigantocellular reticular formation where vasodepressor responses are evoked by glutamate nanoinjections. The GiDA also contains reticulospinal neurons that contain the alpha2A-adrenergic receptor (alpha2A-AR). In the present study, we sought to determine whether nanoinjections of the alpha2-AR agonist clonidine into the GiDA evoke cardiovascular responses and whether these responses can be attributed to the alpha2-AR. We found that nanoinjections of clonidine into the GiDA evoke dose-dependent decreases in arterial pressure and heart rate. These responses were equivalent in magnitude to responses produced by clonidine nanoinjections into the sympathoexcitatory region of the rostral ventrolateral medulla. Furthermore, the vasodepressor and bradycardic responses produced by clonidine injections into the GiDA were blocked in a dose-dependent fashion by the highly selective alpha2-AR antagonist 2-methoxyidazoxan, but not by prazosin, which is an antagonist at both the alpha1-AR and the 2B subtype of the alpha-AR. The antagonism by 2-methoxyidazoxan was site specific because injections of the antagonist into the rostral ventrolateral medulla failed to block the responses evoked by clonidine injections into the GiDA. These findings support the notion that clonidine produces sympathoinhibition through multiple sites within the medullary reticular formation, which is consistent with the wide distribution of the alpha2A-AR in reticulospinal neurons. These data also suggest that clonidine may have multiple mechanisms of action because it evokes a cardiovascular depressive response from regions containing neurons that have been determined to be both sympathoinhibitory and sympathoexcitatory. (+info)
Vasoactive intestinal polypeptide excites medial pontine reticular formation neurons in the brainstem rapid eye movement sleep-induction zone.
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Although it has long been known that microinjection of the cholinergic agonist carbachol into the medial pontine reticular formation (mPRF) induces a state that resembles rapid eye movement (REM) sleep, it is likely that other transmitters contribute to mPRF regulation of behavioral states. A key candidate is the peptide vasoactive intestinal polypeptide (VIP), which innervates the mPRF and induces REM sleep when injected into this region of the brainstem. To begin understanding the cellular mechanisms underlying this phenomenon, we examined the effects of VIP on mPRF cells using whole-cell patch-clamp recordings in the in vitro rat brainstem slice. VIP directly depolarized cells via activation of an inward current; these effects were attenuated and potentiated in low-sodium and low-calcium medium, respectively. The depolarization induced by VIP was slower in onset and longer-lived than that evoked by carbachol. The VIP-induced depolarization was reduced in a dose-dependent manner by a competitive antagonist of VIP receptors. Effects of VIP were attenuated in the presence of guanosine 5'-O-(2-thiodiphosphate, 2'5'dideoxyadenosine, and PKI15-24 and were nonadditive in the presence of 8-bromo-cAMP. We conclude that VIP excites mPRF neurons by activation of a sodium current. This effect is mediated at least in part by G-protein stimulation of adenylyl cyclase, cAMP, and protein kinase A. These data suggest that VIP may play a physiological role in REM induction by its actions on mPRF neurons. (+info)
Fos-like immunoreactivity in the brain stem following oral quinine stimulation in decerebrate rats.
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The present study compared the distribution of Fos-like immunoreactivity (FLI) following intraoral stimulation with quinine monohydrochloride (QHCl) in awake intact rats to the pattern obtained in chronic supracollicular decerebrate (CD) rats. Because the behavioral rejection response to QHCl is evident in the CD rat, it was hypothesized that the pattern of FLI in the lower brain stem should be similar in both groups. Overall, the distribution of FLI in the brain stem was quite similar in both intact and CD groups, and QHCl stimulation increased FLI in the rostral (gustatory) nucleus of the solitary tract, the parabrachial nucleus (PBN), and the lateral reticular formation (RF) compared with an unstimulated control group. The CD group differed from the intact group, however, with a trend toward less FLI in the RF and a shift in the pattern of label away from the external subdivision of the PBN. CD rats also had increased FLI in the caudal nucleus of the solitary tract, with or without intraoral infusions. The distribution of QHCl-induced FLI in the brain stem of intact rats thus indicates both local sensorimotor processing as well as the influence of forebrain structures. (+info)
Fluorescent double-label study of lateral reticular nucleus projections to the spinal cord and periaqueductal gray in the rat.
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Following injections of WGA-HRP into either the spinal cord or periaqueductal gray, labeled neurons were observed bilaterally along the periphery of the lateral reticular nucleus (LRN) magnocellular division. The possibility that some of these neurons in the LRN provide collateral axonal branches to both the periaqueductal gray and the spinal cord was investigated in rats using a retrograde double-labeling method employing two different fluorescent tracers, True Blue and Nuclear Yellow. Following sequential injection of the two fluorescent axonal tracers into the spinal cord and periaqueductal gray in the same animal, a modest number of double-labeled neurons were observed bilaterally near the medial and dorsal perimeter of the magnocellular division of the LRN. The labeled neurons were distinctly multipolar in shape and measured approximately 15-18 mu in their greatest transverse diameter. No double-labeled neurons were observed in the parvocellular or subtrigeminal divisions of the LRN. Based upon these observations, it is suggested that collaterals of the LRN-spinal pathway provide feedback information to the periaqueductal gray that might then be used to modulate the participation of the latter cell group in a variety of pain processing and cardiovascular regulatory functions. (+info)
Mauthner and reticulospinal responses to the onset of acoustic pressure and acceleration stimuli.
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We determined how the Mauthner cell and other large, fast-conducting reticulospinal neurons of the goldfish responded to acoustic stimuli likely to be important in coordinating body movements underlying escape. The goal was to learn about the neurophysiological responses to these stimuli and the underlying processes of sensorimotor integration. We compared the intracellularly recorded postsynaptic responses (PSPs) of 9 Mauthner cells and a population of 12 other reticulospinal neurons to acoustic pressure and acceleration stimuli. All recorded cells received both pressure and acceleration inputs and responded to stimuli regardless of initial polarity. Thus these cells receive acoustic components necessary to determine source direction. We observed that the Mauthner cell was broadly tuned to acoustic pressure from 100 to 2,000 Hz, with a Q(10dB) of 0.5-1.1 over the best frequency range, 400-800 Hz. This broad tuning is probably due to input from S1 afferents and is similar to tuning of the behavioral audiogram. Our data suggest that cells have relatively more sustained responses to acceleration than to pressure stimuli, to which they rapidly adapted. For a given cell, PSP latencies and amplitudes varied inversely with stimulus intensity. For the entire population of cells studied, minimum onset latencies (i.e., those at the highest intensities) ranged from 0.7 to 7.6 ms for acoustic pressure and 0.7 to 9.8 ms for acceleration. This distribution in minimum onset latencies is consistent with earlier EMG and kinematic findings and supports our previous hypothesis that escape trajectory angle is controlled, in part, by varying the activation time of neurons in the escape network. While the Mauthner cell latency did not differ to both onset polarities of pressure and acceleration, this was not true of all cells. Also, the Mauthner cell responses to pressure were approximately 0.6 ms faster than to acceleration; for the other cells, this difference was 1.1 ms with some cells having differences +info)
Divergence of lamina VII and VIII neurones of S1 and S2 segments of the cat's spinal cord to the cerebellum and the reticular formation.
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Cerebellar and reticular projections of neurones located in sacral segments of the spinal cord were electrophysiologically investigated in alpha-chloralose anaesthetized cats. Antidromic action potentials were recorded following stimulation of the contralateral restiform body (coRB), contralateral gigantocellular nucleus (coGRN) as well as ipsi- and contralateral lateral funiculus of the 13th thoracic segment (iTh13 and coTh13). Eighty-seven neurones were found in the medial lamina VII and lamina VIII of the gray matter of S1 and S2 segments. Their axons ascended in lateral funiculi on the contralateral side and in 46 cases also on the ipsilateral side of the spinal cord. A projection to coRB was found in 20 neurones, to coGRN in 10 and dual projections to both coRB and coGRN in 20 neurones. Axons of the remaining 37 cells were found to ascend to the level of Th13 only. Conduction velocities of neurones investigated were comprised in the range 35-83 m/s and no significant differences were found between particular groups. However, an evident decrease in conduction was observed in most neurones when comparing proximal to distal parts of their axons, suggesting the possibility of more extensive divergence than indicated in this study. The pattern of projections revealed that the information from the periphery is conveyed in parallel to various supraspinal and possibly also spinal centres. (+info)
Increased gamma- and decreased delta-oscillations in a mouse deficient for a potassium channel expressed in fast-spiking interneurons.
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Kv3.1 is a voltage-gated, fast activating/deactivating potassium (K(+)) channel with a high-threshold of activation and a large unit conductance. Kv3.1 K(+) channels are expressed in fast-spiking, parvalbumin-containing interneurons in cortex, hippocampus, striatum, the thalamic reticular nucleus (TRN), and in several nuclei of the brain stem. A high density of Kv3.1 channels contributes to short-duration action potentials, fast afterhyperpolarizations, and brief refractory periods enhancing the capability in these neurons for high-frequency firing. Kv3.1 K(+) channel expression in the TRN and cortex also suggests a role in thalamocortical and cortical function. Here we show that fast gamma and slow delta oscillations recorded from the somatomotor cortex are altered in the freely behaving Kv3.1 mutant mouse. Electroencephalographic (EEG) recordings from homozygous Kv3.1(-/-) mice show a three- to fourfold increase in both absolute and relative spectral power in the gamma frequency range (20-60 Hz). In contrast, Kv3.1-deficient mice have a 20-50% reduction of power in the slow delta range (2-3 Hz). The increase in gamma power is most prominent during waking in the 40- to 55-Hz range, whereas the decrease in delta power occurs equally across all states of arousal. Our findings suggest that Kv3. 1-expressing neurons are involved in the generation and maintenance of cortical fast gamma and slow delta oscillations. Hence the Kv3. 1-mutant mouse could serve as a model to study the generation and maintenance of fast gamma and slow delta rhythms and their involvement in behavior and cognition. (+info)