Electrical Stimulation Of Brain Stem Research Articles

Cellular Changes in Injured Rat Spinal Cord Following Electrical Brainstem Stimulation.

Spinal cord injury (SCI) is a major cause of disability and pain, but little progress has been made in its clinical management. Low-frequency electrical stimulation (LFS) of various anti-nociceptive targets improves outcomes after SCI, including motor recovery and mechanical allodynia. However, the mechanisms of these beneficial effects are incompletely delineated and probably multiple. Our aim was to explore near-term effects of LFS in the hindbrain’s nucleus raphe magnus (NRM) on cellular proliferation in a rat SCI model. Starting 24 h after incomplete contusional SCI at C5, intermittent LFS at 8 Hz was delivered wirelessly to NRM. Controls were given inactive stimulators. At 48 h, 5-bromodeoxyuridine (BrdU) was administered and, at 72 h, spinal cords were extracted and immunostained for various immune and neuroglial progenitor markers and BrdU at the level of the lesion and proximally and distally. LFS altered cell marker counts predominantly at the dorsal injury site. BrdU cell counts were decreased. Individually and in combination with BrdU, there were reductions in CD68 (monocytes) and Sox2 (immature neural precursors) and increases in Blbp (radial glia) expression. CD68-positive cells showed increased co-staining with iNOS. No differences in the expression of GFAP (glia) and NG2 (oligodendrocytes) or in GFAP cell morphology were found. In conclusion, our work shows that LFS of NRM in subacute SCI influences the proliferation of cell types implicated in inflammation and repair, thus providing mechanistic insight into deep brain stimulation as a neuromodulatory treatment for this devastating pathology.

Retinal Vessel Diameter Responses to Central Electrical Stimulation in the Rat: Effect of Nitric Oxide Synthase Inhibition.

Recent histological data suggest autonomic innervation of the central retinal artery. In the present study, we investigated the effect of electrical brain stem stimulation at the superior salivatory nucleus (SSN) on the retinal vessel diameter in rats and whether nitric oxide mediates a possible effect. Sprague-Dawley rats (n = 12) were anesthetized using pentobarbital sodium (50 mg/kg intraperitoneally). The animals were artificially ventilated and the femoral artery and vein were cannulated for blood pressure measurement and drug administration. After a craniotomy was performed, a unipolar stainless steel electrode was inserted into the brainstem at the coordinates of the SSN. Stimulations were performed at 20 Hz, 9 μA, 1 ms pulse duration and 200 pulses. Retinal vessel diameters were measured continuously with the Imedos DVA-R, a noncontact fundus camera for rats with image analysis software. After control measurements, L-NAME, a nonspecific inhibitor of NO synthase, was applied intravenously (10 mg/kg), and the SSN stimulations were repeated. Stimulation at the SSN coordinates increased the retinal arterial diameter by 6.41% ± 1.65% and the venous diameter by 3.48% ± 1.93% (both P < 0.05). Application of L-NAME reduced the arterial response significantly to 2.93% ± 0.91%, but did not change the venous response. Mean arterial pressure, carotid blood flow, and heart rate remained unaltered (by the stimulation). The present study demonstrates that the retinal circulation reacts to electric stimulation at the SSN coordinates in rats. Nitric oxide is involved in the response, but it is not the sole neurotransmitter.

Spectroscopic measurement of cortical nitric oxide release induced by ascending activation

The transition from sleep to the awake state is regulated by the activation of subcortical nuclei of the brainstem (BS) and basal forebrain (BF), releasing acetylcholine and glutamate throughout the cortex and inducing a tonic state of neural activity. It has been suggested that such activation is also mediated by the massive and diffuse cortical release of nitric oxide (NO). In this work we have combined the spectroscopic measurement of NO levels in the somatosensory cortex of the cat through its marker methemoglobin, as well as two other hemodynamic markers (oxyhemoglobin – oxyHb – and deoxyhemoglobin – deoxyHb), together with the electrical stimulation of BS and BF – to induce an experimental transition from a sleep-like state to an awake-like mode. The results show an increase of NO levels either after BS or BF activation. The response induced by BS stimulation was biphasic in the three studied markers, and lasted for up to 30s. The changes induced by BF were monophasic lasting for up to 20s. The systemic blockade of NO production abolished the observed responses to BS whereas responses to BF stimulation were much less affected. These results indicate a crucial role for NO in the neuronal activation induced by the ascending systems.

Role of intracortical mechanisms in the late part of the silent period to transcranial stimulation of the human motor cortex.

Transcranial magnetic stimulation (TMS) and transcranial electrical stimulation (TES) of the human motor cortex produce a silent period (SP) following motor evoked potentials (MEPs). The early part of the SP can be explained by decreased alpha motor neuron excitability, whereas the late part is presumably due to suprasegmental mechanisms. In order to determine the level of the suprasegmental contribution of the generation of SPs, we recorded excitatory and inhibitory responses to TMS, TES and percutaneous electrical brainstem stimulation (PBS) in the voluntarily activated first dorsal interosseous muscle of the hand. Stimulus intensities were set so that PBS and TES induced MEPs with areas equal to or larger than those of MEPs obtained with TMS. This procedure revealed that SPs were 49% and 83% shorter with TES and PBS, respectively, than with TMS. As TMS is more effective than TES or PBS in activating cortical interneurons, these findings support the idea that a significant component of the SP arises from intracortical mechanisms.

Remote effects of voluntary teeth clenching on excitability changes of the human hand motor area

The aim of the present study was to investigate effects of voluntary teeth clenching (VTC) on motor evoked potentials (MEPs) from the first dorsal interosseous (FDI) muscle to transcranial magnetic stimulation (TMS) by different oriented currents (anterior-medially (AM), posterior-laterally (PL)) of the human motor cortex. In active FDI, VTC enhanced MEP responses induced by AM directed current but reduced these responses induced by PL. In relaxed FDI, VTC enhanced MEP responses by AM but had no significant effects on those by PL. Thus, the results suggest that any components produced by AM directed current were enhanced, whereas those by PL directed currents were not affected or reduced. The present evidence indicates that I-waves recorded at the same latency were not completely the same between those produced by AM and PL directed currents. Because VTC had no influence on responses to brainstem electrical stimulation (BES) or F-waves just after the onset of teeth clenching [T. Furubayashi, K. Sugawara, T. Kasai, A. Hayashi, R. Hanajima, Y. Shiio, N.K. Iwara, Y. Ugawa, Remote effects of self-paced teeth clenching on the excitability of hand motor area, Exp. Brain Res., 148 (2003) 261–265], these modulatory effects on MEPs to both AM and PL directed currents must be due to changes of the motor cortical excitability. Thus, we conclude that VTC affects the motor cortical circuits activated by PL and AM directed currents differentially; it facilitates the one and inhibits the other. This is the first demonstration of opposite effects of the same maneuver on MEP responses elicited by AM and PL directed currents.

Distribution of fos-like immunoreactivity in the auditory pathway evoked by bipolar electrical brainstem stimulation

Objective—The auditory brainstem implant (ABI) represents a new modality for the treatment of patients deafened as a result of complete excision of a bilateral VIIIth nerve tumor. However, little work has been done on the effect of the ABI on the mammalian auditory pathway. The aim of this study was to demonstrate the effect of the ABI using Fos-like immunoreactivity.Material and Methods—A bipolar electrode was implanted in the dorsal cochlear nucleus of bilaterally deafened Sprague–Dawley rats, and electrical stimulation was presented at an intensity four times that of threshold.Results—Fos-like immunoreactivity was induced in the neurons of various auditory brainstem nuclei and observed in the low-to-middle frequency area. In the ipsilateral dorsal cochlear nucleus, ipsilateral posterior ventral cochlear nucleus and bilateral inferior colliculus, Fos-like immunoreactive neurons were observed as a distinct banding pattern.Conclusions—This study showed that Fos-like immunoreactivity was observed in the restricted area of the primary brainstem auditory pathway with the appropriate tonotopicity. These results indicate that the ABI can provide auditory information suitable for speech recognition.

The excitability of lumbar motoneurones in the neonatal rat is increased by a hyperpolarization of their voltage threshold for activation by descending serotonergic fibres

Previous work has shown there is an increase in motoneurone excitability produced by hyperpolarization of the threshold potential at which an action potential is elicited (Vth) at the onset, and throughout brainstem-induced fictive locomotion in the decerebrate cat. This represents a transient facilitation in the membrane potential for activation dependent on the presence of fictive locomotion. The present study tests the hypothesis that a similar neuromodulatory mechanism facilitating neuronal recruitment also exists in the neonatal rat, and the endogenous pathway mediating the Vth hyperpolarization can be activated by electrical stimulation of the neonatal brainstem. Isolated brainstem-spinal cord preparations from 1- to 5-day-old neonatal rats, and whole-cell recording techniques were used to examine the patterns of ventral root (VR) activity produced, and the effect of electrical stimulation of the ventromedial medulla on lumbar spinal neurones. Hyperpolarization of Vth was seen in 10/11 (range -2 to -18 mV) neurones recorded during locomotor-like VR activity, and appeared analogous to the locomotor-dependent Vth hyperpolarization previously described in the cat. However, in the present study, Vth hyperpolarization was also seen during electrical brainstem stimulation that evoked alternating, rhythmic, or tonic VR activity, or failed to evoke VR activity. Thirty-six of 71 neurones were antidromically identified as lumbar motoneurones and 33/36 showed a hyperpolarization of Vth (-2 to -14 mV) during electrical brainstem stimulation. Of the unidentified lumbar ventral horn neurones, 31/35 also showed hyperpolarization of Vth (-2 to -20 mV) during brainstem stimulation. The hyperpolarization of Vth and VR activity induced by brainstem stimulation was reversibly blocked by cooling of the cervical cord, indicating it is mediated by descending fibres, and application of the serotonergic antagonist ketanserin to the spinal cord was effectively able to block the brainstem-evoked hyperpolarization of Vth. These results demonstrate a previously unknown action of the endogenous descending serotonergic system to facilitate spinal motoneuronal recruitment and firing by inducing a hyperpolarization of Vth. This modulatory process can be examined in the neonatal rat brainstem-spinal cord preparation without the requirement for ongoing locomotor activity.

A reliable technique for the induction of locomotor-like activity in the in vitro neonatal rat spinal cord using brainstem electrical stimulation

The use of brainstem electrical stimulation (BES) to evoke locomotion in in vivo preparations, such as the decerebrate cat, is well established. In contrast, despite the popularity of in vitro rodent spinal cord models, BES has not been adapted for routine induction of locomotion in these preparations. We describe a simple and reliable method of inducing locomotor-like activity in the in vitro neonatal rat spinal cord using BES. Relatively large amplitude (0.5–10 mA), long duration (4–20 ms) and low frequency (0.8–2.0 Hz) pulses were delivered through a metal-in-glass electrode placed in contact with the ventral surface of the brainstem, without the need for precise targeting of specific sites. During continuous BES, locomotor-like activity (0.15–0.63 Hz) persisted for over 45 min. Episodes of locomotor-like activity could be recruited repeatedly for hours, using short periods (60 s) of BES alternating with brief rest periods. Additional observations confirmed that the rhythmogenic effect of BES is mediated by excitation of spinal projections at the brainstem level, rather than spinal cord activation due to electrotonic spread of stimulus from the brainstem electrode. Endogenous activation of locomotor networks using BES offers important advantages over bath-applied application of neurochemicals to induce stepping in the in vitro rat model.

Remote effects of self-paced teeth clenching on the excitability of hand motor area.

We studied remote effects of teeth clenching on motor cortical and spinal cord excitability using transcranial magnetic stimulation (TMS), brainstem electrical stimulation (BES), and ulnar nerve stimulation (F-wave) in eight normal volunteers. The TMS, BES, and ulnar nerve stimulation at the wrist were given at different intervals (0-200 ms) after the onset of masseter contraction. Surface electromyographic responses were recorded from the first dorsal interosseous muscle. Responses at different intervals were compared with the response elicited when the subject made no teeth clenching (control response). In TMS, conditioned responses (during teeth clenching) were significantly larger than the control at all intervals. In contrast, in BES and F-waves, conditioned responses were not larger than the control at an early phase (intervals shorter than 50 ms), whereas they were larger than the control at later intervals (longer than 50 ms). These results suggest that facilitation occurs in the hand motor area at the early phase of teeth clenching, and spinal facilitation dominates at its late phase. This time course of facilitation may indicate that the motor cortex must regulate hand muscles finely at the early phase of teeth clenching, and spinal cord may stabilize them firmly at the late phase. The excitability changes of the hand motor area may be in parallel with that of the masseter motor area which reflects the pattern of masseter contraction when the subject activates the masseter muscle phasically at the early phase and sustains that contraction at the late phase.

Cortical excitability changes induced by deafferentation of the contralateral hemisphere.

Short-term deprivation of sensory input by ischaemic nerve block (INB) leads to functional reorganization in the deafferented motor cortex. Here, we show that INB also elicits functional changes in homotopic regions of the cortex contralateral to the deafferented one. We measured motor evoked potential (MEP) amplitudes elicited by transcranial magnetic stimulation (TMS) in small hand and biceps brachii muscles before, during and after INB of the right hand. INB increased excitability of the cortical representation of (i) the intact hand and (ii) body parts proximal to the deafferented hand (upper arm), in the absence of excitability changes in other body part representations such as thorax or leg muscles. This effect persisted throughout the entire period of deafferentation and returned to baseline values afterward. Motor responses to brainstem electrical stimulation remained unchanged during INB, indicating that the effect is probably of cortical origin. Lorazepam, a GABA(A) receptor agonist, blocked this increased excitability. Interhemispheric inhibition between hand muscles decreased during INB. After chronic deafferentation in amputees, MEP amplitudes and motor output curves in small hand muscles were depressed and motor thresholds were elevated compared with aged-matched controls. These results indicate that acute hand deafferentation can elicit a focal increase in excitability in the hand motor representation contralateral to the deafferented cortex that is influenced by transcallosal interactions and GABAergic transmission, and is balanced in the setting of chronic deafferentation.

Modulation of human corticomotor excitability by somatosensory input

In humans, somatosensory stimulation results in increased corticomotoneuronal excitability to the stimulated body parts. The purpose of this study was to investigate the underlying mechanisms. We recorded motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) from abductor pollicis brevis (APB), first dorsal interosseous (FDI), and abductor digiti minimi (ADM) muscles. MEP amplitudes, recruitment curves (RC), intracortical inhibition (ICI), intracortical facilitation (ICF), resting (rMT) and active motor thresholds (aMT) were recorded before and after a 2-h period of ulnar nerve electrical stimulation at the wrist. Somatosensory input was monitored by recording somatosensory evoked potentials. To differentiate excitability changes at cortical vs. subcortical sites, we recorded supramaximal peripheral M-responses and MEPs to brainstem electrical stimulation (BES). In order to investigate the involvement of GABAergic mechanisms, we studied the influence of lorazepam (LZ) (a GABA(A) receptor agonist) relative to that of dextromethorphan (DM) (an NMDA receptor antagonist) and placebo in a double-blind design. We found that somatosensory stimulation increased MEP amplitudes to TMS only in the ADM, confirming a previous report. This effect was blocked by LZ but not by either DM or placebo and lasted between 8 and 20 min in the absence of (i) changes in MEPs elicited by BES, (ii) amplitudes of early somatosensory-evoked potentials or (iii) M-responses. We conclude that somatosensory stimulation elicited a focal increase in corticomotoneuronal excitability that outlasts the stimulation period and probably occurs at cortical sites. The antagonistic effect of LZ supports the hypothesis of GABAergic involvement as an operating mechanism.

Cochlear implants and electrical brainstem stimulation in sensorineural hearing loss.

Cochlear implants and multichannel auditory brainstem implants enable patients with bilateral total or profound hearing loss to receive at least acoustic information. Both types of prosthesis are based on electrical stimulation of the auditory pathway. Different speech coding strategies and the number of electrodes used may influence the postoperative results. The preoperative evaluation of patients is of utmost importance. The cochlear implant is suitable for patients with hearing loss due to inner ear disorders, but who have functioning hearing nerve. Patients with a defect of the hearing nerve can be provided with an auditory brainstem implant.

Nitric oxide regulates cyclic GMP-dependent protein kinase phosphorylation in rat brain.

Nitric oxide (NO) acts via soluble guanylyl cyclase to increase cyclic GMP (cGMP), which can regulate various targets including protein kinases. Western blotting showed that type II cGMP-dependent protein kinase (cGK II) is widely expressed in various brain regions, especially in the thalamus. In thalamic extracts, the phosphorylation of several proteins, including cGK II, was increased by exogenous NO or cGMP. In vivo pretreatment with a NO synthase inhibitor reduced the phosphorylation of cGK II, and this could be reversed by exogenous NO or cGMP. Conversely, brainstem electrical stimulation, which enhances thalamic NO release, caused a NO synthase-dependent increase in the phosphorylation of thalamic cGK II. These results indicate that endogenous NO regulates cGMP-dependent protein phosphorylation in the thalamus. The activation of cGKII by NO may play a role in thalamic mechanisms underlying arousal.

Development and characterization of pathways descending to the spinal cord in the embryonic chick.

1. We used an isolated preparation of the embryonic chick brain stem and spinal cord to examine the origin, trajectory, and effects of descending supraspinal pathways on lumbosacral motor activity. The in vitro preparation remained viable for < or 24 h and was sufficiently stable for electrophysiological, pharmacological, and neuroanatomic examination. In this preparation, as in the isolated spinal cord, spontaneous episodes of both forelimb and hindlimb motor activity occur in the absence of phasic afferent input. Motor activity can also be evoked by brain stem electrical stimulation or modulated by the introduction of neurochemicals to the independently perfused brain stem. 2. At embryonic day (E)6, lumbosacral motor activity could be evoked by brain stem electrical stimulation. At E5, neither brain stem nor spinal cord stimulation evoked activity in the lumbosacral spinal cord, although motoneurons did express spontaneous activity. 3. Lesion and electrophysiological studies indicated that axons traveling in the ventral cord mediated the activation of lumbosacral networks by brain stem stimulation. 4. Partition of the preparation into three separately perfused baths, using a zero-Ca2+ middle bath that encompassed the cervical spinal cord, demonstrated that the brain stem activation of spinal networks could be mediated by long-axoned pathways connecting the brain stem and lumbosacral spinal cord. 5. Using retrograde tracing from the spinal cord combined with brain stem stimulation, we found that the brain stem regions from which spinal activity could be evoked lie in the embryonic reticular formation close to neurons that send long descending axons to the lumbosacral spinal cord. The cells giving rise to these descending pathways are found in the ventral pontine and medullary reticular formation, a region that is the source of reticulospinal neurons important for motor activity in adult vertebrates. 6. Electrical recordings from this region revealed that the activity of some brain stem neurons was synchronized with the electrical activity of lumbosacral motoneurons during evoked or spontaneous episodes of rhythmic motor activity. 7. Both brain stem and spinal cord activity could be modulated by selective application of the glutamate agonist N-methyl-D-aspartate to the brain stem, supporting the existence of functionally active descending projections from the brain stem to the spinal cord. It is not yet clear what role the brain stem activity carried by these pathways has in the genesis and development of spinal cord motor activity.

Magnetic stimulation of corticospinal pathways at the foramen magnum level in humans

Magnetic stimulation done with a double cone coil placed over the back of the head activated descending motor pathways and produced electromyographic responses in muscles of the arms and legs. The latencies of these responses were the same as those of responses to electrical brainstem stimulation. The threshold was lowest when the coil was placed over the inion or below it on the median line. Placement of the coil on the side ipsilateral to the muscle was more effective than placement on the contralateral side. These results indicate that activation occurs at the foramen magnum level (just below the pyramidal decussation). Collision experiments that used cortical and magnetic brainstem stimulation indicated that the major part of the responses to the latter stimulation were conducted via the large diameter component of the corticospinal tract. Collision experiments done with the peripheral nerve and magnetic brainstem stimulation showed that this stimulation produced a single descending volley in the descending tract. We conclude that magnetic brainstem stimulation produces a single descending volley in the corticospinal tract at the foramen magnum level with less discomfort.

Origins and conducting pathways of motor evoked potentials elicited by transcranial magnetic stimulation in cats.

Spinal cord motor evoked potentials (MEPs-S) were elicited in cats by transcranial magnetic stimulation. The MEPs-S recorded from the epidural electrode at the first lumbar (L1) level consisted of four negative peaks (N1, 2.56; N2, 3.19; N3, 4.06; N4, 4.99 ms) followed by small, multiphasic waves. The mean conduction velocities of N1-N3 of the MEPs-S were calculated to be 90 to 115 m/s, which is consistent with extrapyramidal tract activation. A direct brain stem electrical stimulation and sequential transection of the spinal cord studies showed that N1-N3 of the MEPs-S originated primarily from the brain stem and conducted in the ventral funiculus of the spinal cord, which corresponded to the extrapyramidal tracts (e.g., the reticulospinal and vestibulospinal tracts). We also showed that N1 and N2 of the MEPs-S originated mainly from the lower medulla or upper cervical and that N3 originated from the lower pons or upper medulla (vestibular nucleus). On the other hand, N4 of the MEPs-S had a conduction velocity of 70 m/s, which disappeared by ablation of the sensorimotor cortex and pyramidotomy. A dorsal hemisection of the spinal cord, resulting in the disappearance of N4 of the MEPs-S, indicated that it conducted in the dorsolateral funiculus of the spinal cord. These results suggest that N4 of the MEPs-S originates from the sensorimotor cortex and conducts in the lateral corticospinal tract. MEPs-S by transcranial magnetic stimulation in cats constituted complex responses in both the pyramidal and extrapyramidal tracts.

Effects of pontomedullary reticular formation stimulation on the neuronal networks responsible for rhythmical jaw movements in the guinea pig.

1. In the ketamine-anesthetized guinea pig, electromyographic (EMG) responses of the digastric muscle and vertical and horizontal movements of the mandible were studied when loci within the caudal pontine and rostral medullary reticular formation were stimulated during rhythmic jaw movements (RJMs) evoked by stimulation of the masticatory area of the cortex. 2. Within these regions electrical brain stem stimulation of the pontis nucleus caudalis and nucleus gigantocellularis (PnC-Gi) of the reticular formation completely blocked RJMs at stimulus intensities as low as 10 microA while suppressing the short-latency digastric EMG response that was time locked to each cortical stimulus in the train. PnC-Gi stimulation did not, however, reduce the excitability of the short-latency corticotrigeminal excitatory pathway to digastric motoneurons when tested by short pulse train stimulation at 2 Hz (3 pulses, 500 Hz, 0.3 ms) in the absence of RJMs. 3. Short trains (80 ms) of PnC-Gi stimuli delivered at various phases of the RJM cycle produced a permanent phase shift of the RJM rhythm. If the stimulus train was delivered at an early phase of the cycle (8-40%) the next cycle onset was advanced; if the train was delivered later in the cycle (60-80%) the next cycle onset was delayed. Long trains of PnC-Gi stimuli (100, 200, 300, and 400 ms) increased the time of onset of the next cycle by an amount directly proportional to the duration of the stimulus train. 4. Digastric EMG activity occurring during cortically evoked RJMs occupied nearly 50% of the cycle. If a short train of PnC-Gi stimuli was delivered between approximately 5 and 125 ms after the onset of the burst, the duration of the burst was significantly shortened. 5. These results demonstrate that the suppression of cortically evoked RJMs resulting from PnC-Gi stimulation is due to direct effects on central circuits responsible for the production of the RJM behavior and not on the motoneurons themselves. The evidence presented is consistent with our previously presented hypothesis that the neurons involved in mediating the short-latency corticotrigeminal pathway to digastric motoneurons are separate and distinct from those neurons comprising the central networks responsible for the production of the fundamental jaw oscillation during RJMs.

Effects of adequate vestibular stimulation on locomotor activity in the guinea pig fore- and hindlimb muscles. Tilting around a transverse axis

The effects of adequate vestibular stimulation occurring as the animal tilted around its transverse axis on locomotor activity of the fore- and hindlimb muscles produced by electrical brainstem stimulation were investigated during experiments on guinea pigs decerebrated at the precollicular level. An increase and decrease in forelimb and hindlimb extensor activity, respectively, at the standing phase of the locomotor cycle were observed when the animal was tilted head-downward. The reverse changes took place in the limb extensor muscles when the animal was tilted head-up. Forelimb extensor activity during the swing phase increased and decreased when the animal was tilted head-up and head-downward, respectively. Phase shifts of changes in locomotor activity of the forelimb extensors altered from 60 to −30°, from −150 to 220° in hindlimb extensors, and from −140 to −220° in forelimb flexors during sinusoidal tilting in the 0.02–0.4 Hz frequency range and an amplitude of ±20°. Mechanisms underlying the changes observed in locomotor muscle activity are discussed.

Peripheral venous catecholamines versus adrenal secretory rates after brain stem stimulation in cats.

The relationship between adrenal catecholamine secretion and peripheral venous catecholamine concentration was assessed in samples collected before and after brief (15-s) periods of brain stem electrical stimulation in cats anesthetized with alpha-chloralose-urethan. Adrenal blood flow from the left lumboadrenal vein averaged 0.75 +/- 0.05 ml/min (means +/- SE, n = 56). Peripheral norepinephrine (NE) concentration (1.19 +/- 0.07 ng/ml) was not well correlated with adrenal NE secretion (38.18 +/- 3.99 ng/min) before stimulation (r = 0.334, P less than 0.025). Although brain stem sites that evoked large increases in adrenal NE secretion often caused an increase in peripheral NE, sites that evoked significant decreases in adrenal NE secretion were not accompanied by decreases in peripheral NE. Peripheral epinephrine (E) concentration (0.11 +/- 0.01 ng/ml) was well correlated with adrenal E secretion (23.72 +/- 2.33 ng/min) before stimulation (r = 0.468, P less than 0.001). Brain stem stimulation-evoked changes in adrenal E secretion were generally reflected in changes of peripheral E concentration, although many exceptions were seen. Peripheral dopamine (DA) concentration (0.23 +/- 0.02 ng/ml) was well correlated with adrenal DA secretion (0.94 +/- 0.11 ng/min) before stimulation (r = 0.505, P less than 0.001). However, stimulus-evoked changes in adrenal DA secretion were not reflected in changes of peripheral DA concentration. The data indicate that, whereas brief periods of brain stem stimulation evoke a wide range of adrenal secretory responses, peripheral catecholamine responses best reflected adrenal secretion only when large increases in adrenal secretion were evoked and were poor indicators of decreased adrenal catecholamine secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Frequency-specific RSA-like hippocampal patterns elicited by septal, hypothalamic, and brain stem electrical stimulation

Hippocampal electrographic patterns comprised of specific frequencies of slow waves electrographically similar to the waves comprising normal hippocampaa rhythmical slow activity (RSA, theta) may be generated by appropriate electrical stimulation of specific septal, hypothalamic, and brain stem sites. The waves elicited from some but not all sites are further similar to normal RSA patterns in that they may be differentiated into atropine-sensitive (immobility-related) and atropine-resistant (movement-related) types by the same criteria used to define atropine-sensitive and atropine-resistant RSA. The high degree of behavioral, pharmacological, and electrographic similarity between the electrically elicited hippocampal activity and normal hippocampal RSA would seem to warrant further use of the present technique in the investigation of hippocampal function.