Unrestrained Cats Research Articles

Optokinetic eye and head movements in the unrestrained cat

Eye and head movements of the unrestrained and alert cat were measured with the search coil technique. Optokinetic responses were elicited by a moving random dot pattern. With the head free, slow phase gaze velocity (SPGV) during optokinetic nystagmus (OKN) was not faster than slow phase eye velocity (SPEV) with the head fixed neither with binocular nor with monocular stimulation. Cats with the head free also showed a directional asymmetry of SPGV during monocular stimulation with higher gain values for slow phases from temporal to nasal as compared to slow phases from nasal to temporal. Eye, head and body movements contributed to SPGV to a varying degree. Although SPGV remained rather constant (comparable to the head-fixed condition), the relative contributions of head velocity and eye velocity could fluctuate strongly. During the resetting saccades, the head ended its fast phase later than the eye (102 ± 46 ms). During this period, the eye compensated the remaining part of the fast phase of the head and simultaneously executed an already new slow phase of gaze. It is discussed whether the cerebellar flocculus might provide a system to achieve constant gaze during OKN.

Pressor and intestinal vascular bed responses to vasopressin after cholinergic blockade.

Superior mesenteric arterial flow, aortic blood pressure, and heart rate were recorded, and plasma arginine vasopressin (AVP) concentrations were measured in conscious unrestrained cats during intravenous infusions of AVP (0.1-8.1 mU.kg-1. min-1). Responses to AVP were studied when autonomic nervous system (ANS) function remained intact and when the cholinergic limb of the system had been antagonized by methscopolamine nitrate (0.5 mg/kg) or by pirenzepine (60 micrograms/kg). Elevations in the circulating levels of AVP to approximately 30 and 600 fmol/ml in cats with intact ANS function were associated with decreases in superior mesenteric arterial conductance (SMAC, ml.min-1.kg-1.mmHg-1) of approximately 9 and 50%. The relationship between the dose of AVP and the decreases in SMAC for methscopolamine-treated cats was displaced slightly but significantly to the left of that for intact cats. The relationship between the dose of AVP and the increases in arterial pressure for methscopolamine-treated cats was also significantly displaced to the left of that for intact cats; however, the magnitude of the displacement was much greater than that for the dose-conductance relationship. In contrast to the findings with methscopolamine, pirenzepine did not significantly influence either the dose-conductance or dose-blood pressure response curves. These results are consistent with three conclusions. First, physiologically (less than 30 fmol/ml) and pathophysiologically (less than 600 fmol/ml) relevant concentrations of AVP are capable of inducing intestinal vasoconstriction, even in the presence of intact autonomic function. Second, the cholinergic limb of the autonomic nervous system plays a major role in buffering the vasopressor effects of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Integrated defence reaction elicited by excitatory amino acid microinjection in the midbrain periaqueductal grey region of the unrestrained cat

Unilateral microinjections (0.20 μl) of the excitatory amino acids (EAA), l-aspartate (ASP), d,l-homocysteate (DLH) or kainate (KA) were made into the midbrain of freely moving cats. Injections of DLH (20 nmol) or ASP (200 nmol) made within the midbrain periaqueductal grey matter (PAG) consistently elicited a threat display characteristics of defensive behaviour (i.e., pupillary dilatation, piloerection, retraction of the ears, sideways backing, arching of the back, hissing, howling, growling), whereas injections of DLH or ASP made in the tegmentum bordering the PAG did not elicit such behaviour. Injections of KA (940 pmol) made within the PAG, but not the tegmentum, elicited not only a threat display but also directed attack (striking with unsheathed claws and biting). As injections of EAA depolarize cell bodies, but not axons, the results suggest that a population of neurones whose excitation elicits all of the behavioural signs of defence, including directed attack, is found within the PAG. Histology indicated that the region of the PAG from which the defence reaction was elicited was not confined to any PAG subnucleus. Rather, the ‘defence region’ of the PAG formed a cylindrical column lateral to the midbrain aqueduct, approximately 1.5 mm in diameter and 5.0 mm in length, the rostral end of which lay dorsal to the caudal end. Further, it was found that EAA microinjections made in different portions of the defence region of the PAG elicited defence reactions characterised by different patterns of vocalization and differing intensities of display. It was also observed following unilateral injection of KA into the PAG that defence reactions, including attack, were elicited by approach in the visual hemifield or touch of the body contralateral, but not ipsilateral, to the injection site. The assymmetry of the defence reaction was not due to any obvious ipsilateral motor impairment and thus suggests that the PAG mediation of the defence reaction, in addition to controlling the outflow to the somatic and autonomic motor systems, also affects sensory processing.

Effects of physiological manipulations on locus coeruleus neuronal activity in freely moving cats. I. Thermoregulatory challenge

This and the following two papers examine the activity of locus coeruleus noradrenergic (LC-NE) neurons in response to a variety of physiological manipulations in unanesthetized, unrestrained cats. Unit responses were studied during a constant behavioral state in order to avoid the potentially confounding effects of state changes upon LC-NE unit discharge. In the present study, LC-NE unit activity was recorded during two thermoregulatory challenges: ambient heating and pyrogen-induced fever. These two conditions are particularly interesting since the direction of body temperature change that they produce is the same, but the thermoregulatory responses elicited are opposite, i.e. heat loss and heat gain. LC-NE neurons were activated by both manipulations. In response to ambient heating, neuronal activity increased only with the occurrence of panting, and not during earlier portions of the heating session. Following pyrogen administration, LC-NE neurons responded only during the peak increase in body temperature. Both of these effects on unit activity occurred independent of changes in behavioral state. Since both manipulations similarly increased LC-NE unit activity, despite eliciting opposite thermoregulatory responses, it appears that these neurons do not play a specific role in thermoregulation, but may participate in the response to physiological challenges in general.

Effects of physiological manipulations on locus coeruleus neuronal activity in freely moving cats. III. Glucoregulatory challenge

Insulin-induced hypoglycemia and the subsequent administration of glucose were examined for their effects on single unit activity of locus coeruleus noradrenergic (LC-NE) neurons in unanesthetized, unrestrained cats. LC-NE neuronal activity showed an inverse relationship to blood glucose levels. The activity of most cells increased during sustained hypoglycemia, and then decreased following glucose administration. Some neurons were unaffected by hypoglycemia, but were inhibited following glucose. The activation of LC-NE neurons in response to insulin administration generally paralleled the increase in plasma epinephrine, although the adrenal response was more sensitive. These data, together with those reported in the preceding papers, suggest the following general conclusions: (1) physiological stimuli can influence the activity of LC-NE neurons in unanesthetized subjects (although they do so less strongly than environmental stimuli); (2) these effects of physiological stimuli upon LC-NE neurons can be exerted independent of changes in behavioral state; (3) LC-NE neurons do not appear to play a specific role in the regulation of any of the systems examined, but may instead play a more global role in the response to physiological challenges in general; (4) LC-NE neurons are generally co-activated with both the neural and hormonal components of the sympatho-adrenal system, although sympathetic activation can occur in the absence of increased LC-NE activity. A previously hypothesized role for LC-NE neurons in facilitating the behavioral response to environmental stressors may thus be extended to include the response to physiological challenges, and perhaps facilitation of the physiological as well as the behavioral components of the stress response.

Effects of physiological manipulations on locus coeruleus neuronal activity in freely moving cats. II. Cardiovascular challenge

Several cardiovascular manipulations were examined for their effects on single-unit activity of locus coeruleus noradrenergic (LC-NE) neurons in unanesthetized, unrestrained cats: hydralazine (1 mg/kg, i.v.) was administered to present a tonic hypotensive stimulatus, and to activate preferentially the neural component of the sympathoadrenal system; hemorrhage was used to decrease blood volume and to activate both the neural and hormonal components of the sympathoadrenal system; intravenous infusion of isotonic saline was used to increase blood volume. LC-NE neurons were activated by hydralazine, in parallel with the sympathetic response (indicated by elevated heart rate and plasma NE). LC-NE unit activity was decreased folowing a volume load. However, contrary to previous findings in anesthetized animals, hemorrhage had no effect on LC-NE unit activity, but did activate both components of the sympathetic response. It is concluded that: (1) cardiovascular stimuli can influence the activity of LC-NE neurons, though they show less sensitivity to such stimuli than do primary regulatory mechanisms; (2) the response of LC-NE neurons to physiological stimuli can occur independent of changes in behavioral state; (3) these neurons do not appear to play a specific role in cardiovascular regulation, but may respond to physiological challenges in general; (4) finally, in agreement with previous studies, our data show that LC-NE neurons are generally co-activated with the sympathetic nervous system, but also that the two can be dissociated (e.g. hemorrhage).

Rostral hypothalamus: A new neuroanatomical site of neurochemically-induced emesis in the cat

The localized effect of noradrenergic agonists administered directly in the anterior hypothalamic preoptic area (AH/POA) in inducing emesis in the cat was investigated. Of the noradrenergic agonists tested, which included norepinephrine, clonidine, phenylephrine and methoxamine, only clonidine in doses of 5.0–50.0 μg was found to evoke emesis consistently when micro-injected in a volume of 1.0 μ1 into AH/POA of the unrestrained cat. The emetic response to clonidine was short-lasting, generally dose-dependent in terms of latency and frequency, and occurred in bouts of one to three episodes. The sequence of the vomiting response, beginning with licking and retching, functionally resembled a normal pattern of an emetic response. The clonidine-induced emesis was not antagonized by the following antagonists micro-injected in AH/POA just prior to clonidine: α-adrenergic blocking agents, yohimbine, RX 781094 and phentolamine; the antimuscarinic drug, atropine; the serotonin antagonist, methysergide; the opioid antagonist, naloxone; and the dopamine antagonist, chlorpromazine. There- fore, it would appear that clonidine-induced emesis is not mediated by alpha noradrenergic, serotonergic, dopaminergic, muscarinic and opiate receptor systems within the AH/POA of the cat. Finally, the obtained results show that apart from the area postrema and a circumscribed zone of the brain-stem reticular formation, the hypothalamus is now implicated as a neuroanatomical site in the central nervous system mechanism underlying neurochemically-induced emesis.

Regional differences in the cat caudate nucleus as to the effectiveness in inducing contraversive head-turning by electrical stimulation

An attempt was made to re-examine regional differences in the cat caudate nucleus as to the effectiveness in inducing contraversive head-turning by electrical stimulation and to analyze the time course of head-turning quantitatively. In 5 of the total 9 cats, the right sensorimotor cortex and its surrounding areas had been ablated chronically. While the awake, unrestrained cat maintained a stable standing posture facing forward, stimulation was applied systematically to various points in and around the caudate nucleus with a movable stimulating electrode. Trains of stimulating current pulses of less than 300 μA were given, mostly at a rate of 100 Hz for 5 s. In most experiments in which stimulation was given to the side of the intact cerebral cortex, stimulation of caudal portions of the head of the caudate nucleus was effective in inducing contraversive head-turning, but that of its rostral portions was ineffective. In experiments on the side of chronic cortical ablation, similar results were obtained. These results suggested that head-turning induced by stimulation of the caudate nucleus was brought about not by the activation of the corticofugal fibers from these cortical areas by a current spreading to the internal capsule, but by the activation of caudate neurons. Hence, it was demonstrated that there were regional differences in the cat caudate nucleus as to the effectiveness in inducing head-turning. The mean of the shortest latencies of the onset of head-turning for individual stimulation points was 396 ms (S.D., 210 ms) for the side of the intact cerebral cortex, and 454 ms (S.D., 289 ms) for the side of the cortical ablation. Statistically, there was no significant difference between them. Therefore, it was further revealed that the elimination of the sensorimotor cortex did not affect the caudate-induced head-turning in terms of the latency of its onset.

Sensitivity of Intestinal Resistance Vessels to Vasopressin After Ganglionic Blockade in the Conscious Cat

Superior mesenteric arterial flow, arterial pressure, and heart rate were recorded, and plasma arginine-vasopressin (AVP) concentration was measured, during intravenous infusions of AVP (0.1-8.1 mU X kg-1 X min-1) in conscious unrestrained cats under two experimental situations--when autonomic function remained intact and, on other days, when it had been impaired by pretreatment of the animals with the ganglionic blocking agent pentolinium tartrate (2.5 mg X kg-1 and 0.125 mg X kg-1 X min-1). The dose-related increases in the plasma concentrations of AVP attained during the infusions of the peptide were similar under the two experimental situations. The curve expressing the relationship between the dose of AVP and the decrease in superior mesenteric arterial conductance (ml X min-1 X kg-1 X mm Hg-1) for when ganglia were blocked was similar to the curve for when autonomic function remained intact. Elevations in the circulating levels of the peptide within the physiological range (less than 30 fmol X ml-1) were associated with significant decreases in conductance, both when ganglia were blocked and when they were intact. In contrast to conductance, the curve expressing the relationship between the dose of AVP and the increase in arterial pressure for when ganglia were blocked was displaced markedly to the left when compared with the curve for when reflexes remained intact, even though the effect of ganglion blockade on pressor responses did not reach statistical significance with the two lowest doses of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential control of blood pressure and heart rate by carotid and aortic baroreceptors in unanaesthetized cats.

In unanaesthetized cats the most striking effects of sino-aortic denervation (SAD) consist of a marked increase in blood pressure variability and a concomitant marked reduction in heart rate variability. Because the relative contribution of carotid and aortic baroreceptors to these phenomena has never been assessed, blood pressure (intra-arterial catheter) and heart rate were measured in unanaesthetized, unrestrained cats for 8-10 h under three conditions: intact animals, 1 week after section of the carotid sinus or the aortic nerves and 1 week after SAD. Blood pressure and heart rate signals were analysed by a computer to provide mean values and variation coefficients of variation i.e. blood pressure and heart rate variabilities, for each recording period. In the intact cats the coefficient of variation was 6.6 +/- 0.6% (mean +/- s.e.) for mean blood pressure and 11.2 +/- 1.7% for heart rate. The coefficient of variation for mean blood pressure was not altered by either the aortic or the carotid sinus nerve section, a marked increase being observed only after SAD (11.5 +/- 1.3%, P less than 0.01). On the other hand, the coefficient of variation for heart rate was reduced either by the carotid or by the aortic nerve section. The reduction observed following the carotid baroreceptor denervation accounted for the greater fraction of the overall reduction (74 versus 26%) in coefficient of variation for heart rate observed after SAD (4.8 +/- 0.9%, P less than 0.01). These data show that the carotid sinus and aortic nerves are similarly involved in control of blood pressure variability.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of the temporal lobe amygdala in ponto-geniculo-occipital activity and sleep organization in cats

Ponto-geniculo-occipital (PGO) spikes propagate to different structures of the limbic system, including the temporal lobe amygdala. There is direct connection between the amygdala and the pontine nucleic involved in the generation of PGO spikes. It has also been shown that both the amount and the pattern of PGO spike discharges are under the influence of several brainstem and forebrain structures. In the present work, PGO activity was analyzed in unrestrained cats submitted to low-intensity amygdaloid electrical stimulation during paradoxical sleep (PS) episodes. General sleep organization as well as number, mean duration and percentage of PS episodes, were assessed in 8-h sleep recordings during amygdaloid stimulation. Amygdaloid stimulation significantly increased PGO number, spike density and, specially, PGO burst density. No significant changes were found in PS episodes or in the slow-wave sleep. It is concluded that the amygdala plays a role in the modulation of PGO activity by means of a facilitatory influence. It is proposed that this influence is probably exerted through a positive feedback mechanism. The independence between PGO generation and PS maintenance mechanisms is emphasized.

Hypothermia: Role of α1- and α2-noradrenergic receptors in the hypothalamus of the cat

The purpose of this study was to characterized the α 1- and α 2-noradrenergic receptor sub-types which could mediate the hypothermic response produced by noripinephrine (NE) and other α-noradrenergic agonists applied to the thermosensitive zone of the hypothalamus. An array of four guide tubes was implanted stereotaxically so that their tips rested just above the anterior hypothalamic, preoptic area (AH/POA) of the cat. Following post-operative recovery, a micro-injection of an agonist or antagonist of NE receptors or control CSF vehicle was given in a volume of 1.0–2.0 μl in the AH/POA in each of the unrestrained cats. The α 1-noradrenergic receptor agonist, phenylephrine, but not methoxamine, applied to the AH/POA produced a dose-dependent hypothermia of up to 2.0°C. When applied similarly, the α 2-noradrenergic agonist clonidine, as well as norepinephrine, which acts on both α 1- and α 2-noradrenergic receptors, also induced a decline in the cat's core temperature of up to 1.5°C. The hypothermic response of clonidine was inhibited by pre-treatment of the AH/POA with a micro-injection of the selective α 2-noradrenergic blocking agent, yohimbine. However, yohimbine given similarly in the cat's AH/POA potentiated significantly both the phenylephrine and norepinephrine-induced hypothermia. The combined α 1-, α 2-noradrenergic receptor antagonist, phentolamine, also injected into AH/POA inhibited the thermolytic response evoked by both phenylephrine and norepinephrine, whereas it was virtually ineffective against the clonidine-induced hypothermia. These results, therefore, strongly suggest that both α 1- and α 2-noradrenergic receptors subserve the coordinated thermoregulatory mechanisms in AH/POA which are required for the functional dissipation of body heat and the consequent evocation of hypothermia.

Rate of in vivo verapamil exchange within the hypothalamus of the cat as examined by push-pull perfusion.

To investigate the characteristics of the uptake within hypothalamic tissue of the Ca2+-channel blocker, verapamil, push-pull canulae were implanted bilaterally above the anterior hypothalamic-preoptic area (AH/POA) and posterior hypothalamus (PH) of the cat. The functional reactivity of these two anatomical regions was verified in the unrestrained cat, prior to a push-pull perfusion, by a micro-injection of either 5-7 micrograms norepinephrine (NE) into AH/POA, or by perfusion of 50 mM Ca2+ within the PH, both of which induce a transient decline in the cat's core temperature. Verapamil was perfused in a concentration of 0.4, 2.0 or 4.0 micrograms/microliter for successive 10 and 20 min intervals within these NE and Ca2+-sensitive sites. A quantitative analysis of verapamil in each sample of perfusate was performed double-blind by HPLC-spectrophotometric detection. The results showed that the percent recovery of verapamil after the 10 min interval was always less than that after the next 20 min period of perfusion. These recovery values were independent of the site of perfusion and the concentration of verapamil. However, the mean uptake of verapamil into tissue after 10 min was significantly greater than that after the 20 min period for all concentrations tested. These results demonstrate that the hypothalamus has a time-dependent characteristic to incorporate a Ca2+-channel blocker into the parenchyma. Once the point of tissue saturation is reached, a steady-state level of verapamil uptake is established.

Sleep factors released from brain of unrestrained cats: a critical appraisal.

Sleep factors released from brain of unrestrained cats: a critical appraisal.

Neuroanatomical mapping of hypothalamic regions mediating verapamil hyper- and hypothermia in the cat

Guide cannulae for microinjection and push-pull perfusion in the unrestrained cat were implanted bilaterally in the anterior hypothalamic, prepotic area (AH/POA) and posterior hypothalamus (PH). Postoperatively, the region was first identified in AH/POA which was reactive to norepinephrine or in PH to excess Ca ++ ions; in both cases a hypothermie response was produced. Then either an artificial CSF control vehicle or the Ca ++ ion channel blocking agent, verapamil, was perfused for 30 min by means of push-pull cannulae at a rate of 25.0 μl/min. Verapamil (0.4, 2.0 and 4.0 μg/μl) induced a concentrationdependent hypothermia when perfused within AH/POA sites but hyperthermia when perfused in the caudal hypothalamus. An anatomical analysis of the sites of perfusion revealed that verapamil's thermolytic effect was localized within the classical thermosensitive region of the cat's diencephalon, a region ventral to the anterior commissure and dorsal to the optic chiasm. On the other hand, the loci in which verapamil evoked thermogenesis were localized to a region dorsal to the mammillary bodies and caudal to the descending columns of the fornix. It is suggested that verapamil interferes with Ca ++ ion channels in the PH to shift the cat's “set-point” temperature. Conversely, however, verapamil apparently could act on catecholaminergic terminals in AH/POA to enhance the presynaptic release of norepinephrine which, in turn, stimulates the heat loss pathway to yield hypothermia.

The responses of pericruciate cortical neurones to distal forepaw electrical stimulation in the unanaesthetized, unrestrained cat.

Experiments were performed to examine the responses of cortical neurons in the pericruciate cortex to cutaneous afferent input from the distal forepaw. Ninety-nine cortical neurons responding to electrical stimulation of the forepaw were recorded from four cats. Their response latencies ranged from 6 to 23 ms. The units had cutaneous receptive fields which ranged in size from those restricted to one digit to those extending over the whole forelimb. They were recorded from area 4 and area 3. Intracortical microstimulation at the recording sites activated either the distal or proximal musculature of the forelimb. When the characteristics obtained from each recording site were examined as a group of features, a uniform population emerged which was significantly different from the rest of the sample. These units had the shortest latency responses to distal forepaw electrical stimulation, the shortest duration of evoked discharge, the smallest distal cutaneous receptive fields. Such units were recorded at the border between areas 3 and 4, at sites which on microstimulation resulted in movements of the distal forepaw musculature.

Neuronal activity evoked by chronically implanted intracortical microelectrodes

The averaged evoked compound action potentials (AECAPs) were recorded from the ipsilateral pyramidal tract of awake, unrestrained cats before, during, and after continuous electrical stimulation of the cerebral cortex via chronically implanted activated iridium or platinum-30% iridium (Pt30%Ir) microelectrodes. After stimulating 24 h at 20 pulses per second (pps), using charge-balanced, 200-μs pulse pairs of 40 to 80 μA (400 to 800 μC/cm 2, 8 to 16 nC/phase (ph), 2 to 4 A/cm 2), there was a transient elevation of the threshold of the early (direct) and of the late (transynaptic) components of the AECAP. After cessation of continuous stimulation at 80 μA, the threshold of the early component of the AECAP remained elevated for as long as 24 h and the late component as long as 4 days, indicating significant but reversible depression of the electrical excitability of cortical neurons close to the microelectrodes. In three cats stimulated 23 h/day for 1 week, the AECAP also recovered to their prestimulus threshold. In contrast, pulsing for 24 h at 320 μA (3200 μC/cm 2, 64 nC/ph, 16 A/cm 2) produced marked elevation of the threshold of the AECAPs which was not reversed by 7 to 12 days after termination of intracortical stimulation. The electrical excitability of neurons adjacent to (unpulsed) microelectrodes 2 mm from the pulsed electrode was not affected. The observations resported here, in conjunction with the histologic results reported in the companion paper, indicate that both the Pt30%Ir and the iridium microelectrodes can be operated safely at currents to at least 80 μA, charge/ph of 16 A/cm 2, and a charge density of 800 μC/cm 2 · ph. However, on the basis of the electrophysiologic criteria, both types appear to be unsafe when pulsed at 320 μA (64 nC/ph, 3200 μC/cm 2 · ph, 16 A/cm 2).

Discharge patterns of reticulospinal and other reticular neurons in chronic, unrestrained cats walking on a treadmill.

Recordings were made from single units in the medullary reticular formation (MRF) between AP-4.2 and AP-12.9 and from the midline to 3.7 mm lateral in chronically prepared, unrestrained cats walking on a treadmill. Recordings were made with rigid microelectrodes held in a microdrive, and reticulospinal neurons were identified by antidromic stimulation of their axons through microwires chronically implanted into the spinal cord at the L2 level. Electromyograms (EMGs) were recorded from flexor and extensor muscles of the fore- and hindlimbs as well as from back and neck muscles. In total, 295 cells were recorded from 40 penetrations in 4 cats; 252 of these cells were recorded from the more medial regions of the reticular formation encompassing the gigantocellular, magnocellular, and lateral tegmental fields; 38.5% of these (97/252) were antidromically identified from the spinal cord. The remaining 43 neurons (43/295) were recorded from a more lateral and ventral position. These medial and ventrolateral groups of neurons differed not only in position but also in aspects of their discharge during locomotion. Rank-ordered raster displays, triggered from the onset of each recorded muscle, were used to correlate neuronal and muscular activity. The discharge rate of 31% of the reticulospinal neurons (30/97) was modulated once or twice in each step cycle and was strictly related to one or more of the recorded EMGs (EMG-related neurons) on the basis of the pattern of discharge. The discharge of 33/97 (34%) of the neurons was modulated at the periodicity of the locomotor rhythm but could not be correlated with any of the recorded EMGs (locomotor-related cells), whereas the remaining 34/97 neurons (35%) were either silent, fired tonically, or were not related to the locomotor pattern (unrelated cells). Of the EMG-related neurons 27% were related to flexor muscles and the remaining 63% to extensor muscle activity. The discharge pattern of all except two of the flexor-related neurons was correlated with hindlimb muscle activity, whereas that of the extensor-related neurons was correlated almost equally with fore- and hindlimb muscles. Correlations were found with muscles lying both ipsilaterally and contralaterally to the site of the recordings. Although the locomotor-related neurons showed no preferential relation with any of the recorded EMGs, a comparison of the depth of modulation of their discharge measured from postevent histograms suggested that more of these cells were related to the forelimb than to the hindlimb.(ABSTRACT TRUNCATED AT 400 WORDS)

Respiratory inhibition induced by transient hypertension during sleep in unrestrained cats

The effects of transient blood pressure elevation, induced by intravenous injection of phenylephrine, were studied in drug-free, unrestrained cats during sleep and waking. Transient hypertension evoked an increase in respiratory cycle duration (T tot), an effect which was most prominent during quiet sleep. Transient hypertension evoked no overall change in inspiratory duration (T di) during any sleep-waking state, although reduction of diaphragmatic EMG amplitude was observed. Thus, the ratio of diaphragmatic activity time to total respiratory cycle duration ( T di T tot ) was decreased following blood pressure elevation. Apneic episodes occasionally occurred, and these occurrences were more frequent during sleep states. Apneas induced during quiet sleep were often associated with transient or sustained arousal.

Kinesiological studies of self- and cross-reinnervated FDL and soleus muscles in freely moving cats.

The activity patterns in self- and cross-reinnervated flexor digitorum longus (FDL) and soleus (SOL) muscles were examined during natural movements in awake, unrestrained cats in which electromyographic (EMG) electrodes, tendon-force gauges, and muscle-length gauges had been chronically implanted under anesthesia and aseptic conditions. Kinesiological data were recorded between 13 and 22 mo after nerve surgery. Self-reinnervated FDL and SOL muscles (i.e., FDL----FDL and SOL----SOL, respectively) exhibited locomotor activity patterns that were the same as observed in normal, unoperated FDL and SOL muscles (26). FDL----FDL muscles exhibited primarily brief bursts of activity in early swing, just after the toes had left the ground, whereas SOL----SOL muscles showed bursts of activity just before and during stance. In contrast, the cross-reinnervated muscles (both SOL----FDL and FDL----SOL) that had little or no unwanted self-reinnervation showed the patterns of activity that are associated with the innervating foreign motoneurons. That is, cross-reinnervated SOL----FDL muscles were intensely active in quadrupedal standing and, during the stance phase of stepping, producing large force transients while actively lengthening. Conversely, cross-reinnervated FDL----SOL muscles were active mainly in short bursts at the onset of the swing phase of stepping, just after the foot had left the ground. There was considerable modulation of EMG and peak force output in FDL----SOL muscles with changing speed of locomotion, whereas little modulation was evident in SOL----FDL muscles. The activity patterns in self- and cross-reinnervated FDL and SOL muscles were also recorded during scratch and paw-shaking reflexes. As in locomotion, the observed patterns were in all cases consistent with those expected for the innervating motor pool rather than the innervated muscle. Muscles that had been dually reinnervated by both the original and foreign motor pools displayed activity patterns that were a mixture of the FDL and SOL activity patterns described above. The present results demonstrate that motoneuron activation patterns remain qualitatively unaltered when their motor axons reinnervate foreign muscles. In addition, the observations permit some quantitative estimates of the degree to which cross-reinnervated muscles are subjected to patterns of motoneuron activity and to conditions of mechanical loading that are markedly different from those in the self-reinnervated or normal conditions.