Ultrasonographic investigation of the atlanto-occipital articulation in the horse.

The purpose of this study was to evaluate ultrasonographic imaging as a means of easy and noninvasive diagnosis of articular and periarticular structures of the atlanto-occipital articulation in the horse; and to find a safe approach to the atlanto-occipital joint. Ultrasonographic investigations were performed on 6 healthy horses and 16 specimens from horses humanely destroyed age 2-17 years (mean 9.56 years). Preliminary examinations included anatomical studies and preparation of cross-sections. On 4 horse specimens, puncture of the atlanto-occipital joint under ultrasonographic guidance was performed and a new lateral approach undertaken. For ultrasonographic investigations, the neck was divided into 4 zones according to anatomical and clinical modalities: 1) insertion of the funiculus nuchae; 2) tuberculum dorsale of the atlas; 3) atlanto-occipital joint and 4) region above the foramen alare. Each zone was examined in transverse and longitudinal planes proceeding from cranial to caudal. Ultrasonography was found to be useful for soft tissue imaging of this region and was performed down to the atlanto-occipital joint of which the joint surfaces, joint capsule and collateral ligament could be delineated in both planes. We conclude that ultrasonography of the neck is a useful technique, representing an easy to use and safe method. However, further studies are indicated which should be performed on live subjects.

Angular limb deformity in a calf treated by periosteotomy and wedge osteotomy.

A carpus valgus deformity was diagnosed in a five-week-old Brown Swiss calf. The 45 degrees deformity was caused by the malaligned healing of a fracture of the left metacarpus after birth trauma. The deviation improved to 25 degrees after being treated with a semicircular lateral periosteotomy above the distal physis of the radius. A complete correction was made by means of a wedge osteotomy five months after the first treatment. A 20 degrees wedge of bone was removed. The metacarpus was stabilised with a seven-hole dynamic compression plate which was removed 12 weeks later. Thirty months later the calf was sold as a pregnant heifer at an auction of breeding cattle.

[Electrophoretic studies of serum protein fractions in horses with laminitis]. / Elektrophoretische Untersuchungen der Serumproteinfraktionen hufrehekranker Pferde.

The spectrum of serum proteins was evaluated in 46 horses affected with spontaneous laminitis and correlations between the severity of the disease and changes of the protein pattern were analyzed. The investigation was made in two groups; group A consisted of 21 horses of various breeds (warmblood, thoroughbred, standardbred) and group B of 25 ponys. Each group was subdivided according to the severity of the disease, using the OBEL-grade (OG) classification system. Serum proteins were separated by different one- and two-dimensional electrophoretic methods. Sera analysed by cellulose acetate electrophoresis showed a significant difference in the alpha 1-globulin fraction between OG II and OG IV affected horses. An increasing severity of the disease was correlated with a decrease of the alpha 1-globulins. The other protein fractions didn't show a uniform tendency. In group B there was a significant difference in the alpha 1-globulin fractions of OG II and OG III and in the beta 2-globulin fractions of OG I and OG II affected ponys. The acute phase proteins C3c, C4, Hp and fibronectin could be determined in a preliminary study in horse serum using the cross-reactivity of antibodies against the homologous human proteins.

D2 dopamine receptor-mediated mechanisms in the medial preoptic-anterior hypothalamus regulate effective defense behavior in the cat.

The role of the dopaminergic innervation of the medial preoptic-anterior hypothalamus (mPO-AH) in regulating the expression of affective defense behavior in the cat has been investigated in the present study. Feline affective defense behavior, characterized mainly by autonomic arousal, ear retraction, growling, hissing and paw striking, was elicited by electrical stimulation of the ventromedial hypothalamic nucleus (VMH). Following the establishment of a stable threshold current for eliciting the hissing response of the behavior, the effect of injecting various DAergic agonists and antagonists into the mPO-AH on the hissing threshold was determined. The microinjection of the non-selective DA agonist apomorphine (0.03, 0.16, 0.33, 0.66, 1.56 and 3.3 nmol) into the mPO-AH facilitated hissing in a time- and dose-dependent manner. This effect was mimicked by the D2-selective agonist LY 171555 (0.2 and 1.0 nmol) but not by the D1-selective agonist SKF 38393 (1.7 and 17 nmol), and was blocked by the non-selective and the D2-selective antagonists haloperidol (1.3 nmol) and sulpiride (14.5 nmol), respectively. The injection of the D1-selective antagonist SCH 23390 (0.3 nmol), however, did not inhibit apomorphine-induced facilitation of hissing. In addition, the injection of haloperidol (1.3 nmol) and sulpiride (14.5 nmol), but not SCH 23390 (0.3 nmol), alone inhibited the behavior. It was therefore concluded that dopaminergic stimulation of the mPO-AH may facilitate the expression of affective defense behavior in the cat via a D2 receptor-mediated mechanism. The physiological significance of this effect and the interaction between dopaminergic, noradrenergic and serotonergic innervation of the mPO-AH in modulating the expression of affective defense behavior in response to threatening stimuli are discussed.

Intrahypothalamic injections of norepinephrine facilitate feline affective aggression via alpha 2-adrenoceptors.

The purpose of this study was to investigate the effects of noradrenergic agents infused into the anterior hypothalamus on feline affective defense responses elicited by electrical stimulation of the ventromedial hypothalamus. Anterior hypothalamic sites which are known to receive inputs from both the ventromedial hypothalamus and ascending noradrenergic pathways were selected for pharmacological analysis. Intracerebral infusions of NE (1.2-2.4 nmol) into the anterior hypothalamus significantly reduced the threshold current required to elicit the hissing component of affective defense via electrical stimulation of the ventromedial hypothalamus. Maximal threshold reductions (17 +/- 3% to 20 +/- 3%) were observed 30 min following infusion. Anterior hypothalamic infusions of clonidine facilitated feline affective defense by reducing hissing current thresholds by 18 +/- 4%. Clonidine-induced changes in response thresholds parallel those obtained with NE. Both NE-induced and clonidine-induced reductions in current thresholds were reversible by pre- and post-treatment of the anterior hypothalamic sites with yohimbine. These results demonstrate that the reductions in response thresholds are mediated by post-synaptic alpha 2-adrenoceptors located within the anterior hypothalamus. Thus the noradrenergic system may play an important role in the regulation of affective aggressive behavior.

The role of D1 and D2 receptors in dopamine agonist-induced modulation of affective defense behavior in the cat.

The role of D1 and D2 dopamine (DA) receptor subtypes in mediating DAergic modulation of affective defense behavior in the cat has been investigated in the present study. Feline affective defense, characterized mainly by autonomic arousal, ear retraction, hissing and paw striking, was elicited by electrical stimulation of the ventromedial hypothalamus. Following the establishment of a stable threshold current for eliciting the hissing response of the behavior, the effect of systemic (IP) administration of various DAergic agonists and antagonists on the hissing threshold was determined. The injection of the nonselective DA agonist apomorphine (1.0, 0.3 and 0.1 mg/kg) facilitated hissing in a dose-related manner. This effect was mimicked by the D-2 selective agonist LY 171555 (0.1, 0.03 and 0.01 mg/kg) but not by the D1-selective agonist SKF 38393 (1.0, 5.0 and 10.0 mg/kg), and was blocked by the nonselective and the D2-selective antagonists haloperidol (0.1 and 0.5 mg/kg) and spiperone (0.2 mg/kg), respectively. The D1-selective antagonist SCH 23390 blocked apomorphine-induced facilitation only at a high dose (0.5 mg/kg). In addition, the injection of haloperidol (1.0 mg/kg), spiperone (0.2 mg/kg) or SCH 23390 (0.1 mg/kg) alone inhibited the behavior. It was therefore concluded that DAergic facilitation of affective defense behavior is mainly mediated by the D2 receptors, but that activation of the D1 receptors may play a "permissive" role. The interaction between the D1 and D2 receptors in mediating this facilitation and the behavioral specificity of the effect are discussed.

Carbamazepine regulates feline aggression elicited from the midbrain periaqueductal gray.

Carbamazepine has been utilized both as an anticonvulsant and as a psychotropic drug for the treatment of complex partial seizures and various mood and other emotional disorders such as the episodic dyscontrol syndrome. In the present study, we sought to identify the role of carbamazepine in the regulation of two forms of aggressive behavior--affective defense and quiet biting attack behavior--elicited by electrical stimulation of the midbrain periaqueductal gray matter of the cat in the absence of convulsive activity. The experimental paradigm involved establishment of stable baseline thresholds for affective defense and quiet biting attack responses. Following establishment of a stable baseline, carbamazepine (2.5, 5, or 10 mg/kg) and propylene glycol (vehicle control) were administered peripherally (IP). The response thresholds were tested 5-30, 30-60, 60-90, 120-150, 1440-1470, and 2160-2190 minutes following drug administration. It was observed that carbamazepine administration at 5 and 10 mg/kg dose levels preferentially suppressed affective defense behavior but had no effect upon quiet biting attack, indicating that the selective effects of carbamazepine upon affective attack are not due to any possible sedative effects upon motor responses. The effects of carbamazepine upon affective defense were dose dependent and of long duration when administered at the highest dose level (10 mg/kg).

The effects of intrahypothalamic injections of norepinephrine upon affective defense behavior in the cat.

The effects of norepinephrine microinjected into the anterior hypothalamus were examined in feline affective defense behavior elicited by electrical stimulation of the region of the ventromedial nucleus. Anterior hypothalamic sites from which affective defense behavior could also be elicited by electrical stimulation and which are known to receive inputs from both the ventromedial nucleus and brainstem noradrenergic neurons were selected for pharmacological analysis. Intracerebral injections of 250 ng (1 nM) and 500 ng (2 nM) quantities of norepinephrine placed into the anterior hypothalamus resulted in a significant lowering of the attack thresholds. These reductions in response thresholds which were reversed by either pre- or post-treatment with yohimbine, indicate that the noradrenergic system may play an important role in the regulation of affective defense behavior.

Effects of experimental temporal lobe seizures upon hypothalamically elicited aggressive behavior in the cat.

An experiment was performed in order to determine the effects of temporal lobe seizures upon hypothalamically elicited aggressive behavior in the cat. Seizures were induced by electrical stimulation of the pyriform cortex or those subnuclei of the amygdala which had previously been shown to modulate aggressive responses at subseizure current levels. The results clearly indicate that a significant modification of affective defense thresholds following seizures was a direct function of the locus of stimulation. Specifically, seizures generated from the pyriform cortex and medial aspects of the amygdala (sites associated with prior facilitation of affective defense as determined by subseizure electrical stimulation) were followed by a reduction in threshold for this response. In contrast, an elevation in affective defense thresholds occurred when seizures were generated from the central or lateral nuclei of the amygdala (sites associated with prior suppression of affective defense as determined by subseizure electrical stimulation). The primary pathway utilized in the facilitation of affective defense appears to involve the stria terminalis, its bed nucleus, and the anterior medial hypothalamus. Preliminary data suggest that seizures generated from the pyriform cortex or amygdala can also modify quiet biting attack behavior, but in a manner opposite to that demonstrated for affective defense.

The organization of the hypothalamic pathways mediating affective defense behavior in the cat.

The purpose of this study was to describe the hypothalamic pathways which mediate affective defense in the cat utilizing the methods of [14C]2-deoxyglucose (2-DG) and [3H]leucine radioautography in concert with the technique of electrical brain stimulation. The feline affective defense response, characterized by pupillary dilatation, piloerection, ear retraction, hissing, growling and striking with the forepaws, was elicited consistently by stimulation of sites within the ventromedial hypothalamus and anterior aspect of the medial hypothalamus. In one series of experiments, 2-DG autoradiography was employed to describe the brain regions activated following stimulation of sites in the region of the ventromedial hypothalamus from which affective defense had been elicited. Ventromedial hypothalamic stimulation produced activation primarily in forebrain regions situated rostral to the level of the stimulating electrode. These structures included principally the anteromedial hypothalamus and medial preoptic area, as well as the bed nuclei of the stria terminalis and anterior commissure, diagonal band and lateral septal area. The caudal extent of activation included only the dorsal and perifornical hypothalamus at the level of the stimulation site. In a second series of experiments, affective defense sites in the anteromedial hypothalamus were stimulated and the regional distribution of 2-DG label was identified. In contrast to the results obtained from ventromedial hypothalamic stimulation, these experiments revealed a marked descending distribution of label within the posterior hypothalamus, midbrain central gray and ventral tegmental area. Results obtained from studies in which tritiated amino acids were injected into affective defense sites in both the ventromedial nucleus and anteromedial hypothalamus confirmed the general findings observed with 2-DG autoradiography. From these observations, we have concluded that the organization of the pathway mediating affective defense behavior from the ventromedial hypothalamus to the midbrain involves an initial synapse within the region of the anteromedial hypothalamus and a second synapse in the midbrain central gray substance. The significance of the anteromedial hypothalamus for the expression of affective defense behavior was considered in the Discussion.

The role of the anterior hypothalamus in affective defense behavior elicited from the ventromedial hypothalamus of the cat.

In the preceding paper a hypothalamic circuit subserving feline affective defense behavior was described. This circuit included an ascending component from the ventromedial nucleus to the anterior hypothalamus and a descending component from the anterior hypothalamus to the midbrain central gray substance. The present study was undertaken to test the hypothesis that the anterior hypothalamus plays a central role in the organization of this functional pathway. In the first part of this study, dual stimulation methods were utilized to demonstrate that concurrent stimulation of the ventromedial hypothalamus facilitates the occurrence of affective defense responses elicited from the anterior hypothalamus. In the second part of the study, lesions placed in the anterior hypothalamus significantly increased the latency and threshold current for affective defense responses elicited from the ventromedial hypothalamus. [14C]2-deoxyglucose autoradiography confirmed the fact that anterior hypothalamic lesions effective in blocking affective defense were placed in regions where the vast majority of ventromedial hypothalamic fibers terminate. In contrast, lesions which had little or no effect upon the latency or threshold for affective defense elicited from the ventromedial hypothalamus appeared to leave intact the connections from the ventromedial to the anterior hypothalamus. These findings are consistent with the proposed intrahypothalamic anatomical substrate subserving affective defense behavior described in the preceding paper.

An analysis of the mechanisms underlying hippocampal control of hypothalamically-elicited aggression in the cat.

An experiment was performed to determine the role of the hippocampal formation in the regulation of quiet biting attach behavior elicited from electrical stimulation of the hypothalamus. The results showed clearly that stimulation of the dorsal hippocampus resulted in an increased latency to quiet biting attack and that ventral hippocampal stimulation resulted in a decreased latency to quiet biting attack. In addition, the results indicate that those sites in the ventral hippocampal formation from which facilitation of attack can be produced are linked to sensory mechanisms associated with trigeminal reflexes established during hypothalamic stimulation inasmuch as stimulation of these sites increase the lateral extent of the effective sensory field of the lipline. No effect was observed upon a motor component of the jaw-opening response--the latency to jaw-opening-during ventral hippocampal stimulation. In contrast, no effects were observed upon either sensory or motor components of the hypothalamically-elicited jaw-opening response as a result of stimulation of dorsal hippocampal sites. Deoxyglucose autoradiography revealed that the major effect of stimulation of modulatory sites in both the dorsal and ventral hippocampal formation was exerted upon the lateral septal nucleus. Thus, it is proposed that hippocampal modulation of hypothalamically-elicited quiet biting attack is mediated primarily through the lateral septal nucleus.

The effects of stimulation of substantia innominata and sensory receiving areas of the forebrain upon the activity of neurons within the amygdala of the anesthetized cat.

The present study investigated the response characteristics of individual neurons in the amygdala following stimulation of the substantia innominata (SI), and compared these responses with those elicited by stimulation of insular and temporal polar cortices and the lateral olfactory tract (LOT). Recordings were made from single units within the medial, central, basal, and lateral amygdaloid nuclei of anesthetized, male cats. Stimulating electrodes were located in the SI, LOT, and sylvian cortex (SG). Unit responses were classified as either excitation or inhibition. Excitatory responses were further divided into fixed latency excitation (FLE) and variable latency excitation (VLE) based on the variability of the onset latency of the response. The majority of responses to SI stimulation were of the FLE type, implying a direct orthodromic, monosynaptic activation of amygdaloid units. Proportionally more FLE responses were recorded laterally, especially in the magnocellular basal nucleus, compared to VLE responses which were more common in the medial and central nuclei. SI stimulation consistently affected the activity of many more units than did SG or LOT stimulation. The onset latencies of the population of cells exhibiting excitatory responses elicited by SI stimulation were distributed bimodally, and this may reflect a dual projection pathway of amygdaloid afferents from this basal forebrain region. This correlates with anatomical descriptions indicating that SI projections to amygdala pass via the ventral amygdalofugal pathway as well as in the stria terminalis. Excitatory onset latencies of responses to SI stimulation were the shortest in the lateral and magnocellular basal nuclei and the longest in the parvocellular basal nucleus. Amygdaloid units exhibited convergent input from the stimulus sites. A clear topographical distribution of units was not demonstrated. The data suggests that units receiving a convergent input were rarely driven monosynaptically by more than one stimulus site. The basal nucleus contained the smallest fraction of units exhibiting a convergent input. A small population of antidromic responses was recorded and indicates that within the system studied the caudal aspect of the basal nucleus is a major source of amygdaloid efferents. Antidromically driven units did not exhibit transynaptic responses following stimulation of any of the test sites.

Role of the limbic system in hypothalamically elicited attack behavior.

The present review summarizes our research findings concerning the role of the limbic system in hypothalamically-elicited aggression in the cat. Utilizing a dual-stimulation procedure, our results indicate that much of the limbic system suppresses quiet biting attack behavior. The most potent inhibitory effects were obtained from the basomedial amygdala and the prefrontal cortex. Other structures displaying suppression of attack following electrical stimulation include the dorsal hippocampus, pyriform cortex, lateral septal nucleus, lateral aspect of substantia innominata, and anterior cingulate gyrus. Sites producing facilitation of attack include the ventral hippocampus, far lateral aspect of the lateral septal nucleus, medial aspect of the substantia innominata, and lateral amygdaloid nucleus. Anatomical studies suggest that the medial forebrain bundle and stria terminalis are utilized by limbic structures to provide direct modulation of the hypothalamus while the substantia innominata, mediodorsal thalamic nucleus and bed nucleus of the stria terminalis contain important interneurons in the control of quiet biting attack. Further studies indicate that the amygdala, ventral hippocampus, and substantia innominata may control aggressive behavior by modulating the trigeminal sensory components of the attack response.

On the necessity of the idiotype network: studies with nude mice.

jerne suggested that a quintessentialfeature of the immune system was the recognition of self-idiotypes(1,2). Despite intense interest and investigation, the concept remains a hypothesis. Here the authors discuss data which place in question the necessity of an idiotype network.

Temporary desynchronization among circadian rhythms with lateral fornix ablation.

Lateral or medial fornix suction ablations were performed on adult male rats in order to selectively ablate or leave intact, respectively, fibers which terminate in the region of the suprachiasmatic nucleus and hypophysiotropic area of the hypothalamus. Plasma adrenal corticosteroid secretion, locomotor activity, body temperature, and food and water intake were recorded at 4 h intervals over a period of 48 h in individual animals 7-10 days postoperatively. Lateral fornix ablation specifically disrupted adrenal corticosteroid periodicity. A least-squares spectrum analysis of the data indicated that corticosteroid may be under ultradian control after this lesion. All animals, regardless of treatment, exhibited normal circadian locomotor activity patterns. Aberrations in feeding, drinking and body temperature rhythms were occasionally observed. This represents a temporary dissociation between the rhythmic expression of corticosteroid secretion and activity, temperature, feeding and drinking. The evidence presented lends support to the multi-oscillator theory of circadian organization, and suggests that the anteroventral subiculum, via the medial corticohypothalamic tract, is important in the regulation of some, but not all, circadian parameters. In addition to the observations on the rhythmicity of locomotor activity, the extent to which the animals are active is also significantly different between groups; ie., the hyperactivity of fornix-transected animals previously reported by others was found to be associated with lateral and not medial fornix ablation.

Effects of amygdaloid stimulation upon trigeminal sensory fields of the lip that are established during hypothalamically-elicited quiet biting attack in the cat.

An experiment was performed in order to determine the role of the amygdala and surrounding cortex in quiet biting attack elicited from electrical stimulation of the hypothalamus. Stimulation of basal, cortical, and anterior amygdala as well as pyriform cortex and parahippocampal gyrus resulted in a suppression of the attack response and in a constriction of trigeminal sensory fields that are established during hypothalamic stimulation. Stimulation of lateral and central amygdala resulted in a facilitation of the quiet biting attack response and an expansion of the trigeminal sensory fields, and a decreased latency for the occurrence of jaw opening when the sensory field was held constant. These studies suggest that the amygdala modulated quiet biting attack behavior generated by hypothalamic stimulation at least, in part, by virtue of its control over sensory fields.