Melanotropic peptides in the mammalian brain: the melanin-concentrating hormone.

Melanin-concentrating hormone (MCH) has been identified in neurons of the mammalian brain. This review summarizes some current information regarding the cell biology of this neuropeptide and the topography of MCH-immunoreactive (-IR) neurons in several species including mouse, rat, hamster, guinea pig, rabbit, dog and monkey; and atlas of MCH-IR neurons in the hypothalamus and subthalamus of the brain of guinea pig is presented. Based upon the location of this MCH cell group, it is hypothesized that they may be functionally involved in circuits of extrapyramidal motor systems from striatal centers to the thalamus and cerebral cortex and to the midbrain and spinal cord.

Identification of gonadal steroid receptors in meningiomas from dogs and cats.

Cytosolic assay was used to detect gonadal steroid receptors in brain tumor tissue from 6 dogs and 2 cats. For 4 samples, the maximal number of binding sites and the equilibrium dissociation constant were calculated, using Scatchard analysis. The concentration of receptor protein that was discovered was similar to that detected in hormone-sensitive tumors.

Use of ocular compression to induce vagal stimulation and aid in controlling seizures in seven dogs.

Ocular compression (OC) was used to treat 7 dogs with seizures. Treatment was accomplished by use of digital pressure applied to one or both eyes by veterinarians, hospital staff, or owners. The OC was believed to exert an effect through stimulation of the vagus nerve. Use of OC appeared to be efficacious for aborting seizures in 3 dogs, decreasing heart rate and causing muscle relaxation in 1 dog, and preventing onset of seizures in 2 other dogs. In 1 dog, rhythmic application of OC caused onset of rhythmic facial twitches. Administration of OC may be beneficial in treating seizuring dogs.

Use of physiatry as the sole treatment for three paretic or paralyzed dogs with chronic compressive conditions of the caudal portion of the cervical spinal cord.

Physiatry alone was used to treat 3 large (30- to 40-kg [66 to 88 lb]) mature (6- to 9-year-old) dogs that were tetraparetic or tetraplegic. All 3 dogs had myelographic evidence of multiple chronic compressive extradural lesions of the caudal portion of the cervical spinal cord. All dogs improved substantially after a course of intensive physical treatment. For 2 dogs, an abbreviated treatment regimen was continued by the owners after the dogs were discharged. Both of these dogs regained and retained normal neurologic function. The other dog improved but was treated infrequently at home. That dog's signs recurred, and the dog was euthanatized. Persistent use of physical treatment for paralysis that results from conditions affecting the cervical spinal cord may be useful even without concurrent surgical or pharmacologic treatments.

Clinical evaluation of gamma-vinyl-gamma-aminobutyric acid for control of epilepsy in dogs.

Gamma-vinyl-gamma-aminobutyric acid is a novel antiepileptic drug that exerts its effects by increasing the concentration of gamma-aminobutyric acid in the brain. The mechanism of action involves irreversible inhibition of the metabolic pathway of gamma-aminobutyric acid. The drug was administered to 14 dogs in conjunction with other anticonvulsants, in an attempt to control refractory epilepsy. Four of these dogs had clinically relevant evidence of decreased seizure frequency. In 4 dogs, response to the drug was no better than response to phenobarbital alone. In 2 dogs, seizure control improved, but gamma-vinyl-gamma-aminobutyric acid was withdrawn because of development of hemolytic anemia. For various reasons, the therapeutic effect in the remaining 4 dogs could not be evaluated. This study of only 14 dogs illustrates some of the problems that confound our ability to judge the efficacy of anticonvulsant treatment.

Evaluation of craniotomy in dogs and cats.

Over a reporting period of 5 years, craniotomy was performed in 26 dogs and 5 cats with various intracranial lesions. X-ray computed tomography was performed in all animals prior to surgery. Twenty dogs and all cats had intracranial neoplasms; of these, 14 were meningioma, and 11 represented a wide variety of brain tumors and skeletal tumors. Three dogs were treated surgically for traumatic, open-skull fractures with cerebral damage, and 3 underwent biopsy to evaluate chronic inflammatory brain disease. The overall medium survival time was 212 days, the 1-year survival rate was 39%, and the 2-year survival rate was 20%. Dogs and cats with meningioma survived a mean 198 and 485 days, respectively, with 1-year survival rates of 30% for dogs and 50% for cats. The overall median survival time for animals with tumors other than meningeal intracranial neoplasms was 414 days, with a 1-year survival rate of 40%. The death of 19% of all animals could be related to the combination of advanced brain disease and surgery. Because fatality seldom occurred as a direct result of surgery, morbidity and mortality associated with craniotomy in pet animals can be seen as acceptably low. In 29 of 34 craniotomies, dura mater defects were left unsutured and no adverse effects were seen.

Phencyclidine-induced increases in striatal neuron firing in behaving rats: reversal by haloperidol and clozapine.

Amphetamine and related drugs of abuse facilitate dopamine transmission in the striatum. This action is believed to underlie the increase in firing of striatal motor-related neurons after amphetamine administration in behaving rats. The present study extended this electrophysiological investigation to phencyclidine (PCP), a nonamphetamine psychomotor stimulant that acts primarily as a noncompetitive antagonist of N-methyl-D-aspartate (NMDA) glutamate receptors. Like amphetamine, PCP (1.0, 2.5, or 5.0 mg/kg) increased the activity of striatal motor-related neurons concomitant with behavioral activation. These effects were blocked by subsequent administration of either 1.0 mg/kg haloperidol or 20.0 mg/kg clozapine, typical and atypical neuroleptics, respectively. Dizocilpine (MK- 801), another noncompetitive NMDA antagonist, mimicked the effect of PCP. Collectively, these results indicate that amphetamine and NMDA antagonists exert comparable effects on striatal motor-related neurons, suggesting that the response of these cells to psychomotor stimulants is regulated by a dopaminergic-glutamatergic influence.