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Biomedical subjects

P E Gay

Publications and source records attributed to P E Gay.

At least 19 recordsLinked to original sources
PubMed1995

Behavioral effects of felbamate in childhood epileptic encephalopathy (Lennox-Gastaut syndrome).

The behavioral effects of felbamate were assessed in 20 persons, (ages 2 to 19 years) who were participating in a compassionate plea protocol for children with Lennox-Gastaut syndrome. Parents completed a questionnaire concerning aspects of behavioral change once all medications were in a constant regimen. Significant improvements were suggested in social functioning, intellectual functioning, motor functioning, attention and concentration, alertness, initiative, variability in performance, and memory. There was a tendency for these effects to reverse when the drug was discontinued.

Adolescent↗
PubMed1985

Pilot study of fluzinamide (N-methyl-3-[3-(trifluoromethyl)phenoxy]-1-azetidinecarboxamide) in refractory partial seizures.

We conducted a pilot study of fluzinamide in 15 adults with refractory partial seizures. After a baseline period, fluzinamide was added to the existing regimen of phenytoin and carbamazepine and increased to maximum tolerated dose. Common side effects included dizziness, diplopia, ataxia, headache, nausea, and rash, resulting in patient withdrawal in six cases. Seizures became less frequent in four of the nine patients who completed the 8-week trial.

Adolescent↗
PubMed1984

Effects of antiepileptic drugs and seizure type on operant responding in mentally retarded persons.

The performance of 129 mentally retarded persons was studied on a progressive fixed-ratio schedule of reinforcement. Subjects were selected according to antiepileptic drug (AED) regimen or membership in one of four control groups. The AEDs studied were: phenobarbital (PB); phenytoin (PHT); PB in combination with PHT (PB/PHT); and valproic acid (VPA) in combination with other AEDs . The control groups were: persons without seizure disorders and on no medications (control); persons without seizure disorders, but on the chronic medication thioridazine ( TDZ ); persons with histories of one or more seizures and treatment with PB and/or PHT, but currently on no AEDs ; and, to control for the effects of multiple AEDs , persons on multiple drug regimens (i.e., PB and/or PHT in combination with carbamazepine and/or ethosuximide). Except for the VPA group, response rates per minute were decreased in high intelligence quotient (greater than 40) persons receiving AEDs or with a history of treated seizures. Deficits in responding were particularly marked in persons with partial seizures. Persons on VPA responded at rates comparable with those of the control and TDZ groups, unless they had partial seizures. This effect was independent of seizure frequency and was inversely related to serum level. Persons on PB most frequently exhibited frustration responses during testing, and when these occurred they were rated as being significantly more severe. Persons on PB also most frequently elected to "leave the experiment" and did so primarily for reasons thought to reflect deficits in inhibition. These results suggest that operant tasks can be sensitive to both AED effects and to underlying alterations of function that accompany seizure disorders in the mentally retarded.

Adolescent↗
PubMed1983

Interaction between phenobarbital and thioridazine.

The effects of thioridazine (TDZ) on serum phenobarbital (PB) and phenytoin (PHT) were studied in mentally retarded persons. Persons taking these drug combinations were identified and matched on the basis of age, sex, body weight, and antiepileptic drug (AED) dosage with persons from the same population who were taking only the AEDs. Trough, steady state serum levels were obtained as part of regular AED monitoring schedules. Serum level of PB per unit dose was significantly less with concomitant administration of TDZ (100 to 200 mg/day) than when PB was given alone. This effect seemed to be TDZ dose-responsive. TDZ had no consistent effects on serum PHT.

Anticonvulsants↗
PubMed1978

Despite various drugs, cats continue to kill mice.

Amphetamines (d- at 0.5--4 mg/kg; 1- at 2--4 mg/kg) inhibited spontaneous mouse killing by some, but not all cats. Various other drugs (drugs and maximum tested doses were: imipramine, 64 mg/kg; amitriptyline, 32 mg/kg; tranylcypromine, 2 mg/kg; tripelennamine, 4 mg/kg; scopolamine, 1 mg/kg; methyl scopolamine 1 mg/kg; chlordiazepoxide 16 mg/kg; diazepam 4 mg/kg; meprobamate, 80 mg/kg; pentobarbital, 16 mg/kg; chlorpromazine, 8 mg/kg; and haloperidol, 0.5 mg/kg) did not reliably inhibit such killing. In contrast with rats, mouse killing by cats was not consistently blocked by antidepressants or amphetamines. When individual cats were inhibited, their reduction of killing seemed related to anorexia rather than to affective arousal.

Aggression↗
PubMed1978

Behavioral correlates of social dominance.

The behavioral correlates of dominance in the squirrel monkey were explored using a variety of operant tasks. Compared to more submissive animals, more dominant ones showed higher operant rates, more consistent work output, and a higher degree of "frustration tolerance." These data suggest that dominance in the squirrel monkey is not related solely to physical size, but to a variety of behavioral traits which lead to more adjustive problem-solving behavior.

Animals↗
PubMed1976

Effects of drug-state change on discrimination performance.

A single dose of d-amphetamine (0.25, 0.50, or 1.00 mg/kg), administered in 5 successive sessions, did not seriously impede the discrimination performance of male Holtzman rats under cued reinforcement conditions. A 2.00 mg/kg dose, however, produced a total cessation of operant behavior. In 2 post-drug (saline) sessions, groups previously treated with 0.50 or 1.00 mg/kg demonstrated an initial decrement and subsequent recovery in performance. A second experiment demonstrated that rats administered either saline or 0.50 mg/kg d-amphetamine for 5 successive sessions showed a decrement and subsequent recovery in performance when switched to the opposite treatment condition for the next 2 sessions. These data may be explained in terms of a change in drug state.

Animals↗
PubMed1976

Disinhibition and external inhibition of response following septal lesions in rats.

Septal-lesioned and sham-operate rats were tested for reactivity to extraneous stimuli (clicks or flashing lights) presented during periods of low or high responding generated by a 120-sec FI schedule of reinforcement. While septal-lesioned rats tended to show greater disinhibition and less external inhibition than sham-operates, the magnitude of the deficits was not considered sufficiently great to warrant the conclusion that the septal syndrome results from increased susceptibility to disinhibition.

Acoustic Stimulation↗
PubMed1976

Drinking induced by parenteral injections of pilocarpine.

Parenteral (IP) injections of pilocarpine, in doses from 3.75 - 30 mg/kg, reliably produced drinking in water-satiated rats. This effect was not diminished by pretreatment with either centrally active (scopolaime, atropine) or peripherally active (methyl scopolamine, methyl atropine) cholinergic blocking agents, suggesting that pilocarpine does not induce drinking via a cholingergic meachnism. Repated injections of low doses, but not high doses, of pilocarpine augments drinking over trials.

Animals↗
PubMed1976

Interactions of amygdala lesions with effects of pilocarpine and d-amphetamine on mouse killing, feeding, and drinking in rats.

Repeated injections of 7.5 mg/kg pilocarpine induced mouse killing in both amygdala-lesioned and sham-operated rats, but more injections were required in the lesioned animals. Killing was evoked least readily in rats that showed substantial weight loss after surgery and that had damage to more medial regions of the amygdala. d-Amphetamine (.75, 1.50, or 3.00 mg/kg), administered either before or after a killing test, inhibited pilocarpine-induced killing in both surgical groups. Amygdala lesions attenuated pilocarpine-facilitated drinking in sated animals but did not alter the inhibitory effects of either pilocarpine or d-amphetamine on feeding or drinking.

Aggression↗
PubMed1975

Chlordiazepoxide and diazepam induced mouse killing by rats.

Chlordiazepoxide HCl, at dose levels from 2.5 mg/kg to 80 mg/kg, significantly increased the low base rates of mouse killing (3-9%) observed in large samples (N = 100/dose) of Holtzman strain albino male rats. Maximal killing rates were obtained at doses from 7.5 mg/kg to 20 mg/kg. Diazepam was equally effective, and several times more potent than chlordiazepoxide. Pentobarbital did not increase killing. Killing induced by chlordiazepoxide was blocked by d-amphetamine SO4, but not by l-amphetamine, at dose levels similar to those that block undrugged killing in this strain (ED50 = 1.5 mg/kg). Unlike pilocarpine-induced killing, the effects of chlordiazepoxide were not increased or decreased significantly by either peripherally or centrally active anticholinergic drugs, over wide dose ranges of these agents; nor were the effects of chlordiazepoxide increased by repeated daily administration.

Aggression↗