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B A Pappas

Publications and source records attributed to B A Pappas.

At least 55 records · Page 3Linked to original sources
PubMed1983

Failure to replicate the dorsal bundle extinction effect: telencephalic norepinephrine depletion does not reliably increase resistance to extinction but does augment gustatory neophobia.

Depletion of telencephalic noradrenaline (Ne), caused by lesion of the dorsal tegmental bundle, has been reported to increase persistence of non-reinforced responding in various operant tasks. This has been referred to as the dorsal bundle extinction effect (DBEE). In an effort to reproduce this effect, rats receiving 6-hydroxydopamine lesions of the dorsal Ne bundle (DB-6-OHDA) were compared to controls during extinction of a continuous food rewarded (CRF) lever-press response. While the lesion group showed an increase in responding during initial extinction, no significant difference in resistance to extinction using a 2-min non-response criterion was obtained. Moreover, no differences in reinforced response rates were observed with CRF, fixed ratio (FR-15, FR-30, FR-60) or variable interval (VI-30, VI-60, VI-120 s) schedules of reinforcement. In order to test the hypothesis that the DBEE is dependent on time of behavioral testing after surgery, subsequent experiments were performed where rats began CRF operant training 5, 17, 31 or 110 days post-lesion. No differences in resistance to extinction were observed between lesion and control rats at any post-lesion interval. Neonatal treatment with 6-OHDA which permanently lesions forebrain Ne terminals also failed to prolong extinction. Finally, when both DB-6-OHDA and neonatal rats were given a choice between water and saccharin the lesioned animals exhibited a neophobic reaction whereby they drank significantly less saccharin. We conclude that while the DBEE is not a reliably reproducible phenomenon other effects of forebrain Ne lesions, such as neophobia, appear to be robust.

Afferent Pathways↗
PubMed1983

Behavioral comparison of pentylenetetrazol, clonidine, chlordiazepoxide and diazepam in infant rats.

The effects of various doses of pentylenetetrazol, clonidine, chlordiazepoxide and diazepam on limb and head movement and behavioral seizure signs were examined in 4-, 8- and 16-day old rats tested at ambient temperatures of either 25 or 35 degrees C. All 4 drugs produced intense behavioral activation at the 2 younger ages but there were marked differences among them in the effects of test temperature on this activation and in the relationship between age and their activating effect. A "paradoxical" and intense behavioral energization was observed after the administration of either of the 2 benzodiazepines at 4, 8 but not 16 days, particularly at the lower test temperature. Clonidine and pentylenetetrazol were activating at all 3 ages but while clonidine had greater effect at the low test temperature, the opposite was the case after pentylenetetrazol. The effects of the benzodiazepines and clonidine were clearly distinct from those of pentylenetetrazol and this was the only drug to substantially elicit seizure signs. It is uncertain whether or not the benzodiazepines cause brain seizures in young animals. If so, then their behavioral manifestation is clearly different from that observed after pentylenetetrazol.

Age Factors↗
PubMed1983

Acute exposure to pulsed microwaves affects neither pentylenetetrazol seizures in the rat nor chlordiazepoxide protection against such seizures.

Three experiments failed to provide consistent evidence for an effect of 2.70 GHz pulsed microwave radiation up to 20 mW/cm2 on pentylenetetrazol-induced seizures or on the efficacy of chlordiazepoxide for counteracting such seizures. Microwave radiation counteracted the hypothermic effects of chlordiazepoxide without altering its antiseizure efficacy. This underscores the dissociation between thermal and pharmacological effects of microwaves.

Animals↗
PubMed1982

Infant rat hyperactivity elicited by home cage bedding is unaffected by neonatal telencephalic dopamine or norepinephrine depletion.

Newborn rats received either stereotaxically guided bilateral injections of 6-hydroxydopamine (6-OHDA) in the neostriatum so as to deplete dopamine (DA) there, or subcutaneous 6-OHDA to deplete forebrain norepinephrine (NE). Both the DA and NE depleted rats as well as their respective control rats were significantly more active at 15-16 days of age when tested in a novel environment containing soiled bedding from their home cages, than when tested in the presence of clean bedding material. Furthermore, under both the home cage and clean bedding conditions the DA depleted rats were more active at this age than their controls. Thus while transiently elevated locomotor activity is one consequence of neonatal, neostriatal DA depletion, inattention to olfactory stimuli (which occurs after adult neostriatal DA depletion) is not another. The NE depleted rats in both home cage and clean bedding test conditions showed activity levels equivalent to that of their control groups. Furthermore, the NE depletion did not affect hyperactivity elicited by artificially (peppermint) scented bedding like that in which the rats had been reared. Thus, contrary to expectations based on the reported reduction of preference for conspecific odor after neonatal and adult forebrain NE depletion, these data show that the locomotor activating effects of neither conspecific nor artificial odors associated with the nest odors are attenuated by neonatal NE depletion. The mortality rates among NE depleted rats raised in the peppermint scented shavings was unusually high and overall, these rats were less active than similarly raised controls.

Animals↗
PubMed1982

Chlordiazepoxide-induced released responding in extinction and punishment-conflict procedures is not altered by neonatal forebrain norepinephrine depletion.

The effects of chlordiazepoxide (CDZ) in extinction and punishment-conflict tasks were examined in rats after neonatal systemic administration of 6-hydroxydopamine (6-OHDA) to deplete forebrain norepinephrine (NE). At about 70 days of age the rats were water deprived and trained for three days to drink in a novel apparatus. On the fourth day (test day) drinking was either extinguished by elimination of water from the drinking tube or punished by lick-contingent shock. Just prior to this test session half of the vehicle and half of the 6-OHDA treated rats were given an injection of CDZ (8 mg/kg IP). Both the injection of CDZ and forebrain NE depletion prolonged responding during extinction and reduced the suppressant effects of punishment in male rats, and these effects were of similar magnitude. Furthermore, CDZ was as effective in neonatal 6-OHDA treated male rats as in vehicle treated rats indicating that decreased transmission is ascending NE fibers caused by CDZ is not solely responsible for its behavioral effects in extinction and conflict tasks. Rather, these effects may involve cooperative mediation by both noradrenergic and serotonergic forebrain terminals. Unexpectedly, CDZ's anti-extinction effect was absent in female rats and its anti-conflict effect observed only in NE depleted females.

Animals↗
PubMed1982

The ontogeny of spinal cord monoamines and the post-decapitation reflex.

The ontogeny of the post-decapitation reflex (PDR) was examined in neonatal systemic 6-hydroxydopamine (6-OHDA) treated rats. The PDR was absent in the youngest (5 day) and oldest (60 day) 6-OHDA treated rats but present with attenuated characteristics at around 15 and 20 days. The reappearance of the PDR in these rats closely paralleled age-related fluctuations in spinal cord noradrenaline (NE) which increased until 15 days, then precipitously declined, but did not correlate with spinal dopamine (DA) or serotonin (5-HT). The failure of the alpha noradrenergic blocking agents chlorpromazine, phenoxybenzamine, prazosin, or yohimbine to eliminate the vestigial PDR in the 15-20-day-old, 6-OHDA-treated rats indicates that this is probably not mediated by remaining, undamaged spinal NE neurons at this age. Neither is it likely to be mediated by spinal 5-HT neurons since inhibition of 5-HT synthesis had no effect upon the PDR latency in normal or neonatal 6-OHDA-treated, 17-day-old rats. In contrast to NE levels which increased with age in normal rats, spinal cord 5-HT and DA levels at least as high at 5 days of age as at adulthood.

Aging↗
PubMed1981

Drug alterations of punished responding after chlordiazepoxide: possible screen for agents useful in minimal brain dysfunction.

In the present study, the effect of various stimulant drugs on the action of chlordiazepoxide to increase punished responding was studied. Drugs such as d-amphetamine, methylphenidate and imipramine that are effective in attentional deficit disorder (MBD) were found to reverse this benzodiazepine-induced increase in responding. Phenobarbital which worsens this condition enhanced the benzodiazepine effect. Since the impairment caused by chlordiazepoxide may be analogous to the lack of impulse control noted in MBD, the bupropion antagonism of this action of chlordiazepoxide suggests that bupropion may be useful in MBD.

Animals↗
PubMed1981

Plasma free and total tryptophan, blood serotonin, and the hyperactivity syndrome: no evidence for the serotonin deficiency hypothesis.

Total and free plasma tryptophan and plasma cortisol levels were determined for children diagnosed as hyperactive or learning disabled and in normal siblings of these subjects. No differences were observed among the groups on any of the dependent variables related to a number of parameters measured for the hyperactive children such as degree of hyperactivity, presence of food allergies, favorable response to methylphenidate, and brain dysfunction. Moreover, in further comparisons no differences were found between hyperactive and age-matched controls on these variables as well as blood serotonin, nor were any differences found for a group of hyperactive children between placebo and methylphenidate trials. These data do not support earlier suggestions of a serotonin deficiency in hyperactive children.

Attention Deficit Disorder with Hyperactivity↗
PubMed1980

Monoamine replacement after reserpine: catecholaminergic agonists restore motor activity but phenylethylamine restores atropine-resistant neocortical low voltage fast activity.

A large dose of reserpine abolishes an atropine-resistant form of neocortical low voltage fast activity (LVFA) which normally accompanies certain patterns of motor activity in rats. An attempt was made to reverse this effect by replacement of specific monoamines or by injection of suitable agonists in rats pretreated with reserpine (10 mg/kg). The following compounds, alone or in various combinations, failed to restore atropine-resistant LVFA in reserpinized rats even though spontaneous motor activity was restored in many cases: L-DOPA (150-300 mg/kg) after pretreatment with an inhibitor of peripheral L-aromatic amino acid decarboxylase; 5-hydroxytryptophan (100-200 mg/kg); D-amphetamine (1-2 mg/kg); apomorphine (0.25-2.5 mg/kg); lysergic acid diethylamide (100-300 microgram/kg); and clonidine (0.5-1.0 mg/kg). In contrast beta-phenylethylamine was quite effective in restoring atropine-resistant LVFA and its effects were not diminished by pretreatment with alpha-methyl-p-tyrosine (400 mg/kg), chlorpromazine (15 mg/kg). It is suggested that a trace amine plays an essential role in the production of atropine-resistant LVFA independent of catecholamines.

5-Hydroxytryptophan↗
PubMed1980

Reserpine abolishes movement-correlated atropine-resistant neocortical low voltage fast activity.

Following a large dose of atropine, rats display large amplitude slow waves in the neocortex during immobility, tremor, tooth-chattering and face-washing (Type II behavior) but display low voltage fast activity (LVFA) during walking, struggling, postural changes and head movement (Type I behavior). Rats treated with a large dose of reserpine usually continue to display LVFA during immobility as well as during movement although large amplitude slow waves are present more frequently than normal. A combination of reserpine and atropine abolishes all LVFA even during intense sensory stimulation or electrical stimulation of the reticular formation. Chlorpromazine, lysergic acid diethylamide, methysergide, phenoxybenzamine, pimozide, promethazine, propranolol and trifluoperazine do not have this effect when combined with atropine. In rats treated with nialamide prior to reserpine and atropine, LVFA continues to occur in association with Type I behavior just as in rats given atropine alone. It is proposed that the occurrence of LVFA in the neocortex is determined by two distinct reticulocortical systems. A cholinergic system produces all LVFA occurring during Type II behavior and a second system, dependent on a monoamine, produces LVFA in association with Type I behavior. The view that LVFA is a correlation of arousal or the sleep-waking cycle is criticized.

Animals↗
PubMed1980

Importance of the Locus coeruleus and involvement of alpha-adrenergic receptors in the post-decapitation reflex in the rat.

The latency, duration, hindlimb kick frequency, and total activity components of the post-decapitation reflex (PDR) were measured in the rat using a movement-sensitive transducer. Reduction of brain and spinal cord norepinephrine (NE) caused by neonatal administration of 6-hydroxydopamine (6-OHDA) or 5,7-dihydroxytryptamine, which also reduced brain serotonin, decreased all components of the PDR. Depletion of serotonin or dopamine alone reduced the vigor of the reflex, suggesting that these pathways can influence the PDR but are not essential for the response. Lesions of neurons in the Locus coeruleus, made electrolytically or with 6-OHDA, decreased the intensity of the PDR, with the 6-OHDA-induced lesion being more effective. Depletion of forebrain NE terminals with 6-OHDA did not alter the PDR, consistent with a critical involvement of spinal noradrenergic fibers. The PDR was also decreased by phentolamine and prazosin, but not by propanolol, suggesting an involvement of alpha-adrenergic receptors in the response. This hypothesis was further supported by the finding that the efficacy of a variety of drugs (such as tricyclic antidepressants, phenothiazines, and anti-hypertensive compounds) for blocking the reflex was apparently related to their affinity for alpha-adrenergic receptors. Thus, the PDR is dependent on noradrenergic fibers in the spinal cord and may provide a simple screen for drugs with suspected alpha-adrenergic blocking properties or for agents that disrupt the function of central noradrenergic fibers.

5,7-Dihydroxytryptamine↗
PubMed1980

Intraventricular 6-hydroxydopamine in the newborn rat and locomotor responses to drugs in infancy: no support for the dopamine depletion model of minimal brain dysfunction.

Bilateral intraventricular injections of 6-hydroxydopamine (6-OHDA) after desmethylimipramine (DMI) in rats 1 and 2 days of age, severely depleted brain dopamine (DA) particularly in the neostriatum, where levels in adulthood were about 7% of control. Compared to vehicle-injected controls these rats were hyperactive only at 15 and 20 days of age, and in adulthood were impaired in a two-way avoidance. Rats with similar 6-OHDA treatment but without DMI pretreatment showed severe depletion of brain norepinephrine (NE) as well as DA, and were behaviorally similar to the DA-depleted only rats. This behavioral syndrome is similar to that reported after intracisternal injection of 6-OHDA in 5-day-old rats, which has been argued as a model for minimal brain dysfunction (MBD). Contrary to expectation from this model, however, challenge doses of either d-amphetamine or methylphenidate did not reduce, but instead increased activity of these rats. The 6-OHDA treatments also did not alter the enhancement of locomotor activity by scopolamine, which was present at 30 days but not at 15 days.

Aging↗
PubMed1978

Tyrosine hydroxylase activity in brain regions after intraventricular 6-hydroxydopamine in the neonatal rat.

Intraventricular 6-OHDA treatment to newborn rats produced a marked reduction in tyrosine hydroxylase activity in most brain regions at maturity which correlated moderately well with the catecholamine levels. However, those regions in which NE levels were increased did not show a corresponding increase in total tyrosine hydroxylase activity. There was a much better correlation between NE levels and the particulate form of tyrosine hydroxylase which has been suggested to be the more functionally active form of the enzyme.

Animals↗