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J T Concannon

Publications and source records attributed to J T Concannon.

13 recordsLinked to original sources
PubMed1984

Differential effects of apomorphine in 6-hydroxydopamine-treated and aged rats.

Effects of dopamine depletion and old age were tested on the ability of rats to discriminate the interoceptive cue produced by IP administered apomorphine. In Experiment 1, rats were administered IC injections of 6-hydroxydopamine or its vehicle at 5 days of age. Administration of this dopamine neurotoxin resulted in significant depletion of whole-brain dopamine to 27.2% of controls as indicated when the brains of littermate rats, killed at 35 days of age, were analyzed by high-pressure liquid chromatography. Although this dopamine depletion was significant, toxin-treated rats learned to discriminate 0.16 mg/kg apomorphine from saline at the same rate as control rats. However, the dose-response curve for apomorphine discrimination after doses of 0.04-0.24 mg/kg suggested hypersensitivity to the dopamine agonist in toxin-treated rats. In Experiment 2, senescent rats were similarly trained to discriminate apomorphine in the two-lever food-motivated operant task. Dose-response testing indicated hypersensitivity similar to that found in 6-OHDA-treated rats. This increased behavioral responsiveness of aged rats to dopamine agonists is discussed in relation to receptor supersensitivity, metabolic rates, and blood-brain barrier permeability.

Aging↗
PubMed1983

The development of brain biogenic amines, cyclic nucleotides and hyperactivity in 6-OHDA-treated rat pups.

Developmental changes in the behavior and brain biochemistry of rat pups were investigated in rats administered intracisternal injections of 6-hydroxydopamine (6-OHDA) or its vehicle at 5 days of age. Although pups of both groups were equivalent in their activity at 15 days of age, 6-OHDA-induced hyperactivity emerged at 20 and 30 days of age in a between-group design in which rats were only tested at one age. Body weight measurements revealed that 6-OHDA-treated rats were underweight at 15, 25 and 30 days of age. Furthermore, at 20 days of age, total activity was inversely related to body weights in the 6-OHDA-treated pups. Whole-brain levels of dopamine (DA) were decreased at every age by the 6-OHDA treatment, whereas norepinephrine (NE) levels were virtually unaffected by 6-OHDA at these same ages. Total activity was inversely correlated with whole-brain DA levels at 20 and 30 days of age when 6-OHDA-treated pups were hyperactive. Measures of cerebellar and "rest-of-brain" adenosine 3',5'-monophosphate (cyclic AMP) and guanosine 3',5'-monophosphate (cyclic GMP) were not uniformly altered by either the 6-OHDA treatment or by maturation. Results are discussed both in terms of brain biochemistry modulation of hyperactivity and the contribution of decreased body weights induced by 6-OHDA to the production of hyperactivity.

Aging↗
PubMed1983

Open-field behavior in dopamine-depleted rat pups and their mothers.

Possible changes in the behavior of rat mothers and their pups were investigated by administering intracisternal injections of 6-hydroxydopamine (6-OHDA) or its vehicle to 5-day-old rats. Administration of the neurotoxin resulted in a significant depletion of whole-brain dopamine levels to 23% of control levels, whereas norepinephrine levels were reduced to 83% of controls. Open-field behavior revealed that the 6-OHDA-treated rat pups were hypoactive, in terms of decreased square crossings, at 15 days of age, yet were hyperactive at 30 days of age. Toxin-treated pups also showed lower urination scores at 25 and 30 days of age. Mothers' open-field behavior was virtually unaffected by the treatment status of their offspring (i.e., 6-OHDA vs. vehicle-treated), although several of the mothers' behaviors decreased with repeated measures over days.

Aging↗
PubMed1983

Pre- and postnatal effects of caffeine on brain biogenic amines, cyclic nucleotides and behavior in developing rats.

To examine the perinatal effects of caffeine on pup behavior and brain neurochemistry, rat mothers were exposed to caffeine in a choice situation prenatally, postnatally, at both times or at neither time. Prenatally, caffeine-exposed mothers drank approximately 14 mg/kg/day, an amount ineffective in altering mothers' overall prenatal body weight, although it did reliably decrease birth femur length of offspring. Postnatal pup activity measures revealed that postnatal caffeine exposure depressed activity, with an additional contribution of prenatal caffeine exposure. Those effects occurred at caffeine intake levels (circa 48 mg/kg/day) which minimally affected pup body weight, body length, femur length or eye-opening. Postwithdrawal (35 days of age) biochemical determinations revealed significant postnatal effects of caffeine by depressing cyclic AMP/"whole-brain" and elevating the cyclic GMP/cyclic AMP ratio in cerebellum. Whole-brain levels of dopamine and norepinephrine, however, were not affected by the caffeine treatments. These results suggest that activity profiles may be a more sensitive index of caffeine "toxicity" than other indices of physical development, and that cyclic nucleotides may play at least some role in the hypoactivity-inducing effects of caffeine in developing rats.

Animals↗
PubMed1982

Nonmonotonic age changes in susceptibility to hypothermia-induced retrograde amnesia in rats.

The effects of post-training and/or pretesting body cooling on retention of Pavlovian discriminated fear conditioning were examined in preweanling (16-day) and weanling (23-day) rats. Twenty-four retention was assessed in 16- and 23-day-old rats receiving hypothermia after training, after training and prior to testing, or at neither time. Amnesia was present in the preweanling but not weanling rats. Recovery from amnesia was not observed in the preweanling rats followed a second cooling treatment. Control groups indicated the differential amnesia was not the result of differences in 24 hr baseline retention, depth of hypothermia cooling, rate of recovery from hypothermia treatment, or body temperature immediately post-testing. The results are discussed with respect to current views of infantile amnesia and the growing evidence for similar nonmonotonic functions during ontogeny.

Age Factors↗
PubMed1982

Pre-test epinephrine injections reverse DDC-induced retrograde amnesia.

The effects of pre-test systemic administration of epinephrine on DDC-induced retrograde amnesia (RA) for discriminated Pavlovian fear-conditioning were examined in rats. Epinephrine reversed RA with the optimal dosage being 0.05 mg/kg. Apparently, the effect was specifically reversal of amnesia since (a) performance was restored to control levels, but no higher, and (b) sensitization and activity-related artifacts were minimized. These results are consistent with those showing reversal of RA by pre-test administration of hormones or catecholamine agonists. That is, they suggest that amnesia is due to a retrieval deficit rather than to failure of memory storage. Results are discussed in terms of epinephrine-induced modulation of storage and retrieval processes through central and peripheral mechanisms.

Animals↗
PubMed1982

Haloperidol-induced hyperactivity in neonatal rats: effect of lithium and stimulants.

The effect of chronic subcutaneous administration of haloperidol directly into neonatal rats was investigated as a possible model for the hyperkinetic syndrome in human children in terms of its onset, duration and offset of hyperactivity. In addition, the ability of chronically-administered lithium in the diet of nursing mothers to attenuate the haloperidol-induced hyperactivity was investigated. Experiments with acute administration of the clinically-effective stimulants, amphetamine and methylphenidate, to the pups were also conducted to determine the adequacy of this behavioral model vis-a-vis the human condition. The results indicate that, although chronic haloperidol (2.5 mg/kg) produced hyperactivity relative to controls on the 25th day of life, this hyperactive behavior does not return to control levels at 30 days of age. Moreover, neither the stimulants nor lithium attenuates this hyperactivity and, indeed, lithium, by itself, produces increased activity. Thus, chronic haloperidol administered directly into neonatal rat pups produces hyperactivity possibly by the production of dopaminergic supersensitivity, yet this effect does not model the temporal course seen in hyperkinetic humans. In addition, the administration of drugs that are clinically-useful in treating childhood hyperactivity were unable to decrease the hyperactivity produced by haloperidol in neonatal rats. Taken together, these observations cast doubt upon the usefulness of this animal model to mimic the human condition.

Animals↗
PubMed1982

Failure of amphetamine isomers to decrease hyperactivity in developing rats.

Possible amphetamine-induced changes in locomotor activity were investigated in developing rats administered intracisternal injections of 6-hydroxydopamine (6-OHDA) or its vehicle at 5 days of age. Administration of the dopamine neurotoxin resulted in a significant depletion of whole-brain dopamine to 44% of control levels, whereas norepinephrine levels were not significantly reduced. In normal and 6-OHDA-treated pups activity increased from moderately low levels at 15 days of age to moderately high levels at 25 days of age. However, 6-OHDA-treated rats were hyperactive at 20 days of age. At 25 days, activity in both groups was equal and declined to levels typical for adults. Administration of graded doses of d- and l-amphetamine generally increased activity in both groups of rats, with d-amphetamine being more potent than l-amphetamine. Furthermore, no dose of either amphetamine isomer decreased activity in 6-OHDA-treated, hyperactive rats. Hence, no convincing evidence was found for a "paradoxical calming" effect of amphetamine in hyperactive rats, supporting other recent reports. These results suggest that the neonatal DA-depleted rat does not provide an accurate model system for pre-clinical investigation of the human hyperkinetic syndrome.

Aging↗
PubMed1982

Dopaminergic activity of quipazine.

Rats were trained to discriminate between the stimulus properties of intraperitoneal 0.16 mg/kg apomorphine and saline in a two-lever, food-motivated operant task. Administration of 1.0 mg/kg quipazine, a putative serotonin agonist, produced apomorphine-appropriate responding with a maximal effect occurring at 45 min post-injection. Pretreatment with either 2.0 mg/kg methysergide or 0.4 mg/kg haloperidol reduced quipazine-induced responding upon the apomorphine-appropriate lever to levels observed with methysergide or haloperidol administered alone. These results evidence a dopaminergic action for quipazine and suggest that central serotonergic and dopaminergic pathways may interact cooperatively to control behavior.

Animals↗
PubMed1980

Modulation of conditioned taste aversion by sodium pentobarbital.

The effects of pentobarbital on the formation and expression of LiCl induced taste aversion were examined using a two-bottle preference test. Rats adapted to restricted fluid intake were offered a 15% sucrose solution 15 min after a pentobarbital or saline injection but prior to post-CS LiCl or control injections. All animals were tested 3 days later in either the same or opposite drug state, and were returned to the conditioning day drug state for a second test. The results showed that pentobarbital in testing disrupted evidence for taste aversion in a manner not simply accounted for by its dipsogenic effects. It was suggested that the present paradigm may prove to be a simple behavioral assay for screening putative anxiolytic drugs.

Animals↗
PubMedDate not supplied

Can ACTH analogs support discriminative learning in rats?

Ten rats were trained to discriminate between the stimulus properties of subcutaneously (SC) administered MSH/ACTH4-10 and saline in a two-lever, food-motivated operant task. After 12 weeks of discriminative training with 100 micrograms/kg MSH/ACTH4-10, half the rats received 200 micrograms/kg MSH/ATCH4-10, whereas the other half were administered 400 micrograms/kg, for 6 additional weeks. Subsequently, all rats continued training on 50 micrograms/kg ORG 2766 (SC) and, after 12 weeks of training, were randomly assigned to receive either 100 or 200 micrograms/kg ORG 2766. The results of this extensive 36 week training schedule indicate that only 1 of the 10 rats learned to discriminate the interoceptive cues produced by the ACTH analogs. However, this rat's performance was so sustained and errorless that the possibility exists that it was relatively more sensitive to the effects of MSH/ACTH4-10 and its analogs and that these substances may support discriminative learning in the rat.

Adrenocorticotropic Hormone↗