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Biomedical subjects

T A Patterson

Publications and source records attributed to T A Patterson.

At least 55 records · Page 3Linked to original sources
PubMed1992

Simultaneous quantitation of arecoline, acetylcholine, and choline in tissue using gas chromatography/electron impact mass spectrometry.

A capillary gas chromatography/mass spectrometry (GC/MS) assay for the simultaneous quantitation of arecoline (ARE), acetylcholine (ACh), and choline (Ch) in biological tissue has been developed. The method utilizes hexadeuterated ARE and nonadeuterated ACh and Ch as internal standards. The compounds were ion-pair extracted from tissue using sodium tetraphenylboron in 3-heptanone. GC/MS analysis was achieved using capillary GC and electron impact mass spectrometry. Quantitation was accomplished using selected ion monitoring at m/z 140 and 146 for non-deuterated and deuterated arecoline respectively, and m/z 58 and 64 for non-deuterated and deuterated ACh and Ch respectively. The method easily detected 25 pmol of all three compounds taken through the assay, and was linear through 50 nmol.

Acetylcholine↗
PubMed1992

Memory in the chick: multiple cues, distinct brain locations.

Training chicks on a one-trial passive avoidance task results in memory-dependent synaptic remodeling in the intermediate medial hyperstriatum ventrale (IMHV) and lobus parolfactorius (LPO). Because pretraining IMHV lesions are amnestic and posttraining IMHV lesions are not, the functional significance of this remodeling requires explanation. Chicks use various cues to classify and remember objects. If the IMHV were concerned with memory for only one such cue, then posttraining IMHV lesions would not lead to "amnesia" because animals would still avoid the aversive bead using other contextual cues. This hypothesis was tested using a color discrimination task. IMHV lesions, but not LPO lesions, impair color discrimination, suggesting that the IMHV may be involved in classifying and remembering the bitter bead on the basis of color. Thus, even simple associations are stored in the brain in the form of multiple, dispersed representations.

Animals↗
PubMed1992

Hospital outbreak traced to a case of Norwegian scabies.

A hospital outbreak, traced to a case of Norwegian scabies, resulted in 45 and 32 symptomatic cases in staff and patients, respectively. A total of 228 asymptomatic in-patient contacts and over 500 staff required prophylactic treatment with either 1% gamma benzene hexachloride lotion or 5% permethrin cream. Recurrences occurred in seven staff members and five patients. The outbreak was contained within four months.

Aged↗
PubMed1991

Effects of acute and chronic systemic administration of some typical antipsychotic drugs on turnover of dopamine and potassium ion-induced release of dopamine in the striatum of the rat in vivo.

Chronoamperometry was used to measure the dose dependency of antipsychotic drug (spiperone, haloperidol and chlorpromazine)-induced increases in depolarization-stimulated release of dopamine in the striatum of the rat in vivo. The dose-response curves were found to be at least biphasic (small doses increased release and large doses inhibited release) and different in shape from dose-response curves for increases in the turnover of dopamine, suggesting that the two processes may not be related. The threshold dose to induce increased depolarization-stimulated release of dopamine correlated with the values in the literature for doses required to block stereotype induced by apomorphine and amphetamine and doses sufficient to cause a maximal increase in release correlated with the doses required for the induction of catalepsy. In addition, the ratio of the doses required to obtain half-maximal and maximal increases in stimulated release of dopamine, matched values in the literature of the ratio of doses required to ameliorate psychotic symptoms, whereas the doses required to reverse the increase induced by antipsychotic drugs did not. Chronic administration of haloperidol resulted in alterations in the dose-response curves for both the release and turnover of DA. Chronic administration caused a reversal of the effect of acute administration in the small dose range (inhibition as opposed to enhancement of release), a decrease in the maximum magnitude of release of dopamine obtained and an overall shift to the right of the dose-response curve. Chronic administration of haloperidol decreased turnover, relative to animals receiving the drug acutely and no shift in the position of the dose-response curve was observed.

Animals↗
PubMed1991

Dissociation of brain sites necessary for registration and storage of memory for a one-trial passive avoidance task in the chick.

Although memory formation occurs in a sequence of pharmacologically dissociable stages, many models assume that this sequence is located within a single neuronal ensemble. Three forebrain areas in the young chick-the intermediate medial hyperstriatum ventrale (IMHV), the lobus parolfactorius (LPO), and the paleostriatum augmentatum--have been identified as important structures in mediating learning and memory processes. It has been shown that pretraining lesions placed to the left IMHV produce amnesia for a 1-trial passive avoidance task. Posttraining lesions in the IMHV are not amnestic. The present study demonstrated that bilateral lesions to the LPO are amnestic but only if made subsequent to rather than before training. These results suggest that long-term storage of the memory is dependent on the LPO. Further experiments determined that in the absence of the LPO at training, the right IMHV can act a long-term memory storage site. In the absence of the right IMHV at training, other, as yet undetermined, areas can take up this role.

Afferent Pathways↗
PubMed1990

Pre- and post-training lesions of the intermediate medial hyperstriatum ventrale and passive avoidance learning in the chick.

Three distinct nuclei of the chick forebrain--the intermediate medial hyperstriatum ventrale (IMHV), lobus parolfactorius (LPO), and paleostriatum augmentatum (PA)--show metabolic, morphological, and neurophysiological changes following training on a passive avoidance task, suggesting that these and other areas of the chick forebrain participate in memory formation for this task. Considerable evidence exists for lateralization of memory processes in the chick. Several experiments examined the effects of lesions in the IMHV on the ability of chicks to learn and retain the avoidance task. Pre-training bilateral lesions in the IMHV produced an impairment in avoidance responding tested three hours after training. Pre-training unilateral lesions in the left but not the right IMHV resulted in a similar impairment. However, bilateral IMHV ablations, given either 1 or 6 h post-training, did not impair retention. IMHV lesions did not impair retention of a simple escape learning task. These results are consistent with other studies that have examined the effects of bilateral IMHV lesions on acquisition of passive avoidance and extend these findings by demonstrating lateralization of acquisition involving the left IMHV. The results also suggest that, as early as one hour post-training, the IMHV is not necessary to retain the memory and indicate that other forebrain structures, possibly the LPO or PA, may maintain the memory trace following training. Hypotheses to account for these results and indications of future research are discussed.

Animals↗
PubMed1990

Cholinergic receptor antagonists impair formation of intermediate-term memory in the chick.

Several experiments examined the effects of cholinergic receptor antagonists on formation of memory in the chick. Scopolamine produced amnesia in chicks trained on a one-trial peck avoidance task in a dose-dependent manner. Pretraining injection of scopolamine produced amnesia that developed between 15 and 30 min after training, suggesting that scopolamine interferes with intermediate-term memory (ITM), previously described to be active during this time (Patterson, Alvarado, Warner, Bennett, & Rosenzweig, 1986). Pretraining injection of scopolamine or ouabain, an inhibitor of ATPase activity shown previously to inhibit formation of ITM, produced identical time courses of amnesia development, supporting the hypothesis that scopolamine interferes with ITM. Pirenzepine, an inhibitor of M1 muscarinic receptors, was effective in producing amnesia, whereas gallamine, an M2 receptor inhibitor, did not produce amnesia. These results suggest that M1, but not M2, receptors are involved in memory formation in the chick.

Animals↗
PubMed1989

Anisomycin and amnesia in the chick: state-dependent effects are not present with intracranial injections.

It has recently been suggested that intraperitoneal (IP) injection of anisomycin (ANI) in the chick produces amnesia for a one-trial passive avoidance task in a state-dependent manner. We have examined the behavioral and biochemical effects of IP and intracranial (IC) injections of ANI in chicks trained on a one-trial passive avoidance task. IC injection of ANI produced 35% brain protein synthesis inhibition whereas IP injection produced only negligible amounts of protein synthesis inhibition in the brain. IC injection of ANI produced amnesia and was not state-dependent. Patterns of behavior consistent with state-dependent effects were produced by IP injection of ANI. These experiments indicate that there are differences in the pattern of results produced by IP and IC injection of ANI and support the hypothesis that the expression of long-term memory in chicks is associated with protein synthesis.

Amnesia↗
PubMed1989

Midazolam induces amnesia in a simple, one-trial, maze-learning task in young chicks.

We report a simple, one-trial, learning paradigm which we have developed for use in young chicks. Chicks were separated from their brood mates and placed in a small isolation chamber. A 'T' corridor, or maze, connected the isolation chamber to the brood space, allowing the chick to escape isolation stress and rejoin the brood. When the chick successfully negotiated the corridor, the latency to perform this task was recorded. On a subsequent trial, any improvement in the speed of performance was reasoned to reflect the chick's memory of the task. Undrugged chicks always showed significant improvement in task latency if they were replaced in the maze 3 hours after a successful escape, suggesting that they had remembered the task. Chicks given midazolam (0.1 or 0.3 mg/kg, IP), a benzodiazepine, before the first escape, showed no improvement on their second escape. Improved performance was seen, however, if a second injection of midazolam was given before the second escape, suggesting a state-dependent effect.

Amnesia↗
PubMed1989

Influence of opioid peptides on learning and memory processes in the chick.

Several experiments were conducted to examine the effects of intracranial injection of opioid peptides and antagonists on learning and memory in the chick. Pretraining injection of [leu5]enkephalin and the selective delta receptor agonist [D-Pen2,L-Pen5]enkephalin (DPLPE) into the intermediate medial hyperstriatum ventrale (IMHV) produced impairment. ICI 174,864, a delta-selective antagonist, reversed the impairment produced by either [leu5]enkephalin or DPLE, results indicating that delta receptors may play a role in learning in the chick and suggesting that the impairment produced by [leu5]enkephalin is mediated through delta opioid receptors. beta-endorphin produced a naloxone-reversible impairment in performance, which suggests that this impairment is mediated by opioid receptors. Bilateral injection of beta-endorphin into the IMHV produced impairment, as did unilateral injection into the right, but not left, IMHV. Only bilateral injections into IMHV of [leu5]enkephalin were effective. These results suggest that the effects of beta-endorphin are centrally mediated whereas the effects of [leu5]enkephalin may be localized to other brain regions or are peripherally mediated. These initial results suggest that opioids are associated with learning and memory in the chick.

Animals↗
PubMed1989

Prevention of physostigmine-, DFP-, and diazinon-induced acute toxicity by monoethylcholine and N-aminodeanol.

1. Choline, and the choline analogues monoethylcholine (MEC) and N-aminodeanol (NAD) were examined for prophylactic activity in acute acetylcholinesterase inhibitor toxicity in mice. The rank order of potency of the compounds was MEC greater than NAD greater than choline. 2. Simultaneous administration of MEC (60 mg kg-1) or NAD (200 mg kg-1) with physostigmine reduced lethality to 17 and 13% respectively. MEC (60 mg kg-1) completely protected against disopropylfluorophosphate (DFP) and diazinon toxicity, and NAD reduced lethality to 17% for both agents. Choline (200 mg kg-1) exhibited only negligible antidotal activity against the inhibitors. 3. In vitro concentrations of choline, MEC, and NAD, similar to the estimated concentration obtained in vivo in the acute toxicity study, produced mixed inhibition of mouse brain acetylcholinesterase. The inhibition was dose-related and was additive to the inhibition produced by the cholinesterase inhibitors. 4. All three analogues reduced ligand binding at the nicotinic, M1, and M2 receptors. The rank order of potencies for the analogues at each receptor was nicotinic: (choline greater than MEC greater than NAD), M1: (MEC greater than choline greater than NAD), and M2: (MEC greater than choline greater than NAD). 5. It is proposed that the analogues prevent acetylcholinesterase inhibitor toxicity peripherally by interacting with acetylcholinesterase, and/or by competing with acetylcholine for binding to cholinoceptors.

Animals↗
PubMed1988

Time courses of amnesia development in two areas of the chick forebrain.

The roles of different forebrain structures in stages of memory formation were investigated by injecting agents into either the left medial hyperstriatum ventrale (MHV) or right lateral neostriatum (LNS) close to the time of one-trial taste-avoidance training. With L-glutamate injected into either the left MHV or right LNS 5 minutes pretraining, retention was good 1 minute posttraining but significantly impaired at 5 minutes and each subsequent time point. With emetine injected into either area, retention was still good 60 minutes posttraining but significantly impaired at 90 minutes. With ouabain, retention declined more slowly following injection into the right LNS (at 45 minutes) compared to injection in the left MHV (at 30 minutes). A second experiment confirmed the regional difference in amnesia development produced by ouabain. These results indicate that the duration of short-term memory is longer following inhibition of intermediate-term memory (ITM) in the right LNS, compared to inhibition of ITM in the left MHV.

Animals↗
PubMed1987

Amnesia produced by anisomycin in an appetitive task is not due to conditioned aversion.

Two experiments investigated the effects of lithium chloride (LiCl) and anisomycin (ANI) in a water reward Y-maze task. In Experiment 1, male CD-1 mice given weak or strong training were injected post-training with either saline or LiCl (150 mg/kg), which has been reported to produce conditioned aversion in mice. One day after training, both LiCl groups avoided the rewarded arm of the maze and drank less water than saline-injected controls. Two days after training, the strongly trained LiCl mice showed avoidance, while both LiCl groups drank less water. In Experiment 2, weakly trained mice given pre- and post-training ANI (30 mg/kg) were amnesic on the second test day compared to mice that received post-trial saline. However, water consumption was increased on the test day for both groups. LiCl produced a different pattern of results than ANI in this task. On the basis of these results, it is suggested that amnesia produced by ANI is due to impaired memory formation and not to conditioned aversion.

Amnesia↗
PubMed1987

Analysis of nutR, a site required for transcription antitermination in phage lambda.

Deletions extending from the cro gene into boxA and nutR of the Rho-dependent tR1 terminator of bacteriophage lambda have been generated and cloned between promoters and the galK gene of Escherichia coli on a multicopy plasmid. Terminators placed between the promoters and galK restrict transcription and expression of galK on these plasmids. However, when lambda N protein is provided, and if a functional N interaction site, nutR, is intact, transcription antitermination occurs and galK expression increases. Deletions into the nutR region affect the ability to antiterminate. From the results obtained we conclude that: boxA, a site believed to bind host factors (Nus), is not required for transcription antitermination in this system; the host NusA function is required even in the absence of boxA; nutR is required for N antitermination; translation across the nutR sequence prevents N-dependent antitermination.

Bacteriophage lambda↗