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M D Hamburg

Publications and source records attributed to M D Hamburg.

13 recordsLinked to original sources
PubMed1979

DDC-induced amnesia and norepinephrine: a correlated behavioral-biochemical analysis.

Diethyldithiocarbamic acid (DDC), a dopamine-B-hydroxylase inhibitor, when injected into rats 30 min to 6 h before training of a passive avoidance task, impaired formation of long-term memory as indicated by performance on a retention test 24 h later. Performance of the task was at its minimum when injection occurred 2 to 4 h prior to training; recovery was evident in animals trained 5 or 6 h after drug treatment. Catecholamine assay of brains of temporally yoked animals showed that norepinephrine depletion followed a time course paralleling that of the amnesia. These findings support the hypothesis that the degree of memory storage, as reflected in performance following training in a passive avoidance task, can be directly correlated with the level of norepinephrine existing at the time of training.

Animals↗
PubMed1976

DDC-induced retrograde amnesias prevented by injections of dl-DOPS.

Injection of a dopamine beta-hydroxylate inhibitor, diethyldithiocarbamate (DDC) in rats 30 min prior to training of a step-down passive avoidance task impaired performance of the task 24 hr later. Similarly, injection of DDC 30 min prior to testing blocked retrieval of a passive avoidance habit trained in normal rats the previous day. Injection of a direct norepinephrine (NE) precursor, dl-thero 3,4-dihydroxyphenylserine (DOPS) 60 min before DDC prevented both amnesias. These data support the hypothesis that reduced levels of NE are responsible for DDC-induced amnesias.

Amnesia, Retrograde↗
PubMed1967

Retrograde amnesia produced by intraperitoneal injection of physostigmine.

Intraperitoneal injection of physostigmine in rats produced a retrograde amnesia of a trained task of escaping shock. This amnesic effect was a U-shaped function of the length of the interval between initial training and injection. In all cases, retraining Occurred 30 minutes after injection. A substantial effect was produced by physostigmine if its application was made 30 minutes after training; there was no effect if application and tests were made 1, 2, or 3 days after the original training. When the substance was injected and the rats were retrained 5, 7, or 14 days after the original training, a substantial effect again appeared. These results are similar to those reported in experiments in which another anticholinesterase, diisopropyl fluorophosphate, was applied intracerebrally. The data demonstrate a similar pattern of change of the amnesia with time, and they substantiate the view that neither the place of application nor the brain lesions caused the reported amnesia.

Amnesia↗
PubMed1966

Anticholinesterase-induced amnesia and its temporal aspects.

Injection of the anticholinesterase drug diisopropyl fluorophosphate into the hippocampi of rats, 30 minutes after escape learning, produces partial amnesia with full recovery 5 days after injection. No such amnesia is produced if the injection takes place 3 days after learning. However, with injections 5 days after learning there is again an effect, and at 14 days amnesia is complete though no normal forgetting occurs within this period.

Amnesia↗
PubMedDate not supplied

Evidence for adrenergic neurons in a memory access pathway.

Injection of a beta-adrenergic blocker, propranolol, in rats within 5 min after training of a step-dowm passive avoidance response had no effect on performance either 2 or 6 hr later, however, when testing occurred 1, 3 or 7 days after training and injection a significant performance decrement was observed. If drug injection was postponed until 1 or 3 days after training and testing was conducted 2 hr later, again poor avoidance performance was obtained. No support for a state-dependency explanation [14] of the propranolol amnesia could be found. The amnesia that followed beta-adrenergic receptor block was identical to that previously reported when norepinephrine biosynthesis was reduced [9] and supports the hypothesis of a role for adrenergic neurons in memory formation and retrieval that is different from cholinergic neurons [4,10].

Animals↗