Short-term Memory Formation Research Articles

Long-Term Retention Explained by a Model of Short-Term Learning in the Adaptive Control of Reaching

Extensive theoretical, psychophysical, and neurobiological work has focused on the mechanisms by which short-term learning develops into long-term memory. Better understanding of these mechanisms may lead to the ability to improve the efficiency of training procedures. A key phenomenon in the formation of long-term memory is the effect of over learning on retention-discovered by Ebbinghaus in 1885: when the initial training period in a task is prolonged even beyond what is necessary for good immediate recall, long-term retention improves. Although this over learning effect has received considerable attention as a phenomenon in psychology research, the mechanisms governing this process are not well understood, and the ability to predict the benefit conveyed by varying degrees of over learning does not yet exist. Here we studied the relationship between the duration of an initial training period and the amount of retention 24 h later for the adaptation of human reaching arm movements to a novel force environment. We show that in this motor adaptation task, the amount of long-term retention is predicted not by the overall performance level achieved during the training period but rather by the level of a specific component process in a multi-rate model of short-term memory formation. These findings indicate that while multiple learning processes determine the ability to learn a motor adaptation, only one provides a gateway to long-term memory formation. Understanding the dynamics of this key learning process may allow for the rational design of training and rehabilitation paradigms that maximize the long-term benefit of each session.

Short-time memories in a network with randomly distributed connections

Coupled map lattices are able to store short-term memories when an external periodic input is applied. We consider short-term memory formation in networks with both regular (nearest-neighbor) and randomly chosen connections. The regimes under which single or multiple memorized patterns are stored are studied in terms of the coupling and nonlinear parameters of the network.

Transient Amnestic Syndrome in the Setting of Recurrent Partial Elementary Seizures

Back to table of contents Previous article Next article LETTERFull AccessTransient Amnestic Syndrome in the Setting of Recurrent Partial Elementary SeizuresGregory M. Weiss M.D.David R. Spiegel M.D.,Gregory M. Weiss M.D.Search for more papers by this authorDavid R. Spiegel M.D.Search for more papers by this author,Published Online:1 Jan 2008AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: The amnestic syndrome is a condition in which short term memory is disproportionately affected compared to other cognitive functions. 1 Transient disturbances in memory have been attributed to partial complex seizures, head trauma, transient global amnesia, alcohol abuse, and medication effects. 2 We would like to propose an addition to the causes of transient amnestic syndrome, as we present a case of recurrent partial elementary motor seizures with short term memory loss. Our patient is a 53-year-old black male admitted to our teaching hospital with short term memory loss of 1 month’s duration. During a prior admission he was diagnosed with partial seizures and was discharged on carbamazepine. In the interval, he was noncompliant with carbamazepine. He underwent a comprehensive medical examination, which was within normal limits, except for a magnetic resonance imaging (MRI) scan of his brain which showed interval development of bilateral hippocampal disease. The EEG showed postictal slowing.Cognitively, our patient exhibited marked short term memory loss, remembering 3/3 words immediately but 0/3 words at 3 minutes. The remainder of his Mini-Mental State Examination (MMSE) was normal. The only other significant feature was that our patient had motor symptoms such that his head, neck, and eyes deviated toward the right for about 10 sec. He was unaware of his seizures and resumed speaking postictally. During a typical 15 minute evaluation, our patient would have as many as five of these “motor episodes.” At this time, he was treated for recurrent partial elementary motor seizures and began carbamazepine.By day four of treatment, he no longer demonstrated these motor episodes or short term memory deficits. An MRI of the brain and EEG were repeated. The EEG and hippocampal structure (per MRI) normalized. With significant improvement in transient amnestic syndrome, our patient was discharged on carbamazepine. We have presented a case of recurrent partial elementary motor seizures resulting in hippocampal lesions on MRI and subsequent short-term memory impairment. The latter seems to be consistent with hippocampal function as the suggested site for short-term memory formation. 3 While partial complex seizures have been reported as a cause of transient amnestic syndrome, 2 there is less convincing evidence with partial elementary motor seizures. The mechanisms of transient amnestic syndrome, status/post partial complex seizures, could involve excitotoxicity within the hippocampus, 4 causing memory loss. During our patient’s previous admission, an MRI of the brain showed no hippocampal disease. That study corresponded to the earliest documented seizure activity. After 3 months of noncompliance with carbamazepine, the second MRI revealed interval changes in the hippocampus. Interestingly, the seizure focus for partial elementary motor seizures spares the hippocampus and thus is not associated with transient amnestic syndrome. Because neurons are extensively interconnected, however, it can be proposed that excitatory activity can propagate itself across the brain, 5 possibly resulting in hippocampal lesions, especially with recurrent partial elementary motor seizures. As for our patient, his seizure focus, presumably in the left motor cortex, “spread” to the hippocampus, resulting in the transient amnestic syndrome, which resolved with anticonvulsant therapy. Thus, we would like to suggest that recurrent partial elementary motor seizures be considered as an additional seizure type that could induce transient amnestic syndrome.Department of Psychiatry and Behavior Sciences, Eastern Virginia Medical School, Norfolk, VirginiaReferences1 . Carson AJ, Zeman A, Myles L, et al: Neurology and neurosurgery, in The American Psychiatric Publishing Textbook of Psychosomatic Medicine. Edited by Levenson J. Arlington, Va., American Psychiatric Publishing, 2005, pp 701–732Google Scholar2 . Kaufman D: Clinical Neurology for Psychiatrists, 4th ed. Philadelphia, WB Saunders, 1995Google Scholar3 . Sadock B, Sadock V: Kaplan and Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry, 9th ed. Philadelphia, Lippincott Williams & Wilkins, 2003Google Scholar4 . Jefferys JG: Mechanisms and experimental models of seizure generation. Curr Opin Neurol 1998; 11:123–127Google Scholar5 . Nestler E, Hyman S, Malenka R: Molecular Neuropharmacology: A Foundation for Clinical Neurosciences. New York, McGraw-Hill, 2001Google Scholar FiguresReferencesCited byDetailsCited byNone Volume 20Issue 1 Winter, 2008Pages 115-116 Metrics PDF download History Published online 1 January 2008 Published in print 1 January 2008

Transient Amnestic Syndrome in the Setting of Recurrent Partial Elementary Seizures

Back to table of contents Previous article Next article LETTERFull AccessTransient Amnestic Syndrome in the Setting of Recurrent Partial Elementary SeizuresGregory M. Weiss M.D.David R. Spiegel M.D.,Gregory M. Weiss M.D.Search for more papers by this authorDavid R. Spiegel M.D.Search for more papers by this author,Published Online:1 Jan 2008AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: The amnestic syndrome is a condition in which short term memory is disproportionately affected compared to other cognitive functions. 1 Transient disturbances in memory have been attributed to partial complex seizures, head trauma, transient global amnesia, alcohol abuse, and medication effects. 2 We would like to propose an addition to the causes of transient amnestic syndrome, as we present a case of recurrent partial elementary motor seizures with short term memory loss. Our patient is a 53-year-old black male admitted to our teaching hospital with short term memory loss of 1 month’s duration. During a prior admission he was diagnosed with partial seizures and was discharged on carbamazepine. In the interval, he was noncompliant with carbamazepine. He underwent a comprehensive medical examination, which was within normal limits, except for a magnetic resonance imaging (MRI) scan of his brain which showed interval development of bilateral hippocampal disease. The EEG showed postictal slowing.Cognitively, our patient exhibited marked short term memory loss, remembering 3/3 words immediately but 0/3 words at 3 minutes. The remainder of his Mini-Mental State Examination (MMSE) was normal. The only other significant feature was that our patient had motor symptoms such that his head, neck, and eyes deviated toward the right for about 10 sec. He was unaware of his seizures and resumed speaking postictally. During a typical 15 minute evaluation, our patient would have as many as five of these “motor episodes.” At this time, he was treated for recurrent partial elementary motor seizures and began carbamazepine.By day four of treatment, he no longer demonstrated these motor episodes or short term memory deficits. An MRI of the brain and EEG were repeated. The EEG and hippocampal structure (per MRI) normalized. With significant improvement in transient amnestic syndrome, our patient was discharged on carbamazepine. We have presented a case of recurrent partial elementary motor seizures resulting in hippocampal lesions on MRI and subsequent short-term memory impairment. The latter seems to be consistent with hippocampal function as the suggested site for short-term memory formation. 3 While partial complex seizures have been reported as a cause of transient amnestic syndrome, 2 there is less convincing evidence with partial elementary motor seizures. The mechanisms of transient amnestic syndrome, status/post partial complex seizures, could involve excitotoxicity within the hippocampus, 4 causing memory loss. During our patient’s previous admission, an MRI of the brain showed no hippocampal disease. That study corresponded to the earliest documented seizure activity. After 3 months of noncompliance with carbamazepine, the second MRI revealed interval changes in the hippocampus. Interestingly, the seizure focus for partial elementary motor seizures spares the hippocampus and thus is not associated with transient amnestic syndrome. Because neurons are extensively interconnected, however, it can be proposed that excitatory activity can propagate itself across the brain, 5 possibly resulting in hippocampal lesions, especially with recurrent partial elementary motor seizures. As for our patient, his seizure focus, presumably in the left motor cortex, “spread” to the hippocampus, resulting in the transient amnestic syndrome, which resolved with anticonvulsant therapy. Thus, we would like to suggest that recurrent partial elementary motor seizures be considered as an additional seizure type that could induce transient amnestic syndrome.Department of Psychiatry and Behavior Sciences, Eastern Virginia Medical School, Norfolk, VirginiaReferences1 . Carson AJ, Zeman A, Myles L, et al: Neurology and neurosurgery, in The American Psychiatric Publishing Textbook of Psychosomatic Medicine. Edited by Levenson J. Arlington, Va., American Psychiatric Publishing, 2005, pp 701–732Google Scholar2 . Kaufman D: Clinical Neurology for Psychiatrists, 4th ed. Philadelphia, WB Saunders, 1995Google Scholar3 . Sadock B, Sadock V: Kaplan and Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry, 9th ed. Philadelphia, Lippincott Williams & Wilkins, 2003Google Scholar4 . Jefferys JG: Mechanisms and experimental models of seizure generation. Curr Opin Neurol 1998; 11:123–127Google Scholar5 . Nestler E, Hyman S, Malenka R: Molecular Neuropharmacology: A Foundation for Clinical Neurosciences. New York, McGraw-Hill, 2001Google Scholar FiguresReferencesCited byDetailsCited byNone Volume 20Issue 1 Winter, 2008Pages 115-116 Metrics PDF download History Published online 1 January 2008 Published in print 1 January 2008

Hypoxia suppresses kainate-induced γ-oscillations in rat hippocampal slices

Hypoxia or global ischemia causes rapid loss of consciousness and a sudden increase in spontaneous transmitter release suggesting that coordinated synaptic activity is impaired. Gamma oscillations (30-100 Hz) are thought to provide for binding of parallel processed information in the brain, contributing to cognition and formation of short-term memory. We hypothesized that gamma-oscillations are rapidly blocked by hypoxia and that prolonged hypoxia reduces the capability to generate such activity. In ventral hippocampal slices, kainate-induced gamma-oscillations reversibly declined 40 s after onset of 3 min hypoxia. Repetition of such hypoxic periods led to accumulative impairment of gamma-activities. By contrast, 6 min of hypoxia led to a transient anoxic depolarization after which gamma-oscillations remained almost completely blocked.

The Drosophila ARC homolog regulates behavioral responses to starvation

The gene encoding dARC1, one of three Drosophila homologs of mammalian activity-regulated cytoskeleton-associated protein (ARC), is upregulated in both seizure and muscular hypercontraction mutants. In this study we generate a null mutant for dArc1 and show that this gene is not involved in synaptic plasticity at the larval neuromuscular junction or in formation or decay of short-term memory of courtship conditioning, but rather is a modifier of stress-induced behavior. dARC1 is expressed in a number of neurosecretory cells and mutants are starvation-resistant, exhibiting an increased time of survival in the absence of food. Starvation resistance is likely due to the fact that dArc1 mutants lack the normal hyperlocomotor response to starvation, which is almost universal in the animal kingdom. dARC1 acts in insulin-producing neurons of the pars intercerebralis to control this behavior, but does not appear to be a general regulator of insulin signaling. This suggests that there are multiple modes of communication between the pars and the ring gland that control starvation-induced behavioral responses.

Effect of gestational ethanol exposure on long-term memory formation in newborn chicks

Fetal alcohol syndrome (FAS), a condition occurring in some children of mothers who have consumed alcohol during pregnancy, is characterized by craniofacial malformations, and physical and mental retardation. It is significant that even children with history of gestational ethanol exposure but relatively unaffected overall IQ performance, often exhibit learning difficulties and behavioral problems, suggestive of impaired memory formation. Hence, the specific aim of this study was to examine memory formation in chicks exposed to ethanol during early gestation toward the understanding of neurobehavioral disturbances in FAS. Chicks were exposed to alcohol on gestational days 1–3 by injection of ethanol into the airspace of freshly fertilized eggs. The effects of prenatal ethanol on physical growth and development, and memory formation were studied. The one-trial passive avoidance learning paradigm in 1-day-old chicks was used to study memory formation in these chicks. It was observed that chick embryos exposed to 10% ethanol on gestational days 1–3 had significant reduction in all body parameters when compared with appropriate controls. Further, ethanol-exposed chick embryos had significantly impaired ( P < .05) long-term memory (LTM) formation after training, though short-term or intermediate-term memory formation was unimpaired. Thus, the findings of the current study demonstrate the detrimental effects of ethanol exposure during early pregnancy on developing chick embryos in general and on memory formation in particular. Hence, it is suggested that impairment in LTM could be a fundamental mechanism for learning disorders and neurobehavioral abnormalities observed in FAS.

Attention-Like Processes in Drosophila Require Short-Term Memory Genes

Although there is much behavioral evidence for complex brain functions in insects, it is not known whether insects have selective attention. In humans, selective attention is a dynamic process restricting perception to a succession of salient stimuli, while less relevant competing stimuli are suppressed. Local field potential recordings in the brains of flies responding to visual novelty revealed attention-like processes with stereotypical temporal properties. These processes were modulated by genes involved in short-term memory formation, namely dunce and rutabaga. Attention defects in these mutants were associated with distinct optomotor effects in behavioral assays.

Short-term memory formation and long-term memory consolidation are enhanced by cellular prion association to stress-inducible protein 1

Cellular prion protein (PrP(C)) is a cell surface glycoprotein that interacts with several ligands such as laminin, NCAM (Neural-Cell Adhesion Molecule) and the stress-inducible protein 1 (STI1). PrP(C) association with these proteins in neurons mediates adhesion, differentiation and protection against programmed cell death. Herein, we used an aversively motivated learning paradigm in rats to investigate whether STI1 interaction with PrP(C) affects short-term memory (STM) formation and long-term memory (LTM) consolidation. Blockage of PrP(C)-STI1 interaction with intra-hippocampal infusion of antibodies against PrP(C) or STI1 immediately after training impaired both STM and LTM. Furthermore, infusion of PrP(C) peptide 106-126, which competes for PrP(C)-STI1 interaction, also inhibited both forms of memory. Remarkably, STI1 peptide 230-245, which includes the PrP(C) binding site, had a potent enhancing effect on memory performance, which could be blocked by co-treatment with the competitive PrP(C) peptide 106-126. Taken together, these results demonstrate that PrP(C)-STI1 interaction modulates both STM and LTM and suggests a potential use of ST11 peptide 230-245 as a pharmacological agent.

Early activation of extracellular signal-regulated kinase signaling pathway in the hippocampus is required for short-term memory formation of a fear-motivated learning.

1. According to its duration there are, at least, two major forms of memory in mammals: short term memory (STM) which develops in a few seconds and lasts several hours and long-term memory (LTM) lasting days, weeks and even a lifetime. In contrast to LTM, very little is known about the neural, cellular and molecular requirements for mammalian STM formation. 2. Here we show that early activation of extracellular signal-regulated kinases 1/2 (ERK1/2) in the hippocampus is required for the establishment of STM for a one-trial inhibitory avoidance task in the rat. Immediate posttraining infusion of U0126 (a selective inhibitor of ERK kinase) into the CA1 region of the dorsal hippocampus blocked STM formation. 3. Reversible inactivation of the entorhinal cortex through muscimol infusion produced deficits in STM and a selective and rapid decrease in hippocampal ERK2 activation.4. Together with our previous findings showing a rapid decrease in ERK2 activation and impaired STM after blocking BDNF function, the present results strongly suggest that ERK2 signaling in the hippocampus is a critical step in STM processing.

Brain cholesterol metabolism is important for learning

The brain relies exclusively on de novo synthesis from acetate to fulfill its cholesterol requirement. Turnover of cholesterol within neurons is accomplished by the enzyme cholesterol 24-hydroxylase, a cytochrome P450 that converts cholesterol to the more hydrophilic 24(S)-hydroxycholesterol. This product diffuses out of the brain and is cleared by the liver. We constructed a line of knockout mice in which the cholesterol 24-hydroxylase gene is ablated. Steady state cholesterol content of the brain does not change in the mutant mice but cholesterol synthesis is decreased by 50%, suggesting that cholesterol 24-hydroxylase is responsible for 50% of cholesterol turnover in the brain. The anatomy of the brain in light and electron microscopic analyses does not differ from that of wild type controls. To determine the role of cholesterol 24-hydroxylase in brain function we performed several behavioral tests, including the Morris water maze and cued and contextual fear conditioning tests. Results from these experiments show that the 24-hydroxylase knockout mice have severe deficits in spatial and associative learning and in short and long term memory formation. In vitro studies with hippocampal slices trace these deficits to an impairment of long-term potentiation. Our results suggest that altered cholesterol metabolism in the brain has implications for synaptic plasticity as well as learning and memory. Supported by a grant from the National Institutes of Heart Lung and Blood (HL20948, D.W.R.).

Acteoside of Callicarpa dichotoma Attenuates Scopolamine-Induced Memory Impairments

We previously reported that ten phenylethanoid glycosides including acteoside isolated from the leaves and twigs of Callicarpa dichotoma significantly attenuated glutamate-induced neurotoxicity. In the present study, we examined anti-amnesic activity of acteoside using scopolamine-induced (1 mg/kg body weight, s.c.) amnesic mice with both passive avoidance and Morris water maze tests. Acute oral treatment (single administration prior to scopolamine treatment) of mice with acteoside (1.0, 2.5 mg/kg body weight) significantly mitigated scopolamine-induced memory deficits in the passive avoidance test. It is interesting to note that prolonged oral daily treatment of mice with much lower amount (0.1 mg/kg body weight) of acteoside for 10 d reversed the scopolamine-induced memory deficits. In the Morris water maze, prolonged oral treatment with acteoside (prolonged daily administration of 1.0 mg/kg body weight for 10 d) significantly ameliorated scopolamine-induced memory deficits showing the formation of long-term and/or short-term spatial memory. We suggest, therefore, that acteoside has anti-amnesic activity that may ultimately hold significant therapeutic value in alleviating certain memory impairment observed in Alzheimer's disease.

Endogenous BDNF is required for long-term memory formation in the rat parietal cortex

Information storage in the brain is a temporally graded process involving different memory phases as well as different structures in the mammalian brain. Cortical plasticity seems to be essential to store stable long-term memories, although little information is available at the moment regarding molecular and cellular events supporting memory consolidation in the neocortex. Brain-derived neurotrophic factor (BDNF) modulates both short-term synaptic function and activity-dependent synaptic plasticity in hippocampal and cortical neurons. We have recently demonstrated that endogenous BDNF in the hippocampus is involved in memory formation. Here we examined the role of BDNF in the parietal cortex (PCx) in short-term (STM) and long-term memory (LTM) formation of a one-trial fear-motivated learning task in rats. Bilateral infusions of function-blocking anti-BDNF antibody into the PCx impaired both STM and LTM retention scores and decreased the phosphorylation state of cAMP response element-binding protein (CREB). In contrast, intracortical administration of recombinant human BDNF facilitated LTM and increased CREB activation. Moreover, inhibitory avoidance training is associated with a rapid and transient increase in phospho-CREB/total CREB ratio in the PCx. Thus, our results indicate that endogenous BDNF is required for both STM and LTM formation of inhibitory avoidance learning, possibly involving CREB activation-dependent mechanisms. The present data support the idea that early sensory areas constitute important components of the networks subserving memory formation and that information processing in neocortex plays an important role in memory formation.

Spiking neural nets with symbolic internal state

A type of spiking neural net in which the internal state functions of the neurons are represented symbolically rather than numerically is described. This makes possible subtle forms of short term memory, but also raises both computational and mathematical problems. It is shown how interval arithmetic can be used for event driven simulation. Computational times are given for some tests of an implementation resulting from these ideas. Applications are briefly discussed.

Short-term memories with a stochastic perturbation

We investigate short-term memories in linear and weakly nonlinear coupled map lattices with a periodic external input. We use locally coupled maps to present numerical results about short-term memory formation adding a stochastic perturbation in the maps and in the external input.

ESP-102, a standardized combined extract of Angelica gigas, Saururus chinensis and Schizandra chinensis, significantly improved scopolamine-induced memory impairment in mice

We assessed the effects of oral treatments of ESP-102, a standardized combined extract of Angelica gigas, Saururus chinensis and Schizandra chinensis, on learning and memory deficit. The cognition-enhancing effect of ESP-102 was investigated in scopolamine-induced (1 mg/kg body weight, s.c.) amnesic mice with both passive avoidance and Morris water maze performance tests. Acute oral treatment (single administration prior to scopolamine treatment) of mice with ESP-102 (doses in the range of 10 to 100 mg/kg body weight) significantly reduced scopolamine-induced memory deficits in the passive avoidance performance test. Another noteworthy result included the fact that prolonged oral daily treatments of mice with much lower amounts of ESP-102 (1 and 10 mg/kg body weight) for ten days reversed scopolamine-induced memory deficits. In the Morris water maze performance test, both acute and prolonged oral treatments with ESP-102 (single administration of 100 mg/kg body weight or prolonged daily administration of 1 and 10 mg/kg body weight for ten days, respectively, significantly ameliorated scopolamine-induced memory deficits as indicated by the formation of long-term and/or short-term spatial memory. In addition, we investigated the effects of ESP-102 on neurotoxicity induced by amyloid-β peptide (Aβ 25–35) or glutamate in primary cultured cortical neurons of rats. Pretreatment of cultures with ESP-102 (0.001, 0.01 and 0.1 μg/ml) significantly protected neurons from neurotoxicity induced by either glutamate or Aβ 25–35. These results suggest that ESP-102 may have some protective characteristics against neuronal cell death and cognitive impairments often observed in Alzheimer's disease, stroke, ischemic injury and other neurodegenerative diseases.

Cannabinoid Receptors and Their Relationships with Neuropsychiatric Disorders

Cannabinoids are the constituents of the marijuana plants. The central effects of exogenous cannabinoids are implicated in enhancing mood, altering emotional states, and interfering in the formation of short-term memory. Cannabinoid receptors are G protein-coupled receptors with seven transmembrane domains that are expressed on the cell surface with their binding domain exposed to the extracellular space. To date, two cannabinoid receptors have been cloned, CB1 and CB2. Recent evidence suggests that a third CB3 receptor is out there, waiting to be cloned. The endocannabinoids may represent the first members of a new classes of neuromodulators, that are not stored in cell vesicles, but rather synthesised by the cell on demand. The endogenous cannabinoid system could play a central role in several neuropsychiatric disorders and is also involved in other conditions such as pain, spasticity and neuroprotection. Implication of cannabinoid system in the pathogenesis and development of schizophrenia is also discussed.

Opposing roles for GABA A and GABA C receptors in short-term memory formation in young chicks

The inhibitory neurotransmitter GABA has both inhibitory and enhancing effects on short-term memory for a bead discrimination task in the young chick. Low doses of GABA (1–3 pmol/hemisphere) injected into the multimodal association area of the chick forebrain, inhibit strongly reinforced memory, whereas higher doses (30–100 pmol/hemisphere) enhance weakly reinforced memory. The effect of both high and low doses of GABA is clearly on short-term memory in terms of both the time of injection and in the time that the memory loss occurs. We argue on the basis of relative sensitivities to GABA and to selective GABA receptor antagonists that low doses of GABA act at GABA C receptors (EC 50 approximately 1 μM) and the higher doses of GABA act via GABA A receptors (EC 50 approximately 10 μM). The selective GABA A receptor antagonist bicuculline inhibited strongly reinforced memory in a dose and time dependent manner, whereas the selective GABA C receptor antagonists TPMPA and P4MPA enhanced weakly reinforced in a dose and time dependent manner. Confirmation that different levels of GABA affect different receptor subtypes was demonstrated by the shift in the GABA dose-response curves to the selective antagonists. It is clear that GABA is involved in the control of short-term memory formation and its action, enhancing or inhibiting, depends on the level of GABA released at the time of learning.

Differential effects of THC- or CBD-rich cannabis extracts on working memory in rats

Cannabinoid receptors in the brain (CB 1) take part in modulation of learning, and are particularly important for working and short-term memory. Here, we employed a delayed-matching-to-place (DMTP) task in the open-field water maze and examined the effects of cannabis plant extracts rich in either Δ 9-tetrahydrocannabinol (Δ 9-THC), or rich in cannabidiol (CBD), on spatial working and short-term memory formation in rats. Δ 9-THC-rich extracts impaired performance in the memory trial (trial 2) of the DMTP task in a dose-dependent but delay-independent manner. Deficits appeared at doses of 2 or 5 mg/kg (i.p.) at both 30 s and 4 h delays and were similar in severity compared with synthetic Δ 9-THC. Despite considerable amounts of Δ 9-THC present, CBD-rich extracts had no effect on spatial working/short-term memory, even at doses of up to 50 mg/kg. When given concomitantly, CBD-rich extracts did not reverse memory deficits of the additional Δ 9-THC-rich extract. CBD-rich extracts also did not alter Δ 9-THC-rich extract-induced catalepsy as revealed by the bar test. It appears that spatial working/short-term memory is not sensitive to CBD-rich extracts and that potentiation and antagonism of Δ 9-THC-induced spatial memory deficits is dependent on the ratio between CBD and Δ 9-THC.

Short-term memories with a stochastic perturbation

We investigate short-term memories in linear and weakly nonlinear coupled map lattices with a periodic external input. We use locally coupled maps to present numerical results about short-term memory formation adding a stochastic perturbation in the maps and in the external input.