Dataset Information

Lateral Habenula determines long-term storage of aversive memories.

ABSTRACT: The Lateral Habenula (LHb) is a small brain structure that codifies negative motivational value and has been related to major depression. It has been shown recently that LHb activation is sufficient to induce aversive associative learning; however the key question about whether LHb activation is required for an aversive memory to be formed has not been addressed. In this article we studied the function of the LHb in memory formation using the Inhibitory Avoidance task (IA). We found that LHb inactivation during IA training does not disrupt memory when assessed 24 h after, but abolishes it 7 days later, indicating that LHb activity during memory acquisition is not necessary for memory formation, but regulates its temporal stability. These effects suggest that LHb inactivation modifies subjective perception of the training experience.

SUBMITTER: Tomaiuolo M

PROVIDER: S-EPMC4026688 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Lateral Habenula determines long-term storage of aversive memories.

Tomaiuolo Micol M Gonzalez Carolina C Medina Jorge H JH Piriz Joaquin J

Frontiers in behavioral neuroscience 20140513

The Lateral Habenula (LHb) is a small brain structure that codifies negative motivational value and has been related to major depression. It has been shown recently that LHb activation is sufficient to induce aversive associative learning; however the key question about whether LHb activation is required for an aversive memory to be formed has not been addressed. In this article we studied the function of the LHb in memory formation using the Inhibitory Avoidance task (IA). We found that LHb ina ...[more]

PMID: 24860453

Similar Datasets

Project description:What we already know about this topicChronic alcohol use and withdrawal leads to increased pain perception, anxiety, and depression. These aberrant behaviors are accompanied by increased excitatory glutamatergic transmission to, and activity of, the lateral habenula neurons.Vanilloid type 1, or TRPV1, channels are expressed in the habenula and they facilitate glutamatergic transmission. Whether TRPV1 channel plays a role in habenula hyperactivity is not clear.What this article tells us that is newGlutamatergic transmission in the lateral habenula was inhibited by TRPV1 channel antagonists. In vivo, local administration of TRPV1 antagonists into the lateral habenula attenuated hyperalgesia, anxiety, and relapse-like drinking in rats who chronically consumed alcohol.The data suggest that enhanced TRPV1 channel function during withdrawal may contribute to aberrant behavior that promotes relapse alcohol consumption.BackgroundRecent rat studies indicate that alcohol withdrawal can trigger a negative emotional state including anxiety- and depression-like behaviors and hyperalgesia, as well as elevated glutamatergic transmission and activity in lateral habenula neurons. TRPV1, a vanilloid receptor expressed in the habenula, is involved in pain, alcohol dependence, and glutamatergic transmission. The authors therefore hypothesized that TRPV1 contributes to the changes in both the behavioral phenotypes and the habenula activity in alcohol-withdrawn rats.MethodsAdult male Long-Evans rats (n = 110 and 280 for electrophysiology and behaviors, respectively), randomly assigned into the alcohol and water (Naïve) groups, were trained to consume either alcohol or water-only using an intermittent-access procedure. Slice electrophysiology was used to measure spontaneous excitatory postsynaptic currents and firing of lateral habenula neurons. The primary outcome was the change in alcohol-related behaviors and lateral habenula activity induced by pharmacologic manipulation of TRPV1 activity.ResultsThe basal frequency of spontaneous excitatory postsynaptic currents and firing of lateral habenula neurons in alcohol-withdrawn rats was significantly increased. The TRPV1 antagonist capsazepine (10 µM) induced a stronger inhibition on spontaneous excitatory postsynaptic currents (mean ± SD; by 26.1 ± 27.9% [n = 11] vs. 6.7 ± 18.6% [n = 17], P = 0.027) and firing (by 23.4 ± 17.6% [n = 9] vs. 11.9 ± 16.3% [n = 12], P = 0.025) in Withdrawn rats than Naive rats. By contrast, the TRPV1 agonist capsaicin (3 μM) produced a weaker potentiation in Withdrawn than Naïve rats (spontaneous excitatory postsynaptic currents: by 203.6 ± 124.7% [n = 20] vs. 415.2 ± 424.3% [n = 15], P < 0.001; firing: 38.1 ± 14.7% [n = 11] vs. 73.9 ± 41.9% [n = 11], P < 0.001). Conversely, capsaicin's actions in Naïve but not in Withdrawn rats were significantly attenuated by the pretreatment of TRPV1 endogenous agonist N-Oleoyldopamine. In Withdrawn rats, intra-habenula infusion of TRPV1 antagonists attenuated hyperalgesia and anxiety-like behaviors, decreased alcohol consumption upon resuming drinking, and elicited a conditioned place preference.ConclusionsEnhanced TRPV1 function may contribute to increased glutamatergic transmission and activity of lateral habenula neurons, resulting in the aberrant behaviors during ethanol withdrawal.

Dataset Information

Lateral Habenula determines long-term storage of aversive memories.

Publications

Lateral Habenula determines long-term storage of aversive memories.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets