Librium prevents the analgesia and shuttlebox escape deficit typically observed following inescapable shock

Drugan, Robert C.; Ryan, Susan M.; Minor, Thomas R.; Maier, Steven F.

doi:10.1016/s0091-3057(84)80014-3

Cited by 153 publications

(80 citation statements)

References 40 publications

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“…Also this hypothesis poses that only if norepinephrine depletion is complete, the anxiety will disappear. Therefore the conclusion is that anxiety could play a generalizing role, which is in agreement with the hypothesis of Drugan et al [1984], However, there is a difference between their results and ours. Drugan et al [1984] found that preshock CDP had also an effect which is opposite to our results.…”

Section: Discussionsupporting

confidence: 88%

Effect of an Anti-Anxiety Drug in a Learned Helplessness Experiment

Nijssen

Schelvis²

1987

Neuropsychobiology

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Rats were injected with chlordiazepoxide 30 min before a situation of uncontrollable stress, or 30 min before an FR-3 escape test 24 h after the uncontrollable stress. Only in the latter situation they reduced their response latencies. The conclusion was that helplessness after moderate stress (i.e. electric shock) resembles a state of anxiety. Anxiety can be descibed on a behavioural level as inhibiting the ongoing behaviour. Therefore an explanation in terms of anxiety is in agreement with Weiss’ inactivity hypothesis and with the results of the study by Drugan et al., who also emphasized the role of anxiety or fear in learned helplessness experiments.

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Section: Discussionsupporting

confidence: 88%

Effect of an Anti-Anxiety Drug in a Learned Helplessness Experiment

Nijssen

Schelvis²

1987

Neuropsychobiology

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“…Although the shuttle escape deficit is sensitive to some anxiolytic and antidepressant treatments (e.g., [11,42,55]), escape learning or post-shock freezing have not been extensively validated as animal models of any particular condition. Other behaviors have been used as endpoints in uncontrollable stress experiments, such as reduced duration of swimming when placed in water (e.g., [45]), but to our knowledge there are no published studies demonstrating that reduced swimming was a result of the uncontrollability/controllability of the stressor.…”

Section: Discussionmentioning

confidence: 99%

The role of prior stressor controllability and the dorsal raphé nucleus in sucrose preference and social exploration

Christianson

Paul

Irani

et al. 2008

Behavioural Brain Research

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Research investigating how control over stressors affects behavior often utilizes freezing and shuttle escape learning as the behavioral endpoints. These endpoints have been argued to reflect anxious or depressed states, but these descriptions are problematic. The present study sought to determine the impact of stressor controllability and the dorsal raphé nucleus (DRN) on sucrose preference and juvenile social exploration, putative measures of anhedonia and anxiety that are commonly used in studies of stress per se. In Experiment 1 rats were exposed to escapable (ES) or yoked-inescapable (IS) tailshocks. In Experiment 2 ES or IS was given 7 days before all rats received IS. In Experiment 3 the DRN was inactivated during IS by microinjection of 8-OH-DPAT. Sucrose preference and social exploration were tested for several days after stress. A fourth experiment confirmed that juvenile social exploration is sensitive to traditional β-carboline and benzodiazepine manipulations. Both ES and IS reduced sucrose preference, but only IS reduced social exploration. Prior treatment with ES prevented the effect of IS on social exploration but did not prevent the effect of IS on sucrose preference and inactivation of the DRN prevented the effect of IS on social exploration but did not change sucrose preference. The present results indicate that social exploration but not sucrose preference is sensitive to prior stressor controllability, and that DRN activation mediates the effect of IS on social exploration. We argue that DRN-5-HT activation mediates a state of generalized anxiety produced by uncontrollable stress and that juvenile social exploration is a useful behavioral endpoint in stressor controllability studies.

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“…Additionally, administration of a2 antagonists increases LC firing (Rasmussen and Jacobs, 1986) and increases anxiety-like behaviors (Redmond and Huang, 1979). Agents which decrease LC firing, such as opiates, benzodiazepines, (Drugan et al, 1984;Rasmussen and Jacobs, 1986;Tanaka et al, 1990), and clonidine (Aghajanian, 1978;Aghajanian and VanderMaelen, 1982), on the other hand, decrease anxiety behaviors. In humans trials, clonidine has been shown to be effective in some, but not all, patients with panic disorder (Bremner et al, 1996a).…”

Section: Discussionmentioning

confidence: 99%

Group II mGlu Receptor Activation Suppresses Norepinephrine Release in the Ventral Hippocampus and Locomotor Responses to Acute Ketamine Challenge

Lorrain

Schaffhauser

Campbell

et al. 2003

Neuropsychopharmacol

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Group II mGlu receptor agonists (eg LY379268 and LY354740) have been shown to reverse many of the behavioral responses to PCP as well as glutamate release elicited by PCP and ketamine. In the present set of experiments, we used in vivo microdialysis to show that, in addition to reversing PCP-and ketamine-evoked glutamate release, group II mGlu receptor stimulation also prevents ketamine-evoked norepinephrine (NE) release. Pretreating animals with the mixed 2/3 metabotropic glutamate (mGlu2/3) receptor agonist LY379268 (0.3-10 mg/kg) dose-dependently inhibited ketamine (25 mg/kg)-evoked NE release in the ventral hippocampus (VHipp). Ketamine hyperactivity was also reduced in a similar dose range. Following our initial observation on NE release, we conducted a series of microinjection experiments to reveal that the inhibitory effects of LY379268 on VHipp NE release may be linked to glutamate transmission within the medial prefrontal cortex. Finally, we were able to mimic the inhibitory effects of LY379268 on ketamine-evoked NE release by using a novel mGlu2 receptor selective positive modulator. (+/À) 2,2,2-Trifluoroethyl [3-(1-methyl-butoxy)-phenyl]-pyridin-3-ylmethyl-sulfonamide (2,2,2-TEMPS, characterized through in vitro GTPgS binding) at a dose of 100 mg/kg significantly reduced the NE response. Together, these results demonstrate a novel means to suppress noradrenergic neurotransmission (ie by activating mGlu2 receptors) and may, therefore, have important implications for neuropsychiatric disorders in which aberrant activation of the noradrenergic system is thought to be involved.

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Librium prevents the analgesia and shuttlebox escape deficit typically observed following inescapable shock

Cited by 153 publications

References 40 publications

Effect of an Anti-Anxiety Drug in a Learned Helplessness Experiment

Effect of an Anti-Anxiety Drug in a Learned Helplessness Experiment

The role of prior stressor controllability and the dorsal raphé nucleus in sucrose preference and social exploration

Group II mGlu Receptor Activation Suppresses Norepinephrine Release in the Ventral Hippocampus and Locomotor Responses to Acute Ketamine Challenge

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