Deficits in passive avoidance learning in young rats following mecamylamine injections in the hippocampo-entorhinal area

Blozovski, Denise

doi:10.1007/bf00239211

Cited by 24 publications

(14 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Both drugs (35μg) were dissolved and delivered in a volume of 0.35μl of PBS. Both the concentration and volume of MLA and mecamylamine were selected from previous studies with similar doses that have shown significant deficits in various types of learning and memory and in which diffusion was found to be limited to the targeted area (Barros, et al, 2004;Bettany, & Levin, 2001;Blozovski, 1983;Decker, et al, 1995;Felix, & Levin, 1997;Levin, 2002b;Ohno, et al, 1993;Wallenstein, & Vago, 2001). A relatively high concentration was chosen to examine robust effects of each drug.…”

Section: Intrahippocampal Infusionsmentioning

confidence: 99%

Cholinergic modulation of pavlovian fear conditioning in rats: Differential effects of intrahippocampal infusion of mecamylamine and methyllycaconitine

Vago

Kesner

2007

Neurobiology of Learning and Memory

View full text Add to dashboard Cite

The cholinergic system has consistently been implicated in Pavlovian fear conditioning. Considerable work has been done to localize specific nicotinic receptor subtypes in the hippocampus and determine their functional importance; however, the specific function of many of these subtypes has yet to be determined. An α7 nicotinic antagonist methyllycaconitine (MLA) (35μg), and a broad spectrum non-α7 nicotinic antagonist mecamylamine (35μg) was injected directly into the dorsal hippocampus or overlying cortex either 15 minutes pre-, 1 minute post-, or 6 hours post-fear conditioning. One week after conditioning, retention of contextual and cue (tone) conditioning were assessed. A significant impairment in retention of contextual fear was observed when mecamylamine was injected 15 minutes pre-and 1 minute post-conditioning. No significant impairment was observed when mecamylamine was injected 6 hours post-conditioning. Likewise, a significant impairment in retention of contextual fear was observed when MLA was injected 1 minute postconditioning; however, in contrast, MLA did not show any significant impairments when injected 15 minutes pre-conditioning, but did show a significant impairment when injected 6 hours postconditioning. There were no significant impairments observed when either drug was injected into overlying cortex. No significant impairments were observed in cue conditioning for either drug. In general, specific temporal dynamics involved in nicotinic receptor function were found relative to time of receptor dysfunction. The results indicate that the greatest deficits in long-term retention (1 week) of contextual fear are produced by central infusion of MLA minutes to hours post-conditioning or mecamylamine within minutes of conditioning.

show abstract

Section: Intrahippocampal Infusionsmentioning

confidence: 99%

Cholinergic modulation of pavlovian fear conditioning in rats: Differential effects of intrahippocampal infusion of mecamylamine and methyllycaconitine

Vago

Kesner

2007

Neurobiology of Learning and Memory

View full text Add to dashboard Cite

show abstract

“…The hippocampal formation (HF) is critical to memory and cognition (Blozovski, 1983; Izquierdo et al, 2008), and mediates the influences of nicotine on memory (Blozovski, 1985; Davis et al, 2007). The HF includes four main subregions (Amaral and Witter, 1995); the dentate gyrus, the hippocampal proper (including CA1, CA2 and CA3 regions), the subicular complex (including subiculum (Sb)), and the entorhinal cortex (EC; including layers I through VI).…”

Section: Introductionmentioning

confidence: 99%

“…However, whether nicotine influences neurons in either the subicular complex or EC is still unknown. Because both the EC and Sb play critical roles in memory functions (Blozovski, 1983; Blozovski, 1985; Burhans and Gabriel, 2007; Deadwyler and Hampson, 2004; Harich et al, 2008; Izquierdo et al, 2008; Martin-Fardon et al, 2007; O'Mara et al, 2001; Van Cauter et al, 2008), information about whether and how nicotine influences these structures is important in understanding how nicotine affects memory.…”

Section: Introductionmentioning

confidence: 99%

Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex

Tu¹,

Gu²,

Shen³

et al. 2009

J. Neurosci.

View full text Add to dashboard Cite

The entorhinal cortex (EC) is a part of the hippocampal complex that is essential to learning and memory, and nicotine affects memory by activating nicotinic acetylcholine receptors (nAChRs) in the hippocampal complex. However, it is not clear what types of neurons in the EC are sensitive to nicotine and whether they play a role in nicotine-induced memory functions. Here, we have used voltage-sensitive dye imaging methods to locate the neuronal populations responsive to nicotine in entorhino-hippocampal slices and to clarify which nAChR subtypes are involved. In combination with patch-clamp methods, we found that a concentration of nicotine comparable to exposure during smoking depolarized neurons in layer VI of the EC (ECVI) by acting through the non-␣7 subtype of nAChRs. Neurons in the subiculum (Sb; close to the deep EC layers) also contain nicotine-sensitive neurons, and it is known that Sb neurons project to the ECVI. When we recorded evoked EPSCs (eEPSCs) from ECVI neurons while stimulating the Sb near the CA1 region, a low dose of nicotine not only enhanced synaptic transmission (by increasing eEPSC amplitude) but also enhanced plasticity by converting tetanus stimulationinduced short-term potentiation to long-term potentiation; nicotine enhanced synaptic transmission and plasticity of ECVI synapses by acting on both the ␣7 and non-␣7 subtypes of nAChRs. Our data suggest that ECVI neurons are important regulators of hippocampal function and plasticity during smoking.

show abstract

“…Appropriate control groups for these age differences (yokedand nonreinforced groups, respectively) have been developed for this test (52). Effects of administration of several chemicals on passive-avoidance responding have been described, including postnatal and prenatal benzodiazepines (53)(54)(55) and cholinergic agonists and antagonists (43,56,57).…”

Section: Avoidance Tasksmentioning

confidence: 99%

Appropriate end points for the characterization of behavioral changes in developmental toxicology.

Cuomo

Salvia

Petruzzi

et al. 1996

Environ Health Perspect

View full text Add to dashboard Cite

The present paper is devoted to second-and higher-tier test methods for the characterization of behavioral changes produced in rodents by exposure to noxious agents during development. The paper analyzes a series of end points that are informative about specific processes and underlying regulatory mechanisms but require greater technical sophistication and larger investments than first-tier end points. This applies to ultrasonic emissions in successive postnatal periods; to mother-pup interactions, including appropriate cross-fostering controls; to social (including sexual) interaction tests from the infantile to the young adult stage; and to a variety of conditioning and learning tests using both positive and negative reinforcement. Environ Health Perspect 104(Suppl 2): 307-315 (1996)

show abstract

Deficits in passive avoidance learning in young rats following mecamylamine injections in the hippocampo-entorhinal area

Cited by 24 publications

References 21 publications

Cholinergic modulation of pavlovian fear conditioning in rats: Differential effects of intrahippocampal infusion of mecamylamine and methyllycaconitine

Cholinergic modulation of pavlovian fear conditioning in rats: Differential effects of intrahippocampal infusion of mecamylamine and methyllycaconitine

Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex

Appropriate end points for the characterization of behavioral changes in developmental toxicology.

Contact Info

Product

Resources

About