Mediation of passive avoidance learning by nicotinic hippocampo‐entorhinal components in young rats

Blozovski, Denise

doi:10.1002/dev.420180408

Cited by 15 publications

(12 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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%

See 1 more Smart Citation

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

Section: Introductionmentioning

confidence: 99%

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

show abstract

“…1979; Mattingly & Zolman, 1980;Nagy, 1979;Stehouwer & Campbell, 1980). The age-dependent improvement in response suppression learning has typically been ascribed to the maturation of central muscarinic (Blozovski & Hennocq, 1982;Ray & Nagy, 1978;Zolman, Mattingly, & Sahley, 1978) and nicotinic functioning (Blozovski, 1983(Blozovski, , 1985, with the nicotinic system being critical at an early age (10-to 14-days-of-age in the rat) and gradually being supplanted (at about 15-days-of-age) by the muscarinic system (Blozovski, 1983(Blozovski, , 1985. However, maturational changes in cholinergic functioning are not sufficient for explaining the age-dependent improvement in response suppression learning of the young chick (Zolman & Mattingly, 1982).…”

mentioning

confidence: 99%

“…However, maturational changes in cholinergic functioning are not sufficient for explaining the age-dependent improvement in response suppression learning of the young chick (Zolman & Mattingly, 1982). Moreover, Blozovski has suggested that an additional neurotransmitter system may be involved in the ontogeny of mammalian response suppression learning (Blozovski, 1985;.…”

mentioning

confidence: 99%

Dopamine D‐2 receptor mediation of response suppression learning of young rats

McDougall

Nonneman

1989

Developmental Psychobiology

View full text Add to dashboard Cite

In three experiments, the effects of augmenting or blocking dopamine (DA) D-2 receptor activity on the ontogeny of response suppression learning of preweanling rat pups were determined. In the initial experiment, rat pups were trained to traverse a straight alley for nipple attachment to an anesthetized dam. When footshock (0.2 mA, 0.5 sec) was made contingent on responding, younger (11- and 13-day-olds) rat pups were deficient to older (17- and 19-day-olds) pups at withholding punished responding. In the subsequent experiments, response suppression learning was assessed after injecting 11- and 17-day-old rat pups with the specific DA D-2 agonist, LY 171555 (0.005-, 0.01-, and 0.1-mg/kg, i.p.), or the specific DA D-2 antagonist, sulpiride (5.0-, 15.0-, and 50.0-mg/kg, i.p.). LY 171555 enhanced the punished responding of both the 11- and 17-day-old rat pups; whereas, sulpiride increased the punished responding of the 17-, but not the 11-day-olds. In four additional experiments, the effects of LY 171555 and sulpiride on the locomotor activity, nociception, and reinforcement processes of 17-day-old rat pups was assessed. Rat pups given LY 171555 (0.01 mg/kg, i.p.) exhibited enhanced locomotor activity and a trend towards hyperanalgesia using a hot plate task. Sulpiride (15.0 mg/kg, i.p.) completely antagonized LY 171555's activity enhancing effects and had hyperalgesic properties. In two experiments, sulpiride did not affect the nonpunished appetitive responding of the 17-day-olds; whereas, haloperidol-treated pups responded on fewer reinforced trials than did saline-treated pups. Therefore, these results indicate that the response suppression learning of 17-day-old rat pups is mediated, at least partially, by a DAD-2 receptor system, and that D-2 receptors are also involved in the locomotor activity and nociceptive responses of young rat pups.

show abstract

“…The hippocampus is critical for learning and memory [13, 14, 30, 63] and is an important site for cognitive dysfunction in a variety of neurodegenerative diseases including Alzheimer's disease (AD) [62]. The hippocampal formation is divided into four main subregions: the dentate gyrus, the hippocampal proper (including CA1, CA2, and CA3 regions), the subicular complex, and the entorhinal cortex (EC, including layers I–VI).…”

mentioning

confidence: 99%

Cholinergic receptors: functional role of nicotinic ACh receptors in brain circuits and disease

Yakel

2013

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

The neurotransmitter acetylcholine (ACh) can regulate neuronal excitability throughout the nervous system by acting on both the cys-loop ligand-gated nicotinic ACh receptor channels (nAChRs) and the G protein-coupled muscarinic ACh receptors (mAChRs). The hippocampus is an important area in the brain for learning and memory, where both nAChRs and mAChRs are expressed. The primary cholinergic input to the hippocampus arises from the medial septum and diagonal band of Broca, the activation of which can activate both nAChRs and mAChRs in the hippocampus and regulate synaptic communication and induce oscillations that are thought to be important for cognitive function. Dysfunction in the hippocampal cholinergic system has been linked with cognitive deficits and a variety of neurological disorders and diseases, including Alzheimer's disease and schizophrenia. My lab has focused on the role of the nAChRs in regulating hippocampal function, from understanding the expression and functional properties of the various subtypes of nAChRs, and what role these receptors may be playing in regulating synaptic plasticity. Here, I will briefly review this work, and where we are going in our attempts to further understand the role of these receptors in learning and memory, as well as in disease and neuroprotection.

show abstract

Mediation of passive avoidance learning by nicotinic hippocampo‐entorhinal components in young rats

Cited by 15 publications

References 42 publications

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

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

Dopamine D‐2 receptor mediation of response suppression learning of young rats

Cholinergic receptors: functional role of nicotinic ACh receptors in brain circuits and disease

Contact Info

Product

Resources

About