Effects of ventral hippocampal galanin on spatial learning and on in vivo acetylcholine release in the rat

So, Ogren; Kehr, Ján; Pa, Schött

doi:10.1016/0306-4522(96)00215-1

Cited by 108 publications

(80 citation statements)

References 44 publications

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“…While there is debate on assigning function to each of these hippocampal sub-regions, the DHPC is considered by some to be necessary for learning and memory processes that involve the utilization of spatial information, whereas the VHPC is linked with learning processes that involve an emotional or motivational component (de Hoz et al, 2003;Bannerman et al, 2004;Fanselow and Dong, 2010). This differentiation of function, however, is complicated by several findings showing that VHPC lesions or inactivation interferes with spatial memory processing (eg Ogren et al, 1996;Schott et al, 1998;Wilkerson and Levin, 1999;Levin et al, 1999;Ferbinteanu and McDonald, 2001;de Hoz et al, 2003). Here we show that VHPC leptin signaling modulates the consolidation of memory for the spatial location of food, which further challenges the belief that hippocampal spatial memory processing is mediated exclusively by the dorsal region.…”

Section: Discussionmentioning

confidence: 90%

Hippocampal Leptin Signaling Reduces Food Intake and Modulates Food-Related Memory Processing

Kanoski

Hayes

Greenwald

et al. 2011

Neuropsychopharmacol

137

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The increase in obesity prevalence highlights the need for a more comprehensive understanding of the neural systems controlling food intake; one that extends beyond food intake driven by metabolic need and considers that driven by higher-order cognitive factors. The hippocampus, a brain structure involved in learning and memory function, has recently been linked with food intake control. Here we examine whether administration of the adiposity hormone leptin to the dorsal and ventral sub-regions of the hippocampus influences food intake and memory for food. Leptin (0.1 mg) delivered bilaterally to the ventral hippocampus suppressed food intake and body weight measured 24 h after administration; a higher dose (0.4 mg) was needed to suppress intake following dorsal hippocampal delivery. Leptin administration to the ventral but not dorsal hippocampus blocked the expression of a conditioned place preference for food and increased the latency to run for food in an operant runway paradigm. Additionally, ventral but not dorsal hippocampal leptin delivery suppressed memory consolidation for the spatial location of food, whereas hippocampal leptin delivery had no effect on memory consolidation in a non-spatial appetitive response paradigm. Collectively these findings indicate that ventral hippocampal leptin signaling contributes to the inhibition of food-related memories elicited by contextual stimuli. To conclude, the results support a role for hippocampal leptin signaling in the control of food intake and food-related memory processing.

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Section: Discussionmentioning

confidence: 90%

Hippocampal Leptin Signaling Reduces Food Intake and Modulates Food-Related Memory Processing

Kanoski

Hayes

Greenwald

et al. 2011

Neuropsychopharmacol

137

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“…The interval between the s.c. administration of scopolamine and training in this study was 40 min, which is longer than in most previous PA studies (varying usually between 5 and 30 min) (Bammer, 1982). The choice of this time interval was based on in vivo microdialysis studies, in which s.c. scopolamine produced an increase in the ACh levels in the ventral hippocampus with a peak effect after 40-60 min (Antoniou et al, 1997;Ö gren et al, 1996;Toide and Arima, 1989).…”

Section: Discussionmentioning

confidence: 95%

“…Scopolamine markedly elevates extrasynaptic ACh at the time of PA training mainly because of the blockade of presynaptic M 2 muscarinic receptors (Ö gren et al, 1996;Stillman et al, 1996). At the same time scopolamine blocks and scopolamine (0.2 mg/kg s.c.) 90 and 40 min before the training session, respectively.…”

Section: Discussionmentioning

confidence: 99%

Selective 5-HT1A Antagonists WAY 100635 and NAD-299 Attenuate the Impairment of Passive Avoidance Caused by Scopolamine in the Rat

Misane

Ögren

2003

Neuropsychopharmacol

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Systemic administration of the muscarinic-receptor antagonists atropine and scopolamine produces cognitive deficits in humans, nonhuman primates and rodents. In humans, these deficits resemble symptoms of dementia seen in Alzheimer's disease. The passive avoidance (PA) task has been one of the most frequently used animal models for studying cholinergic mechanisms in learning and memory. The present study examined the ability of two selective 5-HT 1A receptor antagonists WAY 100635 and NAD-299 (robalzotan) and two acetylcholinesterase (AChE) inhibitors tacrine and donepezil to attenuate the impairment of PA retention caused by the nonselective muscarinic receptor antagonist scopolamine in the rat. Although demonstrating differences in their temporal kinetics, both WAY 100635 and NAD-299 attenuated the impairment of PA caused by scopolamine (0.3 mg/kg s.c.). Donepezil did not block the PA deficit caused by the 0.3 mg/kg dose of scopolamine, but it prevented the inhibitory effects of the 0.2 mg/kg dose of scopolamine. In contrast, tacrine was effective vs both the 0.2 and 0.3 mg/kg doses of scopolamine. These results indicate that (1) a functional 5-HT 1A receptor antagonism can attenuate the anterograde amnesia produced by muscarinic-receptor blockade, and (2) the AChE inhibitors tacrine and donepezil differ in their ability to modify muscarinic-receptor-mediated function in vivo. These results suggest that 5-HT 1A receptor antagonists may have a potential in the treatment of cognitive symptoms in psychopathologies characterized by reduced ACh transmission such as Alzheimer's disease.

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“…It was surrounded by visual extra-maze cues throughout the experiment. 27 The tank was filled with opaque water (at 22-231C) and contained a circular transparent escape platform, submerged 1 cm Experimental procedure All animals were habituated to the experimental room for 30 min prior to testing.…”

Section: Drugsmentioning

confidence: 99%

Influenza A virus infection causes alterations in expression of synaptic regulatory genes combined with changes in cognitive and emotional behaviors in mice

et al. 2004

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Epidemiological studies have indicated a link between certain neuropsychiatric diseases and exposure to viral infections. In order to examine long-term effects on behavior and gene expression in the brain of one candidate virus, we have used a model involving olfactory bulb injection of the neuro-adapted influenza A virus strain, WSN/33, in C57Bl/6 mice. Following this olfactory route of invasion, the virus targets neurons in the medial habenular, midline thalamic and hypothalamic nuclei as well as monoaminergic neurons in the brainstem. The mice survive and the viral infection is cleared from the brain within 12 days. When tested 14-20 weeks after infection, the mice displayed decreased anxiety in the elevated plus-maze and impaired spatial learning in the Morris water maze test. Elevated transcriptional activity of two genes encoding synaptic regulatory proteins, regulator of G-protein signaling 4 and calcium/calmodulindependent protein kinase IIa, was found in the amygdala, hypothalamus and cerebellum. It is of particular interest that the gene encoding RGS4, which has been related to schizophrenia, showed the most pronounced alteration. This study indicates that a transient influenza virus infection can cause persistent changes in emotional and cognitive functions as well as alterations in the expression of genes involved in the regulation of synaptic activities.

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Effects of ventral hippocampal galanin on spatial learning and on in vivo acetylcholine release in the rat

Cited by 108 publications

References 44 publications

Hippocampal Leptin Signaling Reduces Food Intake and Modulates Food-Related Memory Processing

Hippocampal Leptin Signaling Reduces Food Intake and Modulates Food-Related Memory Processing

Selective 5-HT1A Antagonists WAY 100635 and NAD-299 Attenuate the Impairment of Passive Avoidance Caused by Scopolamine in the Rat

Influenza A virus infection causes alterations in expression of synaptic regulatory genes combined with changes in cognitive and emotional behaviors in mice

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