<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet type="text/xsl" href="https://www.nitrc.org/themes/nitrc3.0/css/rss.xsl.php?feed=https://www.nitrc.org/export/rss20_forum.php?forum_id=4705" ?>
<?xml-stylesheet type="text/css" href="https://www.nitrc.org/themes/nitrc3.0/css/rss.css" ?>
<rss version="2.0"> <channel>
  <title>NITRC News Group Forum: acute-nicotine-administration-increases-bold-fmri-signal-in-brain-regions-involved-in-reward-signaling-and-compulsive-drug-intake-in-rats.</title>
  <link>http://www.nitrc.org/forum/forum.php?forum_id=4705</link>
  <description>
	&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Acute Nicotine Administration Increases BOLD fMRI Signal in Brain Regions Involved in Reward Signaling and Compulsive Drug Intake in Rats.&lt;/b&gt;&lt;/p&gt;          
        &lt;p&gt;Int J Neuropsychopharmacol. 2014 Oct 31;&lt;/p&gt;
        &lt;p&gt;Authors:  Bruijnzeel AW, Alexander JC, Perez PD, Bauzo-Rodriguez R, Hall G, Klausner R, Guerra V, Zeng H, Igari M, Febo M&lt;/p&gt;
        &lt;p&gt;Abstract&lt;br/&gt;
        BACKGROUND: Acute nicotine administration potentiates brain reward function and enhances motor and cognitive function. These studies investigated which brain areas are being activated by a wide range of doses of nicotine, and if this is diminished by pretreatment with the nonselective nicotinic receptor antagonist mecamylamine.&lt;br/&gt;
        METHODS: Drug-induced changes in brain activity were assessed by measuring changes in the blood oxygen level dependent (BOLD) signal using an 11.1-Tesla magnetic resonance scanner. In the first experiment, nicotine naïve rats were mildly anesthetized and the effect of nicotine (0.03-0.6mg/kg) on the BOLD signal was investigated for 10min. In the second experiment, the effect of mecamylamine on nicotine-induced brain activity was investigated.&lt;br/&gt;
        RESULTS: A high dose of nicotine increased the BOLD signal in brain areas implicated in reward signaling, such as the nucleus accumbens shell and the prelimbic area. Nicotine also induced a dose-dependent increase in the BOLD signal in the striato-thalamo-orbitofrontal circuit, which plays a role in compulsive drug intake, and in the insular cortex, which contributes to nicotine craving and relapse. In addition, nicotine induced a large increase in the BOLD signal in motor and somatosensory cortices. Mecamylamine alone did not affect the BOLD signal in most brain areas, but induced a negative BOLD response in cortical areas, including insular, motor, and somatosensory cortices. Pretreatment with mecamylamine completely blocked the nicotine-induced increase in the BOLD signal.&lt;br/&gt;
        CONCLUSIONS: These studies demonstrate that acute nicotine administration activates brain areas that play a role in reward signaling, compulsive behavior, and motor and cognitive function.&lt;br/&gt;
        &lt;/p&gt;&lt;p&gt;PMID: 25552431 [PubMed - as supplied by publisher]&lt;/p&gt;
    </description>
  <language>en-us</language>
  <copyright>Copyright 2000-2026 NITRC OSI</copyright>
  <webMaster></webMaster>
  <lastBuildDate>Fri, 01 May 2026 12:27:28 GMT</lastBuildDate>
  <docs>http://blogs.law.harvard.edu/tech/rss</docs>
  <generator>NITRC RSS generator</generator>
 </channel>
</rss>
