<?xml version="1.0" encoding="utf-8"?>
<XML>
<JOURNAL>
<YEAR>2006</YEAR>
<VOL>10</VOL>
<NO>3</NO>
<MOSALSAL>22</MOSALSAL>
<PAGE_NO>265</PAGE_NO>


<ARTICLES>

	<ARTICLE> 
		<TitleF>Editorial Committee:</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>1</FPAGE>
			<TPAGE>1</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/14
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1386/5/23
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The effect of bromocriptine on basal and histamine-stimulated gastric acid secretion in anesthetized rats </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: The protective and antisecretory effects of dopamine agonists on the
stomach have been already reported, but the effect of bromocriptine (D2 dopamine agonist)
on histamine stimulated gastric acid secretion (GAS) needs to be investigated.
Methods: For gastric sampling, animals were anesthetized and a polyethylen tube was
introduced into the stomach through esophagus. A cannula was also inserted into the
pyloroduodenal junction and passed up into the stomach.
Results: Our data showed that administration of bromocriptine (2 mg/kg), 60 minutes
before histamine infusion, did not affect basal acid secretion but significantly reduced
histamine-induced GAS (P&#60;0.01). Also, simultaneous application of bromocriptine and
histamine-infusion (0.8 mg/100g/h) had no effect on histamine-stimulated gastric acid
secretion. The inhibitory effect of bromocriptine on GAS did not change by sulpiride, a D2
dopamine antagonist. Plasma glucose level was constant in our experimental conditions.
Conclusion: Based on our data, we concluded that inhibitory effect of bromocriptine (2
mg/kg) on histamine stimulated acid output was probably mediated by non dopaminergic
receptors or unknown subtypes of D2 receptors which are not sensitive to sulpiride.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>173</FPAGE>
			<TPAGE>181</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/18
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1386/4/27
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Ali</Name>
				<MidName></MidName>
				<Family>Ghanbari</Family>
				<NameE>Ali</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ghanbari</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Afsaneh</Name>
				<MidName></MidName>
				<Family>Eliassi</Family>
				<NameE>Afsaneh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Eliassi</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>afeliassi@hotmail.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Bromocriptine. Sulpiride, Stimulated gastric acid secretion, Rat, Histamine</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Study of benzodiazepine like effect of Matricaria recutita extract on acute pain in the presence and absence of paragigantocellularis nucleus in adult male rats </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: In this study the effect of Matricaria recutita extract on acute pain in the 
presence and absence of flumazenil (antagonist of benzodiazepine) and lesioned 
paragigantocellularis (PGi) nucleus was investigated. 
Method: Wistar male rats (250±20 g) were used. Animals were grouped randomly into 
intact, sham and bilateral lesion of PGi nucleus. Intact and lesioned animals, each divided 
into 4 subgroups which received saline, M. recutita hydro-alcoholic extract (25 mg/kg), 
flumazenil (1 mg/kg) and flumazenil + M. recutita. Hot plate test were used for pain 
thereshold evaluation. 
Results: Results showed that: In intact animals M. recutita induced analgesic effect but 
flumazenil had significant hyperalgesic effect. In these animals flumazenil prevented the 
analgesic effects of M. recutita. Lesion of PGi induced significant hyperalgesia. M. recutita 
in absence of PGi nucleus showed significant analgesic effect and flumazenil increased pain 
sensation and caused significant hyperalgesia. The analgesic effect of M. recutita attenuated 
by flumazenil in absence of PGi nucleus. 
Conclusion: It seems that PGi nucleus involves in pain modulation but analgesic effect 
of M. recutita that may be via the benzodiazepine-like activity of some its components does 
not interact with PGi nucleus.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>183</FPAGE>
			<TPAGE>189</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/25
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1386/5/3
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Zahra</Name>
				<MidName></MidName>
				<Family>Abbasi zadeh</Family>
				<NameE>Zahra</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Abbasi zadeh</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mahnaz</Name>
				<MidName></MidName>
				<Family>Kesmati</Family>
				<NameE>Mahnaz</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Kesmati</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>mahnazkessmati@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Hadi</Name>
				<MidName></MidName>
				<Family>Fathi Moghaddam</Family>
				<NameE>Hadi</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Fathi Moghaddam</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Matricaria recutita, Paragigantocellularis nucleus, Flumazenil, Hot plate.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The modulatory effects of orexin B on the calcium channels activity in neuronal cells of Helix aspersa (garden snail) </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: The functional effects of orexin-B on the calcium spikes and excitability
of the neuronal soma membrane of garden snail, Helix aspersa were studied.
Methods: Conventional intracellular recording, under the current clamp conditions was
performed to examine the effects of orexin-B on the configuration and electrophysiological
properties of calcium spikes.
Results: Application of orexin-B (300 nM) led to a membrane depolarization and thereby
the increase in excitability of neurons. It also decreased the duration and the amplitude of
calcium spikes. On the other hand, orexin-B had a dual effect on the amplitude of afterhyper
polarization (AHP) in a time dependent manner. The maximum reduction of the
amplitude of AHP was recorded within 10 min of orexin-B exposure. However a maximum
increase in AHP amplitude was observed later (15 min after exposure to orexin-B).
Inactivation of G-proteins by pertussis toxin (100 nM) was used to test the involvement of
Gi/Go in the orexin-B induced modulation of calcium channels. Pre-incubation of ganglia
for 3-6 h with PTX blocked the depolarization effect of orexin-B on the resting membrane
potential. Orexin-B on pretreated neuronal cells with PTX did not statistically change the
calcium spike parameters, unless the peak amplitude of AHP increased remarkably.
Conclusion: In conclusion, these data suggest that orexin-B (300 nM) may affect the
membrane excitability and modulates the activity of calcium and calcium activated
potassium channels in snail neurons.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>191</FPAGE>
			<TPAGE>200</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/252009/05/6
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1388/2/16
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Ali</Name>
				<MidName></MidName>
				<Family>Rastqar</Family>
				<NameE>Ali</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Rastqar</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mahyar</Name>
				<MidName></MidName>
				<Family>Janahmadi</Family>
				<NameE>Mahyar</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Janahmadi</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>mjanahmadi@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Yaghub</Name>
				<MidName></MidName>
				<Family>Fathollahi</Family>
				<NameE>Yaghub</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Fathollahi</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mahyar</Name>
				<MidName></MidName>
				<Family>Janahmadi</Family>
				<NameE>Mahyar</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Janahmadi</FamilyE>
				<Organizations>
				<Organization>1Neuroscience Research Center and Dept. of  Physiology, Shahid Beheshti University (Medical Campus), Tehran,Iran .</Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>mjanahmadi@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Orexin-B, Pertussis toxin, Calcium  spike, Neuronal excitability, Snail, Electrophysiology.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The modulatory effects of orexin B on the calcium channels activity in neuronal cells of Helix aspersa (garden snail) </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: The functional effects of orexin-B on the calcium spikes and excitability
of the neuronal soma membrane of garden snail, Helix aspersa were studied.
Methods: Conventional intracellular recording, under the current clamp conditions was
performed to examine the effects of orexin-B on the configuration and electrophysiological
properties of calcium spikes.
Results: Application of orexin-B (300 nM) led to a membrane depolarization and thereby
the increase in excitability of neurons. It also decreased the duration and the amplitude of
calcium spikes. On the other hand, orexin-B had a dual effect on the amplitude of afterhyper
polarization (AHP) in a time dependent manner. The maximum reduction of the
amplitude of AHP was recorded within 10 min of orexin-B exposure. However a maximum
increase in AHP amplitude was observed later (15 min after exposure to orexin-B).
Inactivation of G-proteins by pertussis toxin (100 nM) was used to test the involvement of
Gi/Go in the orexin-B induced modulation of calcium channels. Pre-incubation of ganglia
for 3-6 h with PTX blocked the depolarization effect of orexin-B on the resting membrane
potential. Orexin-B on pretreated neuronal cells with PTX did not statistically change the
calcium spike parameters, unless the peak amplitude of AHP increased remarkably.
Conclusion: In conclusion, these data suggest that orexin-B (300 nM) may affect the
membrane excitability and modulates the activity of calcium and calcium activated
potassium channels in snail neurons.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>191</FPAGE>
			<TPAGE>200</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/252009/05/62007/07/25
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1386/5/3
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Orexin-B, Pertussis toxin, Calcium  spike, Neuronal excitability, Snail, Electrophysiology.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The modulatory effects of orexin B on the calcium channels activity in neuronal cells of Helix aspersa (garden snail) </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: The functional effects of orexin-B on the calcium spikes and excitability
of the neuronal soma membrane of garden snail, Helix aspersa were studied.
Methods: Conventional intracellular recording, under the current clamp conditions was
performed to examine the effects of orexin-B on the configuration and electrophysiological
properties of calcium spikes.
Results: Application of orexin-B (300 nM) led to a membrane depolarization and thereby
the increase in excitability of neurons. It also decreased the duration and the amplitude of
calcium spikes. On the other hand, orexin-B had a dual effect on the amplitude of afterhyper
polarization (AHP) in a time dependent manner. The maximum reduction of the
amplitude of AHP was recorded within 10 min of orexin-B exposure. However a maximum
increase in AHP amplitude was observed later (15 min after exposure to orexin-B).
Inactivation of G-proteins by pertussis toxin (100 nM) was used to test the involvement of
Gi/Go in the orexin-B induced modulation of calcium channels. Pre-incubation of ganglia
for 3-6 h with PTX blocked the depolarization effect of orexin-B on the resting membrane
potential. Orexin-B on pretreated neuronal cells with PTX did not statistically change the
calcium spike parameters, unless the peak amplitude of AHP increased remarkably.
Conclusion: In conclusion, these data suggest that orexin-B (300 nM) may affect the
membrane excitability and modulates the activity of calcium and calcium activated
potassium channels in snail neurons.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>191</FPAGE>
			<TPAGE>200</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/252009/05/62007/07/252007/03/10
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1385/12/19
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/152014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Orexin-B, Pertussis toxin, Calcium  spike, Neuronal excitability, Snail, Electrophysiology.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The modulatory effects of orexin B on the calcium channels activity in neuronal cells of Helix aspersa (garden snail) </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: The functional effects of orexin-B on the calcium spikes and excitability
of the neuronal soma membrane of garden snail, Helix aspersa were studied.
Methods: Conventional intracellular recording, under the current clamp conditions was
performed to examine the effects of orexin-B on the configuration and electrophysiological
properties of calcium spikes.
Results: Application of orexin-B (300 nM) led to a membrane depolarization and thereby
the increase in excitability of neurons. It also decreased the duration and the amplitude of
calcium spikes. On the other hand, orexin-B had a dual effect on the amplitude of afterhyper
polarization (AHP) in a time dependent manner. The maximum reduction of the
amplitude of AHP was recorded within 10 min of orexin-B exposure. However a maximum
increase in AHP amplitude was observed later (15 min after exposure to orexin-B).
Inactivation of G-proteins by pertussis toxin (100 nM) was used to test the involvement of
Gi/Go in the orexin-B induced modulation of calcium channels. Pre-incubation of ganglia
for 3-6 h with PTX blocked the depolarization effect of orexin-B on the resting membrane
potential. Orexin-B on pretreated neuronal cells with PTX did not statistically change the
calcium spike parameters, unless the peak amplitude of AHP increased remarkably.
Conclusion: In conclusion, these data suggest that orexin-B (300 nM) may affect the
membrane excitability and modulates the activity of calcium and calcium activated
potassium channels in snail neurons.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>191</FPAGE>
			<TPAGE>200</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/252009/05/62007/07/252007/03/102007/03/10
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1385/12/19
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Orexin-B, Pertussis toxin, Calcium  spike, Neuronal excitability, Snail, Electrophysiology.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The effect of parameters of low-frequency electrical stimulation on piriform-cortex kindled seizures in rat </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Electrical low-frequency stimulation (LFS) has antiepileptic effect, but the
role of different stimulation parameters on this effect has not been determined. In this study
the effect of different LFS parameters (intensity, pulse duration and train duration) on
piriform-cortex kindled seizures was investigated.
Methods: Seizure was produced in animals using kindling model of epilepsy. Then, the
effect of LFS on seizure severity was investigated.
Results: Different patterns of LFS (1 Hz) applied immediately before kindling
stimulation in fully kindled animals, had no significant effect on seizure parameters. In the
second experiment, effect of LFS (1 Hz) on inter-seizure interval was investigated. Data
showed that daily stimulation of animals for 15 min with LFS for one week after the last
kindling stimulation reduced significantly stage 5 seizure duration. Application of the same
LFS protocols for three days and two weeks had no significant effect on seizure parameters.
In the third experiment, effect of LFS (1 Hz) on kindling rate was investigated. Results
showed that when LFS was delivered daily after each kindling stimulation it could decrease
afterdischarge duration in various days during kindling and delayed the appearance of
seizure stages 1 and 2 significantly.
Conclusion: It may be concluded that LFS has antiepileptic effects on kindling
acquisition and inter-seizure interval in kindled animals and that the characteristics of LFS
protocol (intensity, pulse duration and train duration) have an essential role on these effects.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>201</FPAGE>
			<TPAGE>210</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/252009/05/62007/07/252007/03/102007/03/102007/07/25
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1386/5/3
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Parviz</Name>
				<MidName></MidName>
				<Family>Ghorbani Moghadam</Family>
				<NameE>Parviz</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Ghorbani Moghadam</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohammad</Name>
				<MidName></MidName>
				<Family>Mohammad-Zadeh,</Family>
				<NameE>Mohammad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mohammad-Zadeh,</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Javad</Name>
				<MidName></MidName>
				<Family>Mirnajafi-Zadeh</Family>
				<NameE>Javad</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Mirnajafi-Zadeh</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>mirnajaf@modares.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Yaghub</Name>
				<MidName></MidName>
				<Family>Fathollahi</Family>
				<NameE>Yaghub</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Fathollahi</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Low-frequency stimulation, Epilepsy, Kindling, Piriform cortex.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The effects of testosterone and naloxone treatments on fear behavior in gonadectomized rats </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Effective perception of fear signals is crucial for organism survival. When
threated, the organism indicates defensive behaviors.
Methods: Elevated plus–maze has high efficiency for measurement of fear behavior and
is widly used for fear behavior determination. Increase in two parameters percent of openarm
entries (%OAE) and percent of time spent in the open-arm (%OAT) in the elevated
plus- maze were considered as the indexes of fear reduction effect. In this study, the effect
of testosterone and naloxone on fear behavior of gonadectomized rats (GDX) was
investigated. Also, the interaction of testosterone with naloxone was investigated.
Results: Subcutaneous (SC) injections of different doses of testosterone (100, 200, 300,
450 μg /rat) increased the %OAE and %OAT in a dose dependent manner. Maximum
response was obtained by 450 μg/rat dose of testosterone (P&#60;0.001). SC injections of opioid
receptors antagonist, naloxone 1, 2.5, 5, 7.5 mg / kg reduced %OAE and %OAT (P&#60;0.01) .
Conclusion: It may be concluded that testosterone decreases fear behavior and naloxone
increased fear behavior. Also the results indicate that there is an interaction between
testosteone and naloxone (P&#60;0.001).</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>211</FPAGE>
			<TPAGE>217</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/252009/05/62007/07/252007/03/102007/03/102007/07/252007/07/25
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1386/5/3
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Fatemeh</Name>
				<MidName></MidName>
				<Family>Khakpay</Family>
				<NameE>Fatemeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khakpay</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Parvin</Name>
				<MidName></MidName>
				<Family>Rostami</Family>
				<NameE>Parvin</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Rostami</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>rostami@saba.tmu.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Aliasghar</Name>
				<MidName></MidName>
				<Family>Pilevarian</Family>
				<NameE>Aliasghar</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Pilevarian</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Gonadectomy, Testosterone, Naloxone, Open arm entries , Time spent in the open arm.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Study of the effects of Neuropeptide Y injections on plasma concentrations of Thyroxine and triiodothyronine in goat </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Neuropeptide Y (NPY) is the most abundant peptide present in mammals'
brains. The majority of NPY-producing neurons is in arcuate and paraventricular nuclei of
hypothalamus which affect hypophysiotrapic factors secretion. In this study we investigated
the effect of intravenous injections of various doses of NPY on thyroxine (T4) and
triiodothyronine (T3) serum concentrations.
Methods: Sixteen adult male sannan goats were assigned to four treatment groups.
Treatments were included daily injections of 0, 10, 20 and 40 μg NPY per kg body weight
named C, L, M and H, respectively. The duration of experiments was 13 consecutive days
divided into three intervals pre-treatment (days 1-3), treatment (days 4-10) and posttreatment
(days 11-14). Blood collections were being done throughout the experiment at
09:00 via jugular vein and injections were in treatment interval via carotid artery at 08:00.
Blood samples were centrifuged and the sera were harvested and used for hormone assay
via radioimmunoassay.
Results: Results showed that treatment H caused 11-fold increase in T4 concentrations and
4-fold increase in T3 concentrations ones versus treatment C (P&#60;0.001). Treatment M also
increased T4 and T3 significantly (P&#60;0.001). The effect of treatment L on T4 concentrations
was significantly incremental (P&#60;0.001) but it has no effect on T3 concentrations (P=0.877).
The stimulatory effect of NPY on thyroid hormones was transient because in post-treatment
interval, T4 and T3 concentrations in treatments L, M and H tended to decline but were yet
significantly higher versus treatment C.
Conclusion: Previous studies in rodents demonstrated inhibitory effect of NPY on
thyroid hormones but in present study completely stimulatory and dose-dependent effects of
NPY on these hormones secretion in goat were observed. thus, we suggest the stimulatory
effect of NPY on thyrotrop axis in ruminants. This discrepancy can be due to different
methodology and difference in neuroendocrine framework controlling thyrotrop axis of
ruminants with rodents.
Key words: Neuropeptide Y, Thyroxine, Triiodothyronine, Radioimmunoassay, Goat</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>219</FPAGE>
			<TPAGE>227</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/252009/05/62007/07/252007/03/102007/03/102007/07/252007/07/252007/07/25
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1386/5/3
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Farid</Name>
				<MidName></MidName>
				<Family>Moslemipur</Family>
				<NameE>Farid</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Moslemipur</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>Moslemipurf@gau.ac.ir</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Homayoun</Name>
				<MidName></MidName>
				<Family>Khazali</Family>
				<NameE>Homayoun</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khazali</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mohammad Ali</Name>
				<MidName></MidName>
				<Family>Emami meybodi</Family>
				<NameE>Mohammad Ali</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Emami meybodi</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Neuropeptide Y, Thyroxine, Triiodothyronine, Radioimmunoassay, Goat</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The inhibitory effect of Paraoxon on cerebellar synaptosome GABA uptake in rats </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Compounds which are used to treat organophosphate (OP) poisoning are
not able to fully alleviate long lasting effects. They are mainly used to antagonize
cholinergic effects of Ops. However, non-cholinergic effects, such as interference with
different neurotransmitter systems, especially GABA release and uptake, are recently
attracting more attentions. We have tried to investigate any potential interaction between
paraoxon and GABA uptake.
Methods: We used cerebellar synaptosomes. Cerebellum of 250-280 g Wistar rats were
rapidly dissected out, homogenized, centrifuged, and incubated with 0.01 μ M [3H]GABA
in the presence of different doses of paraoxon for 10 minutes at 37 oC. At the end of the
incubation period, synaptosomes were layered in chambers of superfusion system. In order
to assay the amounts of [3H]GABA taken up, radioactivity was measured using a β-counter.
Results: Our findings reveal that mean GABA uptake was 111.42, 95.37, 71.6, 73.53 and
75 percent of the control values in the presence of different concentrations of paraoxon
(0.01, 0.1, 1, 10 and 100μ M) respectively. GABA uptake was significantly reduced at
doses 1, 10 and 100μ M (p&#60;0.05).
Conclusion: It seems that paraoxon at higher doses may interfere with GABA uptake by cerebellar
synaptosomes.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>229</FPAGE>
			<TPAGE>237</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/252009/05/62007/07/252007/03/102007/03/102007/07/252007/07/252007/07/252007/07/25
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1386/5/3
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Ameneh</Name>
				<MidName></MidName>
				<Family>Shahroukhi</Family>
				<NameE>Ameneh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Shahroukhi</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Asghar</Name>
				<MidName></MidName>
				<Family>Qassemi</Family>
				<NameE>Asghar</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Qassemi</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Fereshteh</Name>
				<MidName></MidName>
				<Family>Pourabdolhossein</Family>
				<NameE>Fereshteh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Pourabdolhossein</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Ali</Name>
				<MidName></MidName>
				<Family>Khoshbaten</Family>
				<NameE>Ali</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Khoshbaten</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Alireza</Name>
				<MidName></MidName>
				<Family>Asgari</Family>
				<NameE>Alireza</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Asgari</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>asgari@bmsu.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Organophosphate, Paraoxon, Superfusion, Synaptosome, GABA</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>The interaction of GABA and glutamate on the cardiovascular responses of horizon tal limb of diagonal band of Broca (hDB)</TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: We previously shown that microinjection of glutamate into the hDB of rat
elicited cardiovascular depressive responses. Microinjection of AP5 (an NMDA receptor
antagonist, 2.5 mM, 50 nl) and CNQX (an AMPA receptor antagonist, 1 mM, 50 nl) caused
no significant changes in the blood pressure and heart rate. Microinjection of bicuculline
(BMI: a GABAA receptor antagonist, 1 mM, 50 nl) resulted in the increased blood pressure
and heart rate. In this study we investigated the possible interaction of GABAergic and
glutaminergic systems by coinjection of the antagonists of both systems.
Methods: Experiments were performed on 27 urethane anesthetized rats. Drugs were
microinjected into the hDB using micropipettes. The arterial pressure and heart rate were
continuously recorded and repeated measures ANOVA was used for data analysis.
Results: Our results showed that coinjection of 50 nl of BMI (1mM ) and AP5 (2.5 mM)
significantly (P &#60; 0. 01) decreased the presser effects of BMI. Also, coinjection of 50 nl of
BMI (1 mM) and CNQX (1 mM) significantly (P &#60; 0.01) decreased the presser effects of
BMI. Microinjection of the doses of BMI and two glutamate receptor antagonists produced
the same results.
Conclusion: These findings suggest that the cardiovascular effects of the blockade of
GABAergic system depend on the activation of local NMDA and AMPA receptors. A
possible explanation for the results is that, GABAergic system tonically inhibits the
glutaminergic neurons.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>239</FPAGE>
			<TPAGE>246</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/252009/05/62007/07/252007/03/102007/03/102007/07/252007/07/252007/07/252007/07/252007/07/25
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1386/5/3
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Ali</Name>
				<MidName></MidName>
				<Family>Nasimi</Family>
				<NameE>Ali</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Nasimi</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Masoumeh</Name>
				<MidName></MidName>
				<Family>Hatam</Family>
				<NameE>Masoumeh</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Hatam</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>hatam_m@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Diagonal band of Broca, GABA, Glutamate, Blood Pressure</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Comparison of the effects of topical hydrocortison and clobetasole phonophoresis on reduction of pain in osteoarthritic knee joint </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Phonophoresis is the use of ultrasound to enhancing cellular drug delivery
through the skin. In this study the effect of clobethasole and hydrocortisone ointments
phonophoresis on pain, knee osteoarthritis and some other symptoms was studied.
Methods: An experimental single blind randomized clinical trial (RCT) was used. An
available sampling technique was used for selection of patients. Sixty subjects with
osteoarthritic knee (tibiofemoral) joints were randomly assigned to six groups: 1-Ultrasound
with acoustic gel. 2- Placebo ultrasound with hydrocortisone. 3- Placebo ultrasound with
clobetasole. 4- Hydrocortisone phonophoresis. 5- Clobetasole phonophoresis. 6- Placebo
ultrasound with acoustic gel. All of the patients received treatments for ten sessions. Pain
level was determined by visual analog scale (VAS) at the beginning, day 6 and follow up
day (11th session). Edema and knee range of motion (ROM) were measured at the
beginning, day 4, day 7 and follow up day. 20 meters walking test time was measured at the
beginning and follow up day. Wilcoxon and Friedman statistical tests were used to analyze
data.
Results: At the end of treatment sessions groups 1, 4, 5 showed a significant decrease in
pain and edema and an increase in knee ROM and 20 meters walking test time (P &#60; 0.05).
Additionally, there was a significant difference in improvement rates between group 5 and
groups 1 and 4..
Conclusion: This study showed that both hydrocortisone and clobetasole phonophoresis
were more effective than ultrasound and acoustic gel on osteoarthritic pain of knee joint.
Clobetasole has a faster effect than other treatments.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>247</FPAGE>
			<TPAGE>258</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/252009/05/62007/07/252007/03/102007/03/102007/07/252007/07/252007/07/252007/07/252007/07/252007/07/25
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1386/5/3
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Tohid</Name>
				<MidName></MidName>
				<Family>Sedghimehr</Family>
				<NameE>Tohid</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Sedghimehr</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Farid</Name>
				<MidName></MidName>
				<Family>Bahrpeima</Family>
				<NameE>Farid</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Bahrpeima</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>bahrpeyf@modares.ac.ir</Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>phonophoresis, hydrocortisone, clobetasole, osteoarthrit.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>


	<ARTICLE> 
		<TitleF>Study of interaction between opioid and ?-2 adrenergic systems in analgesic effect of oxytocin in locus coeruleus nucleus </TitleF>
		<TitleE></TitleE>
		<TitleLang_ID>2</TitleLang_ID>
		<ABSTRACTS>
			<ABSTRACT>
			<Language_ID>2</Language_ID>
			<CONTENT>Introduction: Oxytocin is a active neuropeptide of central nervous system. In this study
the effects of naloxone (opioid receptor antagonist) and yohimbine (α-2 adrenergic receptor
antagonist) on analgesic effect of oxytocin applied into the locus coeruleus (LC) nucleus
were investigated.
Methods: Adult male Wistar rats were used. Animals divided into different groups
receiving saline, oxytocin (3 nmol / 2μl), naloxone (3 nmol / 2μl) + oxytocin, yohimbine (3
nmol / 2μl) + oxytocin, and naloxone + yohimbine + oxytocin. Hot-plate and tail-flick tests
were used to evaluate pain threshold.
Results: Data showed that the injection of oxytocin into the LC nucleus increases the
response time to thermal stimulations in both tail flick and hot plate tests. Injection of
naloxone and yohimbine either separately and or in combination inhibite the antinociception
effect of oxytocin.
Conclusion: It seems that oxytocin induces its inhibitory effect on acute pain via LC
nucleus. This effect is probably mediated by the combination of opioid and α-2 adrenergic
systems.</CONTENT>
			</ABSTRACT>
		</ABSTRACTS>

		<PAGES>
			<PAGE>
			<FPAGE>259</FPAGE>
			<TPAGE>265</TPAGE>
			</PAGE>
		</PAGES>

		<RECEIVE_DATE>
			2007/08/142007/07/182007/07/252009/05/62007/07/252007/03/102007/03/102007/07/252007/07/252007/07/252007/07/252007/07/252007/07/252007/07/25
		</RECEIVE_DATE>

		<RECEIVE_DATE_FA>
			1386/5/3
		</RECEIVE_DATE_FA>

		<ACCEPT_DATE>
			2014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/152014/05/15
		</ACCEPT_DATE>

		<ACCEPT_DATE_FA>
			1393/2/25
		</ACCEPT_DATE_FA>

		<AUTHORS>
			<AUTHOR>
				<Name>Nasrin</Name>
				<MidName></MidName>
				<Family>haghighi</Family>
				<NameE>Nasrin</NameE>
				<MidNameE></MidNameE>
				<FamilyE>haghighi</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email>ns_haghighi@yahoo.com</Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Mahnaz</Name>
				<MidName></MidName>
				<Family>Kessmati</Family>
				<NameE>Mahnaz</NameE>
				<MidNameE></MidNameE>
				<FamilyE>Kessmati</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>

			<AUTHOR>
				<Name>Hadi</Name>
				<MidName></MidName>
				<Family>fathi Moghadam2</Family>
				<NameE>Hadi</NameE>
				<MidNameE></MidNameE>
				<FamilyE>fathi Moghadam2</FamilyE>
				<Organizations>
				<Organization></Organization>
				</Organizations>
				<Countries>
				<Country></Country>
				</Countries>
				<EMAILS>
				<Email></Email>
				</EMAILS>
			</AUTHOR>
		</AUTHORS>


		<KEYWORDS>
			<KEYWORD>
				<KeyText>Oxytocin, Pain, Yohembine, Naloxone, Locus coeruleus nucleus.</KeyText>
			</KEYWORD>
		</KEYWORDS>

		<REFRENCES>
			<REFRENCE>
				<REF>## ##</REF>
			</REFRENCE>
		</REFRENCES>

	</ARTICLE>

</ARTICLES>

</JOURNAL>
</XML>
