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1.
Rev Neurol ; 47(9): 471-6, 2008.
Artigo em Espanhol | MEDLINE | ID: mdl-18985597

RESUMO

INTRODUCTION: According to the model of emotions, feelings have their origin in the conscious perception of body changes produced in response to an emotional stimulus. These changes are perceived thanks to the fact that they are represented in the brain by the interoceptive system. During abstinence, addicts experience intense feelings of ill-being that drive them to consume drugs. The purpose of this review is to discuss the role played by the interoceptive system, and more especially the insular cortex, in the perception of the negative feelings that characterise abstinence. DEVELOPMENT: The continuous processing of interoceptive signals in the insular cortex is what accounts for the conscious appreciation of the body changes that accompany an emotional state. Temporary inactivation of the insular cortex suppresses the search for drugs in addicted rats. Neuroimaging studies reveal an increase in the neuronal activity in the insular cortex and in other areas of the brain while addicts are experiencing the craving to consume drugs. Likewise, nicotine addicts who suffer a brain injury that affects the insular cortex give up smoking easily because they lose the desire to do it. The temporary suppression of neuronal activity in the insular cortex in human addicts by means of non-invasive techniques could be a new therapy to treat the craving to consume drugs. CONCLUSIONS: The insular cortex is essential in the perception of the emotional states and in orienting behaviour to match the needs of the body. New therapies that have the insular cortex as their target could be developed to mitigate craving.


Assuntos
Emoções/fisiologia , Drogas Ilícitas , Transtornos Relacionados ao Uso de Substâncias/fisiopatologia , Transtornos Relacionados ao Uso de Substâncias/psicologia , Animais , Comportamento Aditivo/fisiopatologia , Comportamento Aditivo/psicologia , Córtex Cerebral/anatomia & histologia , Córtex Cerebral/fisiologia , Humanos , Transtornos Relacionados ao Uso de Substâncias/terapia
2.
Neuroscience ; 106(4): 745-55, 2001.
Artigo em Inglês | MEDLINE | ID: mdl-11682160

RESUMO

Visceral sensory perception is subjected to modulation by attention or distraction, like other sensory systems. The thalamic reticular nucleus is a key region in selective attention, effecting a change in the mode of thalamocortical transmission. Each major thalamocortical system is connected with a particular sector of the thalamic reticular nucleus. No connections from the thalamic reticular nucleus have been described to the visceral sensory thalamus. We used axonal tracing techniques to study the possible existence of reciprocal connections between the visceral sensory relay in the lateral ventroposterior parvicellular thalamic nucleus, and the reticular nucleus of the thalamus. We also studied the projections from the visceral sensory cortex, located in the granular insular cortex in the rat, to the reticular nucleus of the thalamus. We found a convergent input from both thalamic and cortical sensory visceral regions to the same sector of the reticular nucleus of the thalamus. This visceral sector in turn sent GABAergic feedback connections to the lateral ventroposterior parvicellular thalamic nucleus. In addition, the visceral thalamus received histaminergic projections from the tuberomammillary nucleus, and noradrenergic projections from the locus coeruleus; both nuclei belong to the ascending activating system. Our findings indicate that the visceral sensory thalamocortical pathway is connected to the same subcortical structures that provide attention mechanisms for other thalamocortical systems.


Assuntos
Córtex Cerebral/citologia , Núcleos Intralaminares do Tálamo/citologia , Vias Neurais/citologia , Neurônios/citologia , Núcleos Ventrais do Tálamo/citologia , Fibras Aferentes Viscerais/citologia , Ácido gama-Aminobutírico/metabolismo , Animais , Tronco Encefálico/citologia , Tronco Encefálico/metabolismo , Córtex Cerebral/metabolismo , Glutamato Descarboxilase/metabolismo , Imuno-Histoquímica , Núcleos Intralaminares do Tálamo/metabolismo , Isoenzimas/metabolismo , Sondas Moleculares , Inibição Neural/fisiologia , Vias Neurais/metabolismo , Neurônios/metabolismo , Terminações Pré-Sinápticas/metabolismo , Terminações Pré-Sinápticas/ultraestrutura , Ratos , Ratos Sprague-Dawley , Núcleos Ventrais do Tálamo/metabolismo , Fibras Aferentes Viscerais/metabolismo
3.
Biol Reprod ; 63(2): 635-42, 2000 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-10906075

RESUMO

The mechanism by which GnRH increases sperm-zona pellucida binding in humans was investigated in this study. We tested whether GnRH increases sperm-zona binding in Ca(2+)-free medium and in the presence of Ca(2+) channel antagonists. We also examined the GnRH effect on the intracellular free Ca(2+) concentration ([Ca(2+)](i)). Sperm treatment with GnRH increased sperm-zona binding 300% but only when Ca(2+) was present in the medium. In Ca(2+)-free medium or in the presence of 400 nM nifedipine, 80 microM diltiazem, or 50 microM verapamil, GnRH did not influence sperm-zona binding. GnRH increased the [Ca(2+)](i) in the sperm in a dose-dependent manner. The maximum effect was reached with 75 nM GnRH. The GnRH-induced increase in [Ca(2+)](i) was fast and transient, from a basal [Ca(2+)](i) of 413 +/- 22 nM to a peak value of 797 +/- 24 nM. The GnRH-induced increase in [Ca(2+)](i) was entirely due to a Ca(2+) influx from the extracellular medium because the increase in [Ca(2+)](i) was blocked by the Ca(2+) chelator EGTA and by the Ca(2+) channel antagonists nifedipine and diltiazem. These antagonists, however, were not able to inhibit the progesterone-activated Ca(2+) influx. On the contrary, T-type calcium channel antagonists pimozide and mibefradil did not affect GnRH-activated Ca(2+) influx but inhibited the progesterone-activated Ca(2+) influx. Finally, the GnRH-induced Ca(2+) influx was blocked by two specific GnRH antagonists, Ac-D-Nal(1)-Cl-D-Phe(2)-3-Pyr-D-Ala(3)-Arg(5)-D-Glu(AA)(6)-GnRH and Ac-(3,4)-dehydro-Pro(1),-p-fluoro-D-Phe(2), D-Trp(3,6)-GnRH. These results suggest that GnRH increases sperm-zona binding via an elevation of [Ca(2+)](i) through T-type, voltage-operated calcium channels.


Assuntos
Canais de Cálcio/fisiologia , Cálcio/metabolismo , Hormônio Liberador de Gonadotropina/farmacologia , Interações Espermatozoide-Óvulo/efeitos dos fármacos , Espermatozoides/metabolismo , Zona Pelúcida/metabolismo , Bloqueadores dos Canais de Cálcio/farmacologia , Diltiazem/farmacologia , Ácido Egtázico/farmacologia , Feminino , Humanos , Masculino , Mibefradil/farmacologia , Nifedipino/farmacologia , Pimozida/farmacologia , Verapamil/farmacologia
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