Biomedical subjects

Sharif A Taha

Publications and source records attributed to Sharif A Taha.

6 recordsLinked to original sources

PubMed2006

Endogenous opioids encode relative taste preference.

Endogenous opioid signaling contributes to the neural control of food intake. Opioid signaling is thought to regulate palatability, the reward value of a food item as determined by orosensory cues such as taste and texture. The reward value of a food reflects not only these sensory properties but also the relative value of competing food choices. In the present experiment, we used a consummatory contrast paradigm to manipulate the relative value of a sucrose solution for two groups of rats. Systemic injection of the nonspecific opioid antagonist naltrexone suppressed sucrose intake; for both groups, however, this suppression was selective, occurring only for the relatively more valuable sucrose solution. Our results indicate that endogenous opioid signaling contributes to the encoding of relative reward value.

Animals↗

PubMed2006

Orexin A in the VTA is critical for the induction of synaptic plasticity and behavioral sensitization to cocaine.

Dopamine neurons in the ventral tegmental area (VTA) represent a critical site of synaptic plasticity induced by addictive drugs. Orexin/hypocretin-containing neurons in the lateral hypothalamus project to the VTA, and behavioral studies have suggested that orexin neurons play an important role in motivation, feeding, and adaptive behaviors. However, the role of orexin signaling in neural plasticity is poorly understood. The present study shows that in vitro application of orexin A induces potentiation of N-methyl-D-aspartate receptor (NMDAR)-mediated neurotransmission via a PLC/PKC-dependent insertion of NMDARs in VTA dopamine neuron synapses. Furthermore, in vivo administration of an orexin 1 receptor antagonist blocks locomotor sensitization to cocaine and occludes cocaine-induced potentiation of excitatory currents in VTA dopamine neurons. These results provide in vitro and in vivo evidence for a critical role of orexin signaling in the VTA in neural plasticity relevant to addiction.

Analysis of Variance↗

PubMed2006

Inhibitions of nucleus accumbens neurons encode a gating signal for reward-directed behavior.

The nucleus accumbens (NAcc) is critical in the control of goal-directed behavior. Pharmacological studies suggest that the NAcc may act in both instructive and permissive modes; however, previous electrophysiological studies in behaving rats have reported firing patterns consistent with an instructive, but not permissive, role for NAcc neurons. We now report that a subset of NAcc neurons shows a long-lasting inhibition in firing rate whose onset precedes initiation of goal-directed sequences of behavior and terminates at the conclusion of the sequence. Together with data from previous behavioral studies, this firing pattern suggests that, when active, these neurons tonically inhibit appetitive and consummatory behaviors and that, when inhibited, these neurons permissively gate those behaviors.

Animals↗

PubMed2005

Ocular dominance plasticity is stably maintained in the absence of alpha calcium calmodulin kinase II (alphaCaMKII) autophosphorylation.

The molecule alpha calcium calmodulin kinase II (alphaCaMKII) is known to play a fundamental role in the induction of many forms of synaptic plasticity. A major theory of alphaCaMKII function proposes that autophosphorylation of the molecule mediates not only the induction but also the maintenance of synaptic plasticity. To test this hypothesis, we assessed ocular dominance plasticity in genetically engineered mice that carry a mutation preventing autophosphorylation of alphaCaMKII. These mutant mice are deficient in plasticity after monocular deprivation, but a sufficiently long period of monocular deprivation will induce ocular dominance plasticity. After induction of ocular dominance plasticity, the stability of the induced changes was assayed after binocular deprivation. Plasticity in homozygous mutant animals was as stable as that measured in WT littermates; also, response characteristics did not differ between the two groups. Our results suggest that alphaCaMKII autophosphorylation is required for the induction of ocular dominance plasticity but is not needed for its stable maintenance thereafter.

Animals↗

PubMed2005

Encoding of palatability and appetitive behaviors by distinct neuronal populations in the nucleus accumbens.

Obesity is a major public health problem. Palatability (i.e., the reinforcing value of food, derived from orosensory cues) is a significant factor in determining food intake and contributes to increased consumption leading to obesity. The nucleus accumbens is a ventral striatal region that is important for both appetitive and consummatory behaviors and has been implicated in modulating palatability. In this study, we investigated palatability encoding in the firing of nucleus accumbens neurons in rats. Nucleus accumbens neurons with significant changes in firing rate during consummatory behavior displayed one of two principal firing patterns. Firing in one class of nucleus accumbens neurons was correlated with the palatability of sucrose reinforcers; changes in neural activity in this class consisted primarily of excitations. Within this group of neurons, a subset was sensitive to the relative value of sucrose reinforcers, as assessed by a behavioral contrast paradigm. A second and distinct population of nucleus accumbens neurons, with changes in firing that were pre-dominantly inhibitions, was not sensitive to reinforcer palatability; rather, these inhibitions were present even during unreinforced bouts of licking. In addition, the onset of these inhibitions typically occurred before the initiation of the licking behavior itself. We propose that two primary classes of nucleus accumbens neurons contribute to neural processing immediately before and during reinforcer consumption: inhibitions related to initiation and maintenance of consummatory behaviors and excitations that encode reinforcer palatability.

Animals↗

PubMed2005

Molecular substrates of plasticity in the developing visual cortex.

Ocular dominance plasticity may be the paradigmatic in vivo model of activity-dependent plasticity. More than four decades of intense research has delineated the network-level rules that govern synaptic change in this model. The recent characterization of a murine model for ocular dominance plasticity has facilitated rapid progress on a new front, extending our understanding of the molecular mechanisms underlying ocular dominance plasticity. In this review, we highlight recent advances in this research effort, focusing in particular on signaling pathways mediating shifts in ocular dominance, and mechanisms underlying the timing of the critical period.

Animals↗