Introduction: Introduction: Several studies have demonstrated that orexins may regulate different forms of affective and cognitive processes during wakefulness. The Orbitofrontal Cortex (OFC) and Anterior Cingulate Cortex (ACC), as an essential part of the Prefrontal Cortex (PFC), have a crucial role in cognitive processes such as reward and decision-making. They also have a high amount of orexin receptor type 1 (OX1Rs). 
Methods: In the present study, we inhibited OX1Rs in this area after a 10-min baseline recording to find out the role of OX1Rs in the OFC neuron’s firing rate. Next, we inhibited the lateral hypothalamus (LH) as the primary source of orexinergic neurons. Afterward, using a single-unit recording technique in rats, we detected the effects of the lateral hypothalamus on the firing rate and activity pattern of the ACC or OFC neurons.
Results: Data showed that the blockade of OX1Rs in the OFC could excite 8 and inhibit 1 neuron(s) out of 11. In addition, the blockade of OX1Rs in the ACC could excite 6 and inhibit 3 neurons out of 10. LH inactivation excited 5 out of 12 neurons and inhibited 6 in the ACC. It also excited 8 and inhibited 6 neurons out of 14 in the OFC. These data suggest that the blockade of OX1Rs excites 72% of the neurons, but LH inactivation had a stimulating effect on only 50% of neurons in two main subregions of the PFC. 
Conclusion: Accordingly, PFC neurons may receive the orexinergic inputs from the LH and indirectly from other sources.

Introduction: The developing and promising optogenetic stimulation method can aid functional recovery by carefully regulating neuronal activity in brain circuits damaged by a stroke lesion. This investigation assesses the potential pretreatment effects of optogenetic stimulation on an ischemic stroke animal model. 
Methods: Lentiviruses containing pLenti-CaMKIIa-hChR2 (H134R)-mCherry-WPRE were administered to adult male Wistar rats. It was injected into the right striatum for this purpose. Twenty-six days after the virus injection, the animals were exposed to blue laser light for six days in a row for 30 minutes at a time. Twenty-four hours after the final light stimulation, the transient middle cerebral artery occlusion (tMCAO) was done. One day after reperfusion, the neurological processes and the size of the brain infarcts in ischemic rats were evaluated. The transcript levels of microRNAs 21 and 124a—epigenetic indicators for neuroprotection and neurogenesis—were also assessed in the striatum and hippocampus.
Results: Our findings suggested that pretreatment with glutamatergic striatum optogenetic stimulation could reduce neurological impairments in rats and boost neuronal survival in both striatum and hippocampal regions. Also, the expression of microRNA-21 (miR-21) in the striatum was significantly increased in rats that had been optogenetically stimulated. Additionally, miR-124a expression was elevated in both regions in rats given tMCAO, and pretreatment with optical stimulations may considerably lower its expression in the hippocampus.
Conclusion: According to our findings, optogenetic stimulation pretreatment of the striatum positively affects stroke recovery. The effect is partially mediated by altering miRNAs involved in neurogenesis and subsequently activating its downstream signaling cascade.