Answer:
Frontal lobe
Explanation:
They areas of the cerebral cortex is divided into major four compartments.
- The frontal lobe
- The temporal lobe
- The parietal lobe
- The occipital lobe
The frontal lobe is situated at the anterior part of the brain whose main function is required in handling of mental processes such as thought, language, memory and speech. With the aid of the frontal lobe, we are able to think, communicate and process information.
The temporal lobe which is located beneath the frontal,parietal and occipital lobe helps to fine tune sounds and plays an integral role in hearing.
The parietal lobe is found at the back of the frontal lobe and also just above the temporal lobe helps to maintain body balance and trigger the body in cases of alertness.
The occipital lobe is located at the posterior region of the brain whose main function is reserved for visual perception.
Answer:
it britens up off the water My Dog Told Me
Long-term potentiation (LTP) is considered a cellular correlate of learning and memory. The presence of G protein-activated inwardly rectifying K(+) (GIRK) channels near excitatory synapses on dendritic spines suggests their possible involvement in synaptic plasticity. However, whether activity-dependent regulation of channels affects excitatory synaptic plasticity is unknown. In a companion article we have reported activity-dependent regulation of GIRK channel density in cultured hippocampal neurons that requires activity oF receptors (NMDAR) and protein phosphatase-1 (PP1) and takes place within 15 min. In this study, we performed whole-cell recordings of cultured hippocampal neurons and found that NMDAR activation increases basal GIRK current and GIRK channel activation mediated by adenosine A(1) receptors, but not GABA(B) receptors. Given the similar involvement of NMDARs, adenosine receptors, and PP1 in depotentiation of LTP caused by low-frequency stimulation that immediately follows LTP-inducing high-frequency stimulation, we wondered whether NMDAR-induced increase in GIRK channel surface density and current may contribute to the molecular mechanisms underlying this specific depotentiation. Remarkably, GIRK2 null mutation or GIRK channel blockade abolishes depotentiation of LTP, demonstrating that GIRK channels are critical for depotentiation, one form of excitatory synaptic plasticity.
Learn more about receptors here:
brainly.com/question/11985070
#SPJ4
