it is considered feedback mechanisms because the menstrual cycle only happens when the hormone is released, it causes the target tissues to react, that reaction is the feedback.
Answer:
It has been suggested that these kinds of lesions may be indicative of fighting with other members of its species or the attacks of predators
Explanation:
The Neandertals were exposed to very hard environmental conditions, thereby these lesions may be indicative of such conditions to which this species was exposed.
<span>The epidermis is mainly a composition of cells called keratinocytes. Defensive cells are known as Langerhans cells and are one of the three types of specialized epidermal cells, The epidermis is bonded to the dermis. Hairs grow in the dermis and up to the epidermis. So, the dermis and the epidermis both have cells and hair. </span>
Answer:
DNA.
Explanation:
Chromosones use a molecule called DNA to carry genetic information. A DNA exists in a cell's nucleus within structures named chromosones.
Good luck~!
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
