The following contains spoilers for love and death season 1

HBO love death concludes in the courtroom. Candy Montgomery (Elizabeth Olsen) details the events of her murder rampage by Getty Gore, which included an ax brought into the living room by Gore, a fight, and a trigger — “shhh” — that drove Candy into such a frenzy that she repeatedly stabbed Mountain. Psychotic break described in another testimony by Dr. Fred Faison as a dissociative event whose description was apparently bought by the jury and deemed sufficient for the defense to find Candy not guilty.

Candy Montgomery’s real-life case developed in a similar fashion when lawyer Don Crowder enlisted Dr. Candy’s support. Fred Faison, a psychologist and hypnotist, testifies in Candy’s defense. Through hypnosis, Faison reportedly helped Candy uncover moments of emotional trauma from the age of 4 when her mother really “shhh” Candy. At the booth, Candy said that Gore had also used the phrase and that Candy had “pissed off”.

The jury found Candy not guilty, apparently influenced by both testimony. (You can read about the real trial in 1984. Texas Monthly articles”Love and Death on Silicon Prairie Part 2: The Killing of Betty Gore“, itself taken from the book Proof of Love: A True Story of Suburban Passion and Death by John Bloom and Jim Atkinson.)

But while the lawsuit could end the events of the case and the source material for the HBO series, will it be the end of the show?

Want love death get season 2?

There have been no announcements for a second season yet. HBO himself only mentioned love death as a “limited series”, meaning it will most likely only run for one season.

If the series had continued the storyline, it would have done so without much source material. The lives of its protagonists were not widely publicized after the trial. Any future drama is likely to be fabricated.

We finally know how Botox gets into the neurons. The discovery could help develop an antidote for the molecule’s neurotoxic effects, which can lead to paralysis or even death.

Botox uses a type of botulinum neurotoxin, a highly toxic substance produced by bacteria. The toxin disrupts communication between neurons, resulting in muscle paralysis. In small therapeutic doses, it can ease muscle spasms, cure migraines, or more commonly, reduce wrinkles. However, in high doses, this molecule causes botulism, a potentially fatal disease that does not require large amounts of treatment.

Frederic Meunier from the University of Queensland in Australia and colleagues analyzed how botulinum neurotoxin type A enters neurons using a technique called single molecule imaging. This allowed them to capture the movement of molecules labeled with a fluorescent dye.

The researchers placed the toxin in a dish of rat neurons. They tuned one camera to a neurotoxin and the other to receptors in neuronal membranes, also labeled with different colors of dyes.

Previously, only two receptors, called polysialoganglioside (PSG) and synaptic vesicle glycoprotein 2 (SV2), were thought to be key for toxin entry into cells. But when they tracked SV2’s response to the toxin, they saw that it moved in tandem with another receptor known as synaptotagmin 1 (Syt1).

“Basically we started thinking, ‘Oh, this is weird,'” Meunier says. The researchers genetically modified rat neurons to prevent Syt1 from binding to SV2 and repeated the experiment. If you suppress the binding between these two receptors, the toxin can no longer enter the cell, Meunier says.

The same was true when they genetically modified neurons to lack PSG, indicating that all three receptors are required for botulinum neurotoxin type A to enter cells. Future drugs that block the binding of the three receptors could prevent neurons from being infected by the toxin, Meunier said.

“By understanding more about the mechanism of cell entry, we are one step closer to preventing cell entry and preventing botulism,” says Sabine Pellett at the University of Wisconsin-Madison.